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NERVOUS SYSTEM

Organisms increase their chance of survival by responding to changes in their environment.


Stimulus: Change in an organisms environment that can be detected by receptor cells
Receptor: Specialised cell that detects a stimulus and initiates a nerve impulse by creating a generator
potential
Kinesis: Change in the speed of random movement in response to environmental stimulus (nondirectional response)
Example of Kinesis: woodlice who breathe using gills, use kinesis to stay in damp environments, in dry
environments, they move quickly so as to exit the dry environment and enter the
damp environment
Taxes: Directed movement toward or away from a stimulus (directional response)
Positive Taxes: Organism moves towards stimulus
Negative Taxis: Organism moves away from stimulus
Tropism: Response to stimulus by growing in a certain direction
Central Nervous System: The brain and the spinal cord
Peripheral Nervous System: Pairs of nerves that go to and from
the brain and spinal cord (the CNS)
Sensory Neurones: Carries nerve impulses from receptors TO
the CNS
Motor Neurones: Carries nerve impulses FROM CNS to the
effectors, it is of two types:
1) Voluntary Nervous System: Caries nerve impulses to body
muscles and is voluntary
2) Autonomic Nervous System: Carries nerve impulses to
glands, smooth muscles and cardiac muscle and is
involuntary

The Autonomic Nervous System is of two types:


1) Sympathetic Nervous System: Stimulates effectors and therefore speeds up any activity
2) Parasympathetic Nervous System: Inhibits effectors and therefore slows down any activity
The Sympathetic Nervous System and the Parasympathetic Nervous System are antagonistic. An
example is found in control of heart rate:
The heart is controlled by the Medulla Oblongata in the brain. The Medulla Oblongata speeds up heart
rate via the Sympathetic nerve and slows down the heart via the Parasympathetic nerve.
The Medulla Oblongata changes the heart rate in response to two receptors:
1) Chemoreceptors in the Carotid and Aortic arteries which are sensitive to a change in CO 2 level in
blood
When CO2 levels high (e.g. during exercise):
There is a change in pH which is detected by chemoreceptor
Chemoreceptor sends impulses to Medulla Oblongata
Medulla Oblongata increases frequency of impulses down Sympathetic nerve to SAN
Heart beats faster

Increased
blood flow
removes CO2
faster
2)
Pressure
receptors in
the
Carotid
Sinus
which are
sensitive to
a
change in
blood
pressure
If blood
pressure is
high,
pressure
receptors
cause
Medulla
Oblongata to
increase frequency of impulses down the Parasympathetic nerve to slow down the heart rate

Some other receptors:


1) Pacinian
Corpuscle; it is a
pressure
receptor found on the
skin and it detects SPECIFIC pressures and vibrations
Pressure on skin changes shape of pacinian corpuscle and Lamella layers are distorted
Distortion of lamella layers causes Stretch Mediated Sodium Channels to open which are
on the sensory neurone
Sodium Channel allow positive Na+ ions to enter the negative sensory neurone causing
depolarisation
This is known as a generator potential, if it reaches the threshold it triggers an action
potential
The amount of sodium channels that open depends on the pressure applied by the
stimulus
Therefore objects with small surface area cause a large stimulus as they cause a lot of
pressure, like a pin

Feature
Shape
Connections
Visual Acuity

Visual
Pigments
Distribution
Sensitivity

2) Rod and Cone Cells; they are photoreceptors that


are found on the retina and they detect light, they
then send impulses to the Optic Nerve which takes
it to the brain
Rods
Cones
Rod-shaped outer segment
Con-shaped outer segment
Many rods converge to one neurone
Only single cone per neurone
(RETINAL CONVERGENCE)
Low giving unclear image
High giving sharp image
As brain cannot distinguish between the
As brain can distinguish where the
separate rods that generated the
impulse came from as impulse was sent
impulse
by single cone
Rhodopsin
Iodopsin
Found evenly all over retina
Very sensitive to light due to RETINAL
CONVERGENCE
Black and white vision in poor light

Overall
Function
RETINAL CONVERGENCE:

All over retina but more concentrated at


fovea, therefore we move our heads to
see stuff properly
Only functions in bright light, i.e not as
sensitive to light
Seeing colour and detail in bright light

Stimulation of several rods results in enough Neurotransmitters being released to reach the threshold
value for an action potential in the bipolar neurone in low light
intensities (also called spatial summation)
Why we have a high degree of visual sensitivity in low light
levels:
1) Several rod cells connected to each bipolar cell
2) Additive effect of small amount of light striking several rod
cells
3) This creates a large enough depolarisation to generate
an action potential
Why we have a high degree of visual acuity:
1) Each cone cell connected to an individual neurone
2) Light strikes individual cone cell to generate a separate
action potential
3) Very small area of
retina stimulated,
so very accurate
vision
Reflex Arc/Spinal Reflex
(this is a special pathway
of neurones):
Rapid automatic
response to a
stimulus
Involves just 3
neurones
Does not involve the brain
One neurone is inside the Spinal Cord which is called the Intermediate/Relay Neurone, the other
two neurones are the Sensory and Motor neurone
They are under genetic control and are effective from birth
The sequence is:
Stimulus Receptor Sensory neurone Intermediate neurone Motor neurone Effector
Response
Importance of the Reflex Arc/Spinal Reflex:
1) Brain is not overloaded with situations in which the response would be the same
2) Brain is free to carry out more complex responses
3) Protects from harmful stimuli as it is fast
Neurone: specialised elongated cell that is capable of carrying impulses from one end to the other
Along the axon, there is:
1) Active Transport: Na+/K+ pump; 3Na+ leaves axon and 2K+
enters. Therefore the p.d. of the axon is -70mV.
The splitting of ATP controls this active transport.
2) Facilitated Diffusion: There are Sodium and Potassium ion
channels (INTRINSIC PROTEINS) in the membrane. The Na +
ions come into axon through their channel and K + ions
come out of axon through their channel. There are more K +
channels than Na+ channels. At resting, both channels are
closed, but they still leak.
Therefore, the resting potential is -70mV
The Myelin Sheath: provides protection and electrical insulation

Action Potential:
1) Depolarisation:
Neurone stimulated causing a few chemical-gated Na + channels to open allowing Na+ ions
to diffuse into axon
If stimulus large enough to make enough Na+ move in that the potential changes from -70
to -50 (threshold value), then all the other Na+ channels open that are VOLTAGE gated
More Na+ enter (positive feedback change creating
more change)
2) Repolarisation:
When potential reaches +40mV, then K+ channels
open causing K+ to rush out making potential
negative again
3) Hyperpolarisation:
The K+ channels remain open a little longer causing a
little extra K+ to leave, making the potential -80mV
At -80mV, the K+ channels close and the Na+/K+
pump restores the potential to -70mV using
ATP
All action potentials are the same size
Speed of transmission:
1) Axon Diameter: the larger, the quicker the impulse
WHY?
Less resistance to flow of ions in/out of axon,
therefore depolarisation reaches other parts of
neurone cell membrane quicker. Also this allows
less leakage of ions.
2) Temperature: the higher, the quicker the impulse
WHY?
Ions diffuse faster in facilitated diffusion, also in
Na+/K+ pump is controlled by active transport
which needs ATP from respiration, respiration
depends on enzymes which rely on temperature
3) Saltatory Conduction; action potential goes from one Node of Ranvier to another due to
insulating myelin. Therefore action potentials can only occur at Nodes of Ranvier
Therefore is something has a very low temperature, to compensate, it may have a large axon diameter.
In exam, if asked to explain Depolarisation:
1) Sodium ion channel proteins open allowing Sodium ions to enter
2) Changes membrane potential and reaches
threshold
3) More channel open this is called positive
feedback
In exam, if asked to explain Repolarisation:
1) Potassium channels open
2) Potassium leaves axon
3) Sodium channels close
Always say nerve IMPULSES, never nerve signals,
etc.
All or nothing principle: Nerve impulses cannot
vary in size, instead the strength of stimulus is
indicated by frequency
Purpose of Refractory Period:
1) Separates nerve impulses as another nerve
impulse cannot happen during the
refractory period
2) Limits number of impulses per second
Synaptic Transmission:
Process of transmission across a neuromuscular junction:
1) Nerve impulse depolarises the presynaptic membrane
2) Calcium channels open allowing Ca2+ ions to enter presynaptic membrane
3) Synaptic vesicle move towards presynaptic membrane
4) Release of transmitter across cleft using exocytosis
5) Transmitter attaches to receptor sites on post synaptic membrane

6) Sodium channels on post synaptic membrane open causing


an influx of sodium ions resulting in a depolarisation
7) Neurotransmitter broken down by enzyme
Acetylcholinesterase in the cleft
8) The products are reabsorbed by pre-synaptic knob where
they are re-synthesis using energy from ATP in
mitochondria
Temporal Summation: where two or more impulses arrive in quick succession down the same neurone,
due to the post synaptic membrane having a
high threshold
Spatial Summation: where two or more impulses arrive at the same time down different neurone, due
to the post synaptic membrane having a high
threshold
How transmission of information in the nervous system may be modified by summation:
1) Summation is the addition of a number of impulses converging on a single post synaptic neurone
2) This allows integration of stimuli from a variety of sources, this is called SPATIAL SUMMATION
3) This allows weak background stimuli to be filtered out before reaching the brain, this is called
TEMPORAL SUMMATION
How a neurotransmitter contributes to a synapse being unidirectional:
1) Neurotransmitters released from presynaptic neurone
2) Diffusion of neurotransmitter from high concentration to lower concentration
3) Only the synaptic neurone contains receptors which the neurotransmitter can bind to
How inability to break down Acetylcholinesterase (enzyme) will lead to death:
1) Acetylcholine (neurotransmitter) will not be broken down and will stay bound to receptor
2) Na+ ions continues to enter and continues to cause depolarisation
3) Muscles stay contracted
Inhibitory Ion Channel Synapses: Neurotransmitter is Cl- ions which causes hyperpolarisation making
action potential unlikely
Skeletal Muscle: You need to know about the skeletal muscle for the exam
Muscle is made up of large bundles of long CELLS called muscle fibres, the membrane if muscle fibre
CELLS is called sarcolemma, bits of sarcolemma fold inwards into a sarcoplasm, these bits are called Ttubules and they help to spread electrical signals, there are sarcoplasmic reticulums that run through
the sarcolemma which release Ca2+ ions needed for contraction. The sarcolemma also has the
myofibril, where the main muscle contractions take place. LEARN THIS PICTURE:

Types of Muscle Fibre:


1) Slow-twitch fibres: FOUND IN HEART
Contract more slowly and are provide less powerful contractions over a long period,
therefore for endurance
Suited to their role by being adapted for aerobic respiration by:
1) Large store of myoglobin
2) Supply of glycogen to provide source of metabolic energy
3) Supply of blood vessels to deliver good amount of Oxygen and Glucose to maintain
aerobic respiration
4) Numerous mitochondria to provide AT

The mitochondria in the slow-twitch fibre will be distributed to the edges of the fibre because:
Allows rapid diffusion of Oxygen
Oxygen is used in the mitochondria
5) Site for Krebs Cycle and
Electron Transport Chain
2) Fast-twitch fibres: FOUND IN FINGER
MUSCLES, ARM MUSCLES
Contract more rapidly and
provide more powerful
contractions over a short
period, therefore for intense
exercise
They are adapted to their role
for anaerobic respiration by:
1) Thicker and more
numerous myosin
filaments
2) High concentration of enzymes used in aerobic respiration
3) High store of Glycogen which can be broken down into glucose, there is a high store
because anaerobic respiration is not very efficient

Muscle Contraction:
This is how a myofibril inside a muscle fibre looks:

How Myosin and Actin really looks:

The Myosin:
1) has a tail (fibrous protein)
2) has a head (globular protein) which contains ADP
Actin:
A globular protein which has ACTIVE SITES that are covered by a protein called TROPOMYOSIN
When muscle contracts:
1) I-Bands become narrower
2) Z-Lines move closer
together

3) H-Zones become narrower


4) A-Bands remain the SAME
(This fact proves that the
myosin does not shorten
and therefore is a Sliding
Filament Mechanism)
Overall, the whole sarcomere gets shorter

Sliding Filament Theory:


1) Action potential arrives through neuromuscular junction (motor neurone meets muscle fibre)
2) Action potential goes through tubules which are connected to the endoplasmic reticulum of the
muscle
3) Endoplasmic reticulum has actively absorbed Ca2+, the action potential opens Ca2+ channels on
the endoplasmic reticulum
4) Ca2+ diffuses out of endoplasmic reticulum into muscle cytoplasm

5) Ca2+ ions cause TROPOMYOSIN protein on the actin to pull away, uncovering the active sites on
the actin
6) Myosin head combines with the active site on the actin through the help of ATP forming
actinomyosin bridge
7) The myosin head change their angle pulling actin filament INWARDS, as they do this, the ADP on
the myosin head is released
8) ATP attaches to myosin head causing it to detach from active site of Actin
9) Ca2+ ions activate enzyme ATPase, which hydrolyses the ATP on the myosin head to ADP whilst
releasing energy to allow myosin head to retain its angle
10)
Myosin head now attaches itself to another active site on the actin that is further along
the actin filament
How you write the above in the exam:
1) Calcium ions bind to troponin
2) This removes the TROPOMYOSIN in the actin, therefore exposing actin binding sites
3) ATP allows myosin to bind to actin
4) As myosin attaches, it changes its angle causing the actin to slide along and also causing the
release of ADP
5) ATP combines to myosin allowing detachment of myosin from the actin binding site
6) ADP combines with myosin therefore causing normal angle to be assumed
7) Phosphocreatine allows regeneration of ATP without respiration by releasing Pi which combines
with ADP to form ATP
Energy for muscle contraction is provided by: hydrolysis of ATP to ADP and Pi
Energy (ATP) is used for:
1) Attachment between actin and myosin
2) Pulling of actin
3) Detachment of myosin heads
4) To move myosin head back to original position
5) Absorption of Ca2+ into endoplasmic reticulum by active transport

Sometimes a muscle may be so active


that Oxygen is rapidly used up and
therefore ATP has to be generated using a
chemical called Phosphocreatine.
Phosphocreatine is stored in muscle and
breaks down into ATP when Oxygen is
being rapidly used up. When the muscles
are relaxed, the phosphocreatine is made,
and when short burst exercise takes
place, e.g. 100m sprint, then
phosphocreatine is converted to loads of
ATP
They could give a vague statement like:
How energy released in mitochondria
during respiration produces contraction of
a muscle fibril:
1) Hydrolysis of ATP releases energy
2) Energy used to form cross-bridges
between actin and myosin
3) Action moves towards centre of
sarcomere

HOMEOSTASIS (POSITIVE & NEGATIVE FEEDBACK)

Homeostasis: Ability of an organism to maintain a constant internal environment


Negative Feedback: When a change to the normal initiates a response which reduces the effect of the
change
Positive Feedback: change stimulates further change; can be dangerous if it is not natural; often
associated with breakdown of control systems
Two example of Negative Feedback:
1) Regulating Body Temperature
Endotherms (warm blooded): control their body temperature by physiological and behavioural means,
thus keeping it constant

Ectotherms (cold blooded): control their body temperature by behavioural means only, NO
physiological cooling/heating mechanism, therefore usually Air Temperature =
Body Temperature
Temperature is detected by hypothalamus which has a heat loss and heat gain centre
The skin plays an important role for regulating temperature as it serves as a receptor.
When we are too cold, heat gain centre in hypothalamus detects this via a receptor in the skin and
inhibits the heat loss centre, then the heat gain centre sends nerve impulses to appropriate part of
the body to do the following:
1) Shivering: creates heat
2) Vasoconstriction: constriction of arteriole walls allows less heat in blood to be lost from skin
3) Making your hair stand on end: traps layer of insulating air
4) Increasing metabolic and respiration rate: achieved via hormones; respiration and
metabolism releases heat
(REMEMBER: metabolic rate is measured by measuring the uptake of Oxygen or
production of CO2)
5) Less blood flow to surface capillaries
You can also add to this list: putting on clothes
There is an advantage and disadvantage that as humans we are able to maintain body temperature
when it is cold:
ADVANTAGE: enzyme reactions are not affected and we are more independent of the environment
DISADVANTAGE: requires more respiration and therefore more loss of energy
Role of blood vessels in conserving heat:
1) Vasoconstriction of arterioles
2) Therefore less radiation
3) Therefore less blood to the surface
When we are too hot, heat loss centre in hypothalamus detects this due to a receptor in the skin via
nervous impulses, and inhibits the heat gain centre, then the heat loss centre sends nerve impulses
to appropriate part of the body to do the following
1) Sweating: cools the body as it evaporates, this is because evaporation removes heat from the
skin, higher rate of sweating leads to lower skin temperature, in the exam if it mentions hot, dry
conditions, think heat loss by evaporation via sweating, sweat leaves the body through
osmosis, this is why humidity causes heat stroke or HYPERTHERMIA, because humid air has a
lot of water particles hence reducing water potential gradient, therefore body struggles to sweat
by releasing water via osmosis, therefore without sweating, the body is burning from inside.
This is also why we drink more when its hot, because when you sweat youre losing water; therefore
water is needed for replacement.
2) Vasodilatation: dilation of arterioles, allowing heat in blood to be transferred to sweat
3) More blood flow to surface capillaries
4) Lowering of hairs causes less insulation
5) Decreasing metabolic rate and respiration rate
You can also add to this list: taking off clothes and migrating, also our ears are designed with a large
surface area so as to allow heat loss
When we measure body temperature, put a thermometer in our mouths instead of on our skin because:
Skin temperature fluctuates more as it is more affected by environment
Why we produce heat during exercise:
1) Respiration is carried out for muscular activity
2) However respiration is INEFFICIENT and therefore releases extra energy as heat
Why we get tired from exercise in hot conditions quicker than we do when it is cold:
1) The heated conditions cause vasodilatation and cause more blood flow to the surface capillaries
2) This results in less blood flow to muscles requiring oxygen
Large mammals with small surface area to volume ratio will heat up a lot quicker than smaller animals
as they have reduced heat loss through skin, therefore large animals will activate their heat loss
centre in hypothalamus a lot quicker than small mammals
As temperature increases, respiration rate increases in ECTOTHERMS, (in us it decreases), this is
because:
1) Increased temperature increases kinetic energy
2) Increased kinetic energy increases rate of reactions
3) More ATP is produced
4) Therefore more ATP used, therefore higher respiration rate required to remake lost ATP
Importance of maintaining a constant body temperature (i.e. importance of homeostasis):
1) If body temperature is too high, the excess heat denatures active sites of enzymes
2) Therefore substrate can no longer form a complex with it therefore reactions are ceased
3) If body temperature is too low, there is too little kinetic energy, therefore molecules move too
slowly

4) Therefore few collisions and thus fewer enzyme-substrate complexes formed, therefore too slow
reactions
The above two situations are both NEGATIVE FEEDBACK
Why the activity of Ectotherms that live in deserts varies so much:
1) Their body temperature varies with that of environment
2) Temperature of desert fluctuates greatly
3) Metabolic reactions inside the Ectotherm are controlled by enzymes
4) Enzyme activity changes according to body temperature
5) Speed of bodily actions dependent on metabolic rate
6) Reptiles seek shade when hot and seek Sun when cool
How the movement of Ectotherms between Sun and shade is related to their body temperature:
The further away the temperature is from the optimum body temperature, the greater the movement
When Ectotherms feel too hot, they may start panting (behavioural) to help cool down, panting helps
because:
1) It causes evaporation of water from lining of mouth
2) Heat transferred from blood
2) Regulating Blood Glucose Levels
Hyperglycaemia: too much glucose in blood, lowers water potential of blood and produces symptoms of
thirst
Hypoglycaemia: too little glucose in blood, produce symptoms of dizziness, tiredness, etc. As the brain
does not have glucose
Pancreas:
Contains Islets of Langerhans that make two types of cells:
-cells produce the hormone glucagon
-cells produce the hormone insulin
These hormones are antagonistic
Second-Messenger hormones: hormones which bind to a receptor on the membrane which then
activates an enzyme
Glycogenesis: the production of glycogen by the polymerisation of glucose
Glycogenolysis: the breakdown of glycogen to release glucose
Gluconeogenesis: the production of glucose from non-carbohydrate sources
If blood glucose levels too high:
1) -cells detect the rise and secret insulin (notice how the -cells are the RECEPTORS and
EFFECTORS.)(-cells are inhibited)
2) Insulin fits into specific receptor proteins on membranes of cells
3) This causes extra glucose channels to open allowing glucose to enter cell via facilitated diffusion
(this is done through the second messenger IRS) and allow it to become metabolised, in Liver
cells, insulin causes IRS to activate glycogen synthase enzyme which causes glucose to be
converted to glycogen (Glycogenesis)
4) Once glucose levels stabilise, -cells reduce secretion of insulin
Type 1 Diabetes: body cannot make insulin; therefore glucose cannot pass from blood into cells,
therefore starving the cells
Type 2 Diabetes: body does not make enough insulin or the receptors are not responding well to
insulin, therefore glucose cannot be fully passed from blood into cells which is the job of
the insulin
Therefore, taking insulin tablets has little effect on type II diabetes as type II diabetes is a failure to
RESPOND to insulin
Usually, diabetic people feel very thirsty, this is because of osmosis of water from cells to the blood
which has lower water potential due to it containing high levels of glucose
How diet and exercise may help maintain low glucose concentration in the blood of a type II diabetic
person:
1) Eat polysaccharides therefore slower digestion, therefore no surge in blood sugar level
2) Exercise increases respiration
If blood glucose levels too low:
1) -cells detect the low levels and secret glucagon
2) Glucagon fits into specific receptor proteins on membrane of cells that CONTAIN glycogen which
are called liver cells
3) Glucagon activates an enzyme that converts glycogen to glucose (Glycogenolysis) and
proteins/lipid to glucose (Gluconeogenesis), glucose can pass through cell membrane, therefore
increasing glucose concentration of blood
4) Once glucose levels stabilise, -cells reduce the secretion of glucagon

REMEMBER: As mentioned, the cells that contain the glucagon receptors are only those which contain
glycogen, one of the places where these cells are found is in the LIVER

The above two situations were examples of NEGATIVE FEEDBACK, the high glucose concentration is
reduced and low glucose concentration is increased through negative feedback.
Usually, after eating something, your glucagon levels will do down as glucose levels will be going up.
Even though people with diabetes have high glucose levels, their glucose levels can still go down
without insulin, this is through:
1) The loss of glucose in urine
2) Glucose gets used up in cell respiration
When a diabetic person takes an insulin injection, and then does not eat a meal, his glucose levels do
not fall dangerously low because:
1) Glucagon is still active which produces glucose using Glycogenolysis
2) Person is not active so little glucose used up in respiration
There is one other hormone that can increase glucose levels:
Adrenaline: 1) Activates an enzyme called Adenyl Cyclase that causes the breakdown of glycogen to
glucose
2)
Glucose produced is then used
for
respiration (this is why you can
run much
faster with adrenaline)
3)
Inhibits enzyme that synthesises
glycogen
from glucose
In any experiment
on blood glucose
concentrations, we
ensure the candidates are not
fed at least 6 hours
before the test because:
1) Glucose in
food would affect results
2) Allows time
for blood glucose level to return
to normal
One example of
Negative and Positive Feedback
working together:
Menstrual Cycle:
There are 4 key hormones (REMEMBER: hormones are globular proteins!):
1) FSH: stimulates development of follicles in ovary, the follicle contain eggs, and stimulates
follicles to produce oestrogen
2) Oestrogen: causes rebuilding of uterus lining and inhibits LH and FSH production (NEGATIVE
FEEDBACK), on day 10, oestrogen reaches a critical point and it stimulate pituitary gland to
release FSH and LH (POSITIVE FEEDBACK)
3) LH: causes one of the follicles in the ovary to release its egg (ovulation-day 14) and stimulates
empty follicle to develop into a structure called Corpus Luteum which produces progesterone,
therefore evidence of ovulation will be a peak in LH and a drop in the diameter of the follicle
which is now empty
N.B. The diameter of a follicle will be largest just before ovulation
4) Progesterone: maintains lining of uterus in readiness for sperm and inhibits production of FSH
and LH from pituary gland (NEGATIVE FEEDBACK)
How you describe Menstrual Cycle in the exam:
1) FSH increase causes follicles to develop
2) Developing follicles produce Oestrogen
3) Oestrogen inhibits FSH
4) High Oestrogen stimulates FSH and LH release from pituary gland
5) LH causes ovulation which results in the production of Progesterone

The corpus Luteum is essential as it produces Progesterone which maintains the uterus lining.
Although fertilisation happens after ovulation, sexual intercourse can take place a day before ovulation
as sperm can survive for a few days.
If egg is not fertilised:
1) Corpus Luteum degenerates and stops producing progesterone
2) No more progesterone causes uterus lining to break and also allows FSH to be released which
causes follicle development, thus restarting the cycle
Evidence that fertilisation has not occurred:
1) Progesterone levels drop
2) Another follicle develops
If egg is fertilised:
1) A hormone called Human Chorionic Gonadotrophin (HCG) acts as a signal to Corpus Luteum to
keep producing progesterone
2) Progesterone maintains uterus lining
How would you know from a graph that fertilisation has occurred/not occurred:
See if the Progesterone concentration has been maintained/ has fallen
How FSH release is controlled by negative feedback (i.e. how do we make sure FSH doesnt keep
rising):
1) FSH stimulates development of follicles which release Oestrogen
2) Oestrogen inhibits FSH
How LH concentration is controlled by negative feedback (i.e. how do we make sure FSH doesnt keep
rising):
1) LH rise causes a rise in Progesterone
2) Progesterone inhibits LH
Role of LH and FSH in the Menstrual Cycle:
1) FSH stimulates growth of a follicle which produces Oestrogen
2) LH causes ovulation
3) LH stimulates formation of Corpus Luteum which produces Progesterone
4) Fall in FSH would result in no Oestrogen
Role of Progesterone in the Menstrual Cycle:
1) Maintains uterus lining
2) Stimulates growth of blood vessels in uterus lining
REMEMBER: ovulation will coincide with a rise in progesterone and a fall in LH because:
1) Progesterone is produced by the corpus luteum
2) Corpus Luteum is formed after ovulation
3) LH is now inhibited by the Progesterone produced
How excess Oestrogen causes infertility (some oral contraceptives contain oestrogen):
1) Oestrogen inhibits production of FSH through negative feedback
2) Therefore prevents follicles developing
3) Oestrogen inhibits LH, this prevents ovulation
Some oral contraceptives add Progesterone as well as Oestrogen as progesterone also inhibits FSH and
LH, FSH causes follicle development and LH causes ovulation.
Why women who have passed menopause will have low levels of oestrogen:
1) Their follicles are no longer active
2) Therefore oestrogen is secreted by follicles, due to the follicles being inactive, the oestrogen
concentration is low
3) Therefore oestrogen is not enough to inhibit pituary gland

4) Therefore there will remain a high concentration of FSH (which wont do anything because
follicles are inactive)
For a girl, the first ovulation takes place late in puberty, this is advantageous because:
Ensures sex organs are mature before conception can occur
N.B. When
HORMONAL CO-ORDINATION
NERVOUS CO-ORDINATION
male sweat
is
exposed to
Slow
Rapid, i.e. response is rapid
a
female, the
Broadcast
Direct
pheromones
Long term
Short-lived/Short duration
in
the male
Chemical
Mainly electrical
sweat will
Delivery via blood vessels
Delivery via nerves
stimulate
Interacts with receptors in membrane of
Causes depolarisation of target cell
the
target cell
membrane
Hypothalamus to produce FSH.

Plant Growth Factors:


1) They are a type of hormone, but unlike animal hormones, they are made by cells throughout the
plant rather than by particular organs
2) Unlike animal hormones, some plant growth factors actually affect the tissues that release them
3) They move around the plant using diffusion
Difference between Hormones and Chemical Mediators:
1) Hormones have widespread effect
2) Hormones only affect cells with right receptor
3) Hormones travel in blood whereas Chemical Mediators travel by diffusion
EXAMPLE OF PLANT GROWTH FACTOR: Idoleacetic Acid (IAA), this growth factor causes GROWTH
INHIBITION wherever it is found, if IAA is found in the root tips; it
causes the root tip to move towards gravity
How IAA causes root tips to grow towards gravity:
1) IAA moves to lower side of root and inhibits growth of lower side
2) Upper side grows more therefore causing the root to bend downwards

REMEMBER: Auxin is produced by the root TIP; therefore if I cut of the tip, the root will continue to grow
horizontally
When light is directed towards the plant, IAA builds up on the shaded side causing the shaded side to
elongate, resulting in the plant bending towards the light. This is called POSITIVE PHOTOTROPISM
Why growth of IAA on the shaded side helps to maintain the leaves in a favourable environment:
1) Causes plant to bend towards light
2) Light is required for photosynthesis
IAA can be sprayed onto plants leaves, allowing it to diffuse through the leaves; however, the surface
of the leaves has to be thin to allow a short diffusion pathway.
REMEMBER: Even plants can reproduce sexually
Why plants that reproduce sexually are very variable in their yield:
1) Meiosis is involved which includes independent assortment and crossing over

2) Fertilisation is random
However plants grown from tissue culture will be clones as they are produced via mitosis.
Paracrine Signalling: communication between close cells using chemicals called Local Chemical
Mediators

Chemical mediators are released into tissue fluid but not into the blood; therefore they only
affect cells that are in their immediate vicinity
Examples of chemical mediators are Histamine and Prostaglandins

DNA TRANSCRIPTION & TRANSLATION

DNA: made up of two polynucleotides containing sequences of nucleotide bases that determine the
sequence of amino acids
Protein is made in the ribosomes, but DNA is too large to leave the nucleus, therefore mRNA takes the
code out of the nucleus through the nuclear pores.
Gene: A specific section of a chromosome that codes for an amino acid
TRICK QUESTION: why are the percentages of bases from the middle part of the chromosome and the
end part different?
They are different genes! Therefore they will have different base sequences

Genetic Code: Sequence of nucleotide bases on the mRNA that code for amino acids
Genetic Code:
1) Universal; same codons code for same amino acid
2) Non-overlapping; each base is part of only one codon
3) Degenerate; some amino acids are coded for by several different codons
4) Three codons do not code for amino acid, they are called stop codons and mark the end of a
polypeptide chain
Codon: Sequence of three nucleotide bases on the mRNA that code for a single amino acid
Anticodon: Group of bases complimentary to bases on the mRNA/ complimentary to codon
Introns: Non-coding, DNA, this means DNA that does not code for a protein
Degeneracy of DNA Code: some amino acids coded for by more than one triplet, the degeneracy will be
on the third base, i.e. UGU, UGC, UGA, UGG all code for the same amino acid and UUU, UUC, UUA, UUG
all code for the same amino acid
RNA is of two types:
1) mRNA
2) tRNA
In RNA (whether its mRNA or tRNA), the base Thymine is replaced with Uracil
Differences between DNA and RNA:
1) DNA has deoxyribose, RNA has ribose
2) DNA has Thymine, RNA has Uracil
3) DNA is double stranded, RNA is single (even tRNA is considered single stranded because it has
just been folded up)
4) DNA is larger and longer, RNA is smaller and shorter
5) There is only one type of DNA, whereas there are 2 types of DNA
6) In DNA, The amount of Adenine = amount of Thymine and amount of Guanine = amount of
Cytosine, in RNA there is variable amounts
Similarities between DNA and RNA:
1) Both have Phosphate
2) Both have Adenine, Cytosine and Guanine
3) Both have nucleotides
4) Both
Protein Synthesis has two stages:
1) Transcription: base sequence on a particular gene is copied onto molecules of mRNA. This takes
place in nucleus.
2) Translation: base sequence on the mRNA is used to assemble a protein using tRNA. This takes
place ON ribosomes.
Transcription:
1) Transcription Factors allow DNA Helicase to break the hydrogen bonds between the bases in the
DNA molecule
2) The enzyme RNA Polymerase moves along one of DNA strands (this strand is called the
sense strand), known as template strand, and free nucleotides to join with the complimentary
bases on the template strand
3) RNA POLYMERASE JOINS THE NEW NUCLEOTIDES TOGETHER TO FORM MRNA
4) As RNA Polymerase moves along the DNA strand, the DNA strands behind it rejoin, like a zip
5) When the RNA polymerase reaches a stop triplet code, it detaches, and thus we have a premRNA strand
6) Pre-mRNA contains Introns, which do not code for an amino acid, therefore we must remove
Introns using splicing
7) The pre-mRNA is spliced by cutting out the Introns and joining the exons together to form mRNA
using proteins called snurps (REMEMBER: Prokaryotic DNA does not have Introns)
REMEMBER: DNA is made up of two polynucleotide strands, the sense strand and antisense stand,
mRNA is transcribed from the DNA sense strand, which CONTAINS THE GENETIC CODE.
Also notice how in DNA Replication, DNA Polymerase was involved, here RNA Polymerase is involved,
theyre not the same.
Role of RNA Polymerase in transcription:
Attach nucleotides to form a strand
Why the number of bases in the DNA sense strand is the same as the number of bases in the DNA
antisense strand:
Complimentary sense strand (obvious)
Why the number of bases in the DNA sense strand is not the same as the number of bases in the mRNA
strand:
DNA contains Introns which are non-coding
Role of DNA antisense strand:
1) Provides DNA with stability

2) Acts as a template for a new strand in DNA Replication


Why some errors during copying of a sequence of bases are not severe:
1) Some amino acids have more than one code, therefore error may not affect amino acid
2) If amino acid is changed, the new amino acid may not affect the functioning of the protein, i.e.
the changed amino acid was not an important amino acid in terms of the structure and function
of the protein
Translation:
1) mRNA leaves nucleus via nuclear pore and enters ribosome where proteins are made which are
to be used in the cell
2) Each codon on the mRNA has a complimentary anticodon on the tRNA
3) Each amino acid has its own tRNA molecule which it attaches to
4) Therefore each tRNA brings an amino acid to the mRNA which it attaches to using the anticodon
via HYDROGEN BONDS
5) The ribosomes
move along the mRNA
bringing two tRNA
molecules (which contain
the amino acid) at
a time each pairing up
with
corresponding codons on
the mRNA
6) When two amino
acids are together on the
tRNA, they are
joined together with a
peptide bond
using enzymes and ATP
7) As the two amino
acids join, the ribosome
moves onto the
next two codons and tRNA
molecules leave
to collect amino acids

8) This continues until the ribosome reaches a stop codon


9) Usually there is modification after translation too, enzymes add specific methyl or phosphate
groups to amino acids
Role of tRNA:
1) Carries specific amino acid to the polypeptide chain, the amino acid is attached to the tRNA by
specific aminoacyl tRNA synthase enzyme
2) Has an anticodon which is complimentary to the codon on the mRNA
3) Attaches to ribosome and holds amino acids in place
Similarities between DNA REPLICATION (making another copy of DNA) and Transcription (making
protein):
1) Both involve Hydrogen bonds breaking between complimentary bases
2) Both involve complimentary nucleotides acting as templates
Differences between DNA REPLICATION (making another copy of DNA) and Transcription (making
protein):
1) Transcription involves Uracil, Replication involves Thymine
2) One strand used in transcription, two strands used in replication
3) DNA used in replication, mRNA used in Transcription
Why only 1% of genetic information of a mammalian cell is transcribed, the rest is untouched:
1) Only some genes are transcribed
2) Different proteins required by different cells, therefore only some genetic information needed
3) Some DNA does not code for anything (Introns)
Features of a gene that enables it to code for a protein:
1) Gene is a length of DNA
2) Gene is a sequence of bases

3) Gene has a triplet code that codes for an amino acid


4) Degenerate code allows different triplets to code for the same amino acid
How different base sequences code for different proteins:
1) Proteins are made of amino acids
2) Each amino acid has its own triplet code
How copying bases more than once may give rise to a difference in the protein:
It Changes base sequence of later triplets

How a protein is made by a gene (SIMPLIFIED):


1) Growth factors allow a gene to be switched on
2) Unzipping of DNA involves the breaking of hydrogen bonds using DNA Helicase
3) Free mRNA nucleotides assemble and form complimentary base pairs
4) RNA Polymerase joins newly formed mRNA nucleotides
5) mRNA leaves nucleus via nuclear pore and enters ribosome
6) mRNA has a codon which is complimentary to the anticodon of a specific tRNA molecule which is
associated with a specific amino acid, therefore mRN attaches to its complimentary tRNA
7) Once amino acids come together, peptide bonds are formed between them
8) tRNA detaches and collects another amino acid
9) Ribosome moves along mRNA
10)
Polypeptide will be complete when a stop codon is reached
REMEMBER: We can convert one protein to another protein by re-arranging its amino acids.
mRNA:
Single helix, each nucleotide contains: 1) Nitrogenous base 2) Phosphate 3) RIBOSE (not
deoxyribose)
Involved in transcription of DNA bases
Leaves nucleus via the pores and enters cytoplasm where it associates with the ribosomes
mRNA is suited to its function because:
1) Possesses correct sequence of triplets that code for specific polypeptides
2) Easily broken down, therefore exists only while it is needed
How tRNA is suited to it functions:
1) End chain for attaching amino acids
2) Anticodon for pairing with codon of mRNA
Difference between tRNA and mRNA:
1) mRNA has no base-pairing/mRNA is linear, whereas tRNA is folded via base-pairing
2) tRNA is cloverleaf shape whereas mRNA is straight
3) mRNA has no binding site for amino acids whereas tRNA does
4) more types of mRNA than tRNA
5) tRNA is a fixed length whereas mRNA is variable length

GENE MUTATION
Gene Mutation: change to one or more bases or arrangement of bases
1) Nonsense Mutation: a base changes resulting in the formation of a stop codon, therefore
polypeptide production stopped prematurely
2) Mis-Sense Mutation: a base changes resulting in a different amino acid being coded for
How a Mis-Sense Mutation causes only one different amino acid in the polypeptide chain:
1) Three bases code for one amino
2) However here only one codon is changed, i.e. there is NO frame shift
3) Therefore the other codons are not affected
3) Silent Mutation: a base changes however the resulting codon still codes for the same amino acid
due to the degeneracy of the generic code, this substitution will be on the third base as
degeneracy is found on the third base
4) Deletion Mutation: when a base/s is completely removed from the DNA sequence, resulting in a
frame shift to the left
Why mutation involving deletion of a base is more severe than mutation involving substitution of a
base:
1) Deletion causes frame shift
2) This changes many amino acids

3) Substitution alters only one amino acid


4) Substitution at times causes no problems due to the degeneracy of the triplet code
So overall, mutation affects the structure of a gene by adding, substituting or deleting a base.
How mutation of a gene may result in a non-functional enzyme:
1) Mutation causes change in base of DNA
2) This results in a change in base sequence of mRNA, thus changing the codons
3) Incorrect tRNA molecules coded for
4) Incorrect amino acids coded for
5) Different amino acids results in different tertiary structure of the enzyme
6) The different tertiary structure means the active site has a different shape due to different bonds
being formed
7) The active site shape no longer complimentary to shape of substrate
How mutation of base may cause the production of a complete new protein (a bit like the above):
1) Base sequence is changed
2) Different mRNA
3) mRNA attracts different tRNA
4) Different amino acid is inserted into protein
Why mutant genes are more easily identified in haploid cells than diploid cells:
1) Haploid cells have one set of chromosomes whereas diploid have two sets of chromosomes
(homologous pair)
2) In haploid cells, all the alleles are expressed, whereas in diploid cells recessive alleles are often
hidden
How mutation can be detected from a sample of cells:
1) Extract DNA
2) Remove specific section using Restriction Endonucleases
3) Find the base sequence using a gene probe
4) Compare the base sequence with a normal base sequence
Causes of mutation:
They can occur spontaneously. How mutation rate is increased by factors known
as Mutagenic Agents, these agents ionise the bases so that they dont form the
correct base pairs:
1) Ultraviolet Light
2) X-Rays
3) and radiation
4) Chemicals such as mustard gas and cigarette smoke
Mutations produce the genetic diversity needed for natural selection and
speciation.
Genetic Control of CELL DIVISION:
Proto-Oncogenes: stimulate cell division
1) Growth factors attach to receptor protein on cell-surface membrane
2) This allows relay proteins to switch on the genes necessary for DNA Replication
Mutation can turn Proto-Oncogene into Oncogenes.
Oncogenes:
1) Permanently activate receptor proteins even without growth factors leading to cell division
2) Codes for growth factors that are then produced in excess stimulating cell division

Tumour Suppressor Genes: slows cell division and overrides the effect of oncogenes
If a Tumour Suppressor Gene becomes mutated, it becomes inactivated. This mutation can be inherited
too.
Tumour Suppressor Genes may also be inactivated when cells with genetically modified genes are
added to the body, this is because the Tumour Suppressor Genes will not have recognised the new
genes, therefore will not know how to stop division.
Why all cancer cells must be destroyed in a tumour:
1) Cells can metastasise
2) It can spread to other parts of the body

3) Remaining cells continue to divide


All cells contain the same genes however only certain genes are expresses in any cell at one time.
Some gene are permanently switched off, whilst others come on and off according to requirement.

TOTIPOTENCY & HOW GENE EXPRESSION IS CONTROLLED

Totipotent Cells: cells that can mature into any type of body cell, i.e. they are undifferentiated
Where we get totipotent cells from: adult stem cells, embryonic stem cells (however they only occur for
a limited amount of time), induced pluripotent stem cells
When a cell becomes specialised, we say it has lost its totipotency.
Whilst it has totipotency, it can be used to treat genetic diseases.
Features of totipotent cells:
1) Will replace themselves, i.e. they are immortal (except for
multipotent cells which divide to form only a limited number)
2) They are undifferentiated

In plants some cells remain totipotent throughout life. These plants


are used naturally and artificially in 3 ways:
1) Vegetative Propagation
2) Cuttings
3) Tissue culture
Cells specialise themselves by controlling which genes are
expressed in two ways:
1) Oestrogen; only works in Target Cells, target cells are cells
2) SiRNA
1) Oestrogen:
Transcription begins when the gene being transcribed is
stimulated by Transcription Factors
Transcription Factors have an active site which binds to a
specific sequence of DNA to start transcription, this specific
sequence is called the PROMOTER SEQUENCE
This active site is blocked by an inhibitor molecule which is
attached to the Transcription Factor and Receptor, this
inhibitor molecule prevents transcription and thus prevents
the gene from being expressed
Oestrogen diffuses into cell via LIPID DIFFUSION
Oestrogen then binds to the active site of the RECEPTOR
This changes the shape of the RECEPTOR molecules, therefore
releasing the inhibitor molecule and thus leaving the active
site of the Transcription Factor vacant
This allows Transcription Factor to ENTER THE NUCLEUS and
attach itself to a specific base sequence on a DNA promoter
How Transcriptional Factors are important for synthesis of particular proteins:
1) They bind to DNA at specific region called the PROMOTER
SEQUENCE
2) They then stimulate RNA Polymerase to arrive and begin
transcription
If we want a cell to stop expressing its genes, we can introduce a molecule to compete with Oestrogen
for the active site of the RECEPTOR.
2) SiRNA
An enzyme cuts large double stranded RNA into smaller sections called Small Interfering RNA
(SiRNA)
One of the strands of the SiRNA combines with an enzyme called RNA-induced silencing complex
SiRNA guides enzyme to mRNA and forms complimentary base pairs with a specific mRNA
The enzyme still attached to the SiRNA then breaks the mRNA into smaller pieces
mRNA no longer capable of translation
Therefore target gene can no longer make a specific protein as mRNA has been cut into pieces
SiRNA is used to block genes that cause diseases, i.e. can be used to stop genetic diseases by stopping
the gene from producing proteins.

GENE MODIFICATION & ITS PROCESS

Genetic Modification:
1) Isolation: finding DNA fragments that have the desired gene that produces the desired protein,
then separating it
2) Insertion: putting the desired DNA fragments into a vector
3) Transformation: transferring the DNA into a suitable host cell
4) Identification: deducing which host cells have taken up the DNA and which havent
5) Growth: making more copies of the host cell
1) Isolation
Isolation can be done in two ways:
1) Use Reverse Transcriptase
Reverse Transcriptase catalyses the production
of DNA FROM RNA
PROCESS:
Find cell that produces desired protein and
remove mRNA from this cell
Add Reverse Transcriptase to make a

strand of DNA from mRNA, this


strand that is made is called
Complementary DNA (cDNA)
To make the other strand of DNA, the
enzyme DNA Polymerase is used to
form
complimentary base pairs with cDNA, therefore cDNA acts as a template for the second
strand

This process is better than taking actual DNA from the organism because:
1) DNA contains Introns too whereas mRNA will contain only activated desired genes
2) Makes stable copy of a gene since DNA is less readily broken down by enzymes than RNA
3) It makes genes easier to find, as there are thousands of genes but only a few types of mRNA
exist
2) Use Restriction Endonucleases
Restriction Endonucleases cut a DNA double strand VIA HYDROLYSIS at a specific sequence of
bases called a recognition sequence in order to isolate the useful DNA sequence
Usually, the DNA sequence the Restriction Endonucleases will cut will be a PALINDROMIC
SEQUENCE, which means: sequence of one strand is the reversal of the corresponding strand.
Restriction Endonucleases cuts DNA in two ways:
Blunt Ends
Sticky Ends
The sticky ends/blunt ends can be attached to other sticky ends/blunt ends that have been cut by the
SAME Restriction Endonucleases using DNA LIGASE to form a Recombinant DNA VIA CONDENSATION:

Sometimes, there are quite a few recognition sequences leading to Restriction Endonucleases causing
many fragments, but scientists only need one specific fragment containing the desired DNA fragment,

therefore they will use Gel Electrophoresis to separate the fragments. (Gel Electrophoresis will be
explained shortly) Once the fragments are separated, they will use a DNA Probe (will be explained
shortly) which will bind to a complimentary base sequence in the gene, the fluorescence/radioactivity
of the DNA Probe will tell us which fragment contains the desired gene. Then we will movie onto
insertion, etc.
The overall isolation using Restriction Endonucleases:
1) Restriction enzymes cut DNA at specific base sequences VIA HYDROLYSIS forming a sticky end
2) Same restriction enzyme also cuts DNA into which gene is inserted forming another sticky end
3) DNA Ligase joins the two pieces of DNA together which happen to be complimentary VIA
CONDENSATION to form recombinant DNA
Why DNA base sequences must be cut with the SAME Restriction Endonucleases:
So that it cuts VIA HYDROLYSIS at the same base sequence therefore allowing pairing of bases when
DNA Ligase is used
Why Restriction Endonucleases (enzyme) will cut DNA only at specific recognition sites:
1) Different lengths of DNA have different base sequences
2) The enzymes active site has different shapes
3) Therefore only specific sequence will fit active site of an enzyme
One the DNA sequence has been isolated; we may continue the process of insertion, transformation,
etc. in two ways:
1) In Vivo: using living cells
2) In Vitro: using the Polymerase Chain Reaction
Before a plasmid with the desired gene is put into, the bacteria, the gene for conjugation is removed
from the plasmid because:
1) This prevents bacteria cells from conjugating
2) Therefore stops the transfer of DNA, thus reducing the risk of other organisms getting altered
genes
Why biologists will often use plasmids which contain antibiotic resistant genes:
1) It can act as a marker
2) This allows detection of the cells containing the desired DNA
If in the exam it asks for the definition of the term sticky ends, you will write:
1) Cut ends of DNA
2) One strand longer than the other
3) Can attach to complimentary DNA

In Vivo
1) Isolation: This has been completed
2) Insertion: putting the desired DNA fragments into a vector
Using Restriction Endonucleases we can combine the DNA of one organism with that of another
organism as long as the Restriction Endonucleases used to create the sticky ends in both was the
same.
PROCESS OF INSERTION:
1) DNA isolated from cell which manufactures desired protein
2) DNA and a plasmid both cut using the same Restriction Endonucleases, therefore creating DNA
fragment with sticky end and plasmid with a hole that has a sticky end
3) DNA fragments and plasmid with holes are mixed together with DNA LIGASE, the DNA fragment
fits into the hole in the plasmid like a jigsaw puzzle therefore forming recombinant DNA
Recombinant DNA: Contains genes of 2 types of organisms (plasmid will become like this)
4) The plasmids containing the DNA fragment will be the vectors, which are materials used to
transport DNA into the HOST CELL
If asked in the exam, how a DNA fragment in inserted into a vector, you will write:
1) Cut vector DNA with same Restriction Endonucleases used to cut DNA containing desired gene
2) Use DNA Ligase to join the sticky ends
Why plasmid is described as a vector:
It can carry foreign DNA into a bacteria cell
Properties of a vector:
1) Big enough to hold gene
2) Circular so that it is less likely to be broken down
3) Contains control sequences so that it can replicate the gene
After the DNA fragment is inserted into the plasmid, the plasmid will function differently, i.e. if you
replaced a resistance gene with the desired gene, then the plasmid will no longer be resistant like it
was before because:
1) The plasmid DNA base sequence has been altered

2) Therefore different proteins will be made


3) Transformation: putting the vector into the host cell
Transformation is obtained by mixing the plasmids and bacterial cells together in a medium of Ca 2+ ions
which causes the bacterial cells to become permeable to the plasmids
4) Identification: deducing which host cells (bacterial cells) have taken up the DNA and which
havent
The method used for Identification is Gene Markers
PROCESS OF IDENTIFICATION:
Antibiotic-Resistance Markers:
PROCESS:
1) Remove resistance gene to a certain antibiotic from a plasmid and add the desired gene in its
place, put this plasmid into bacterial cells
2) Put bacterial cells on nutrient agar plates
3) Transfer a small colony of the bacterial cells onto a second plate in exactly the same position
as the original plate
4) Add the antibiotic to the second plate (the antibiotic for which the plasmid containing the
desired gene no longer has resistance)
5) The cells that die are the ones that have taken up the desired gene as they have replaced
their antibiotic resistance gene with the desired gene
6) The colonies in exactly the same position on the original plate are the ones that possess the
required gene
Fluorescent Markers:
PROCESS:
1) Transfer gene of Jellyfish that produces a green light into the plasmid, put all plasmids into
bacterial cells which will all begin to glow
2) Now transplant the desired gene into centre of the green light gene in plasmid
3) The bacterial cells which contain the plasmids that have taken up the desired gene will stop
glowing as the desired gene has stopped the green light gene from working

Enzyme Markers:
PROCESS:
1) Lactase turn colourless substrate into blue
2) Therefore put the desired gene into the gene that makes lactase and insert into plasmid, then
insert plasmid into bacterial cells
3) Therefore whichever bacterial cells have a plasmid with the desired gene, their lactase gene
will not work
4) Therefore when the bacterial cells are put in a colourless substrate, the bacterial cells
containing the plasmid with the required gene will not change to blue
Importance of Markers:
Allows transformed bacteria to be separate from non-transformed bacteria
5) Growth: The bacterial cells that have the plasmid with the desired gene are now replicated
PROCESS: Using a fermenter
OVERALL, THE PROCESS OF GENETIC ENGINEERING/GENETIC MODIFICATION:
1) Cut desired gene out of cell using Reverse Transcriptase/Restriction Endonucleases
2) Cut plasmid using the same Restriction Endonucleases
3) Insert the gene into the plasmid, thereby joining the sticky ends using DNA Ligase
4) Transfer the plasmid into a cell
5) Use gene markers to identify which cells have taken up the new gene
6) Cells which have taken up the new gene cloned
Sometimes, instead of a bacteria cell, a virus is used for genetic engineering.
Advantages of using a virus to introduce genes into cells:
1) Virus can enter cells and replicate inside cells
2) Viruses target specific cells

Disadvantages of using a virus to introduce genes into cells:


1) May cause disease
2) Immunity may develop to the virus
In Vitro
This process is automated, making it both rapid and efficient
DNA polymerase: An enzyme that joins free nucleotides with their complimentary bases on the DNA,
but it does work for the start and end sequence of the DNA strand
Primers: have base sequence complimentary to that of the start and end sequence of the DNA strand
PROCESS (POLYMERASE CHAIN REACTION):
1) The desired DNA fragments, primers and DNA polymerase are placed in a vessel in a
thermocycler
2) The temperature is increased to 95oC, causing the two strands of the desired DNA fragments to
separate
3) Mixture is cooled to 55oC, causing primers to join with complimentary bases on the start and end
of the two desired DNA strands, therefore original DNA strands are unable to rejoin
4) Now DNA Polymerase begins to join free nucleotides to the middle sections of the two desired
DNA strands
5) The temperature is increased to 72oC, this is the optimum temperature for DNA polymerase to
work
6) We then have two copies of the original DNA fragment, so the cycle is repeated
In the exam, you describe PCR as:
1) Heat DNA to 95oC to allow strands to separate
2) Add primers and nucleotides
3) Cool so that primers bind to DNA and nucleotides attach by complementary base pairing
4) Temperature then taken to 72oC to allow DNA Polymerase to form a new strand
How a Polymerase Chain Reaction may stop by itself:
1) Free nucleotides get used up therefore nothing to make complementary chains
2) Primers get used up there cannot start complementary chains
3) Enzymes lose activity so no polymerisation of complementary strands
As a recap, the reasons for the following are:
Heating sample of DNA above 90oC: separate stranded DNA
Adding primers: attaches to start of gene and replication of base sequence starts from here
DNA Polymerase used at high temperatures: DNA polymerase not denatured by high temperatures thus
allowing rapid replication of DNA
How PCR differs from DNA Replication:
1) PCR uses heat to separate strands
2) PCR replicates pieces of DNA because DNA has been cut
3) Primer is added in PCR to initiate replication

How PCR
transcription:
1)
RNA
DNA
2) In
strand,
two
One use of
Provides
DNA fragment
Number of
produced =
DNA molecules

differs from
Transcription uses
Polymerase, PCR uses
Polymerase
transcription, the
template is one
in PCR, the template is
strands
PCR:
multiple copies of a
DNA molecules
Original number of
X 2Number of PCR Cycles
In Vitro
1) Extremely rapid
2) Does not require living cells
3) Very little purification of final
sample needed
4) Very sensitive, can clone DNA
molecule up to 1kpb long

In Vivo
1) Useful when we wish to introduce a gene
into another organism
Advantage 2) No risk of contamination
s
3) Very accurate
4) Cuts out specific genes
5) transformed bacteria can be used to
produce large quantities of gene products
Disadvanta 1) Relatively slow
1) Mistakes in copying in bases take
ges
2) complex purification
place
Cystic Fibrosis: caused by a mutation in the gene for the protein CFTR, which is a chloride ion channel
Effect of Cystic Fibrosis: too much sticky mucus produced by epithelial cells
Gene Therapy: replacing defective genes with healthy genes
Gene Therapy can be done in two ways:
1) Gene Replacement: defective gene replaced with healthy gene
2) Gene Supplementation: healthy copy of gene added alongside defective gene, the healthy genes
will be dominant
There are two ways in gene therapy may be adopted:
1) Germ-line Therapy: replacing or supplementing the defective gene in the fertilised egg;
prohibited due to ethics
2) Somatic-cell Therapy: targets just the affected areas, but the treatment needs to be repeated
periodically
Somatic-cell Therapy is carried out in two ways:
1) Using a virus called Adenoviruses as vectors for the healthy gene
2) Wrapping the plasmids containing the healthy gene in lipid molecules to form a liposome which
can pass through phospholipid bilayer
Somatic-cell Therapy is not always effective because:
1) Adenoviruses may cause infection
2) Patients may develop immunity from Adenoviruses
3) Liposome may not be able to pass through phospholipid bilayer
4) Healthy gene may not be expressed
5) Healthy gene may enter genome of another gene such as tumour suppressor genes, thus
causing cancer
How a person may become cured through Gene Therapy:
1) Healthy gene is expressed
2) Healthy genes replicated with cells
Why Gene Therapy may still result in children with the genetic disease:
1) Gamete cells do not take up the healthy gene
2) Therefore the person is able to pass on defective gene
Effectiveness of gene therapy:
1) Effect is short lived
2) It can induce an immune response
3) Using viral vectors to deliver the gene present problems
4) The genes are not always expressed
5) Not effective in treating conditions that arise in more than one gene
Gene Therapy can also be used to replace the defective gene in a gamete, however this is illegal in the
UK because:

Changes to genetic make-up of individual may affect normal development


Concerns regarding Gene Therapy:
1) High cost compared with conventional treatments
2) Unknown side-effects
3) Use of animals in preliminary testing
4) Other genes introduced which may have damaging effects

LOCATING A GENE

How to find WHERE a particular DNA sequence (gene) is located (the following
can also be used to see if the desired base sequence actually exists in the DNA
or not):
DNA Probe: short single-stranded section of DNA with base sequence
complimentary to part of target gene, it is labelled either
radioactively or fluorescently
DNA Probe will be made that has bases complimentary to the portion of DNA
whose position we want to find
1) The DNA strands are separated
2) The DNA strands are mixed with the DNA Probe, if the desired base
sequence is present, the DNA Probes will binds to complimentary bases
of the desired gene, this is called DNA Hybridisation
3) The site at which the DNA Probe has attached itself can be distinguished by looking for the
radioactive/fluorescent probe
Therefore, DNA Probes have two benefits:
1) It tells you if desired gene is present
2) If desired gene is present, it binds to it, therefore telling you where to find the desired gene
How DNA Probes can help against cancer:
1) They can help identify carrier of the cancer gene
2) They can identify which cancer gene is present

METHOD OF FINDING BASE SEQUENCE OF A GENE

But to first make the probe, we need to KNOW THE BASE SEQUENCE of the DNA sequence we are
investigating (DNA Sequencing/Sanger Sequencing):
1) Make four test tubes, one containing many single stranded strands of the DNA sequence as well
as a mixture of nucleotides as well as a small quantity of the terminator base Adenine
(terminator bases do not form hydrogen bonds) as well as a primer that is
fluorescently/radioactively labelled as well as DNA Polymerase. In the second tube, put the same
ingredients except put a small quantity of the terminator base Thymine instead of Adenine. Do
the same for the other two tubes, with terminator Guanine and terminator Cytosine
2) The DNA strand being investigated will be copied many time using Polymerase Chain Reaction
and added to the four tubes, each DNA strand in the four tubes can bind to a normal nucleotide
or the terminator nucleotide forming a DNA fragment using DNA Polymerase
3) Depending on exactly where the terminator nucleotide binds, DNA synthesis will be terminated
after only a few nucleotides of after a long fragment of DNA has been synthesis
4) The primer will tell us where the binding started and the terminator bases will tell us where it
ended
5) We now need o separate the different length fragments of DNA which is done through Gel
Electrophoresis
Obviously before attempting to find the base sequence of the gene, we must find the amino acid
sequence, and then find DNA base sequence using the method described above.
DNA Primer: Short length of DNA which is single stranded and has a specific base sequence which
indicates where replication will start
Why the DNA fragments formed in the tubes have different base sequences:
They have different lengths as strand synthesis stops at terminator nucleotide
Gel Electrophoresis:
1) The DNA fragments are placed onto an agar gel and a voltage is applied across it
2) Each fragment is negatively charged due to the Phosphate group, therefore will try to move
towards the anode (+)
3) The resistance of the gel means that the larger the fragments, the more slowly they move
4) The DNA fragments on the gel cannot be seen
5) Therefore sheet of photographic film placed on agar gel for several hours,
radioactivity/fluorescence from each fragment shows where it is on the gel, this method is
extremely sensitive

6) In this way DNA fragments of different lengths are separated


In the exam, for Gel Electrophoresis you will write:
1) Current switched on
2) Fragments move due to electrical attraction
3) DNA transferred to nylon membrane
4) Photographic film placed on gel
5) Film developed, the radioactivity darkens the film
If exam asks you to define electrophoresis in 1 mark, then write:
Using electric current to separate fragments
REMEMBER: DNA fragments will move out with smallest to largest as can be seen in the picture
Remember that two fragments that have the same size will be represented by a single bar on the gel
electrophoresis film
How scientists can use electrophoresis to estimate the NUMBER OF BASE PAIRS in the separated
fragments:
Compare the distance moved by the fragment with the distance moved by a fragment of known size
Why base pairs are a suitable way of measuring the length of a piece of DNA:
1) DNA is made of base pairs
2) Each base pair is same length
How the fragments separated by Gel Electrophoresis may be located by the radioactivity of the Primer:
1) Lay gel close to X-ray film
2) Develop film
Why it is necessary for the Primer to be radioactively/fluorescently labelled:
DNA is not visible on the gel, therefore radioactive/fluorescent label shows up on the photographic film
Restriction Mapping: only small DNA fragments can be sequences in the way described above, larger
genes must be cut into smaller fragments by Restriction Endonucleases and each
fragment sequenced. Therefore a restriction map is simply a diagram of a piece of
DNA marked with the locations of sites where it is cut by restriction enzymes. The
fragments are then compared with fragments of known size
If in restriction mapping, three fragments/bands were produced, then we know it has two recognition
sites.
Restriction Mapping is useful because:
1) Can be used to choose restriction enzymes to generate known-sized fragments
2) It can aid DNA sequencing of long pieces of DNA (this is the most useful use)
How scientists ensure that the enzyme (Restriction Endonucleases) has completely digested the
plasmid DNA:
Add the size of the fragments together, if they add up to more than the total length of the original DNA,
then they know the enzyme has not fully digested the DNA
Automation of DNA sequencing & Restriction mapping:
1) Instead of a radioactively labelled primer, the four types of terminators are labelled with the
fluorescent due
2) DNA synthesis takes place in a single test tube
3) DNA synthesis is speeded up by using PCR cycles
4) Electrophoresis is carried out in a single narrow capillary gel
5) Results are scanned by lasers and interpreted by computers
6) PCR can be used to provide fragments required in these techniques
IF the question is only 2 marks and it is asking the method for finding the base sequence of a gene,
then write:
1) Use Restriction Mapping on the gene
2) Then use DNA Base Sequencing
Genetic Screening:
1) Use DNA sequencing and PCR to produce DNA Probes that are complimentary to bases of the
defective gene
2) Fix hundreds of different probes in an array on a glass slide
3) Add a sample of DNA to the array, any complimentary DNA sequences in the investigated DNA
will bind to one or more probes
4) If it binds, then the individual is said to be a carrier of a genetic disease

If a person is informed that he is at a greater risk of cancer through genetic screening, he may choose:
1) To give up smoking

2) Lose weight
3) Eat more healthy
4) Avoid mutagens
5) Regularly check themselves for cancer
6) To undergo gene therapy
Implication of genetic screening:
1) Who decided who should be screened
2) Who has access to the test results
3) Would employers refuse insurance cover if they knew a person has a genetic disorder
4) What are the responsibilities of someone who carries a gene for an inherited disease
5) Does mankind have a responsibility to maintain genetic diversity
6) Who decided what is a defect or a disease
Southern Blotting:
1) DNA is cut using restriction enzyme
2) Electrophoresis separates DNA fragments according to length
3) DNA made single-stranded
4) Transfer to positively charged nylon membrane to which the negatively charged DNA stick
5) Probe is applied which does complimentary base pairing to the DNA fragments in the nylon
membrane
6) Radioactive strand detected on film
7) Pattern unique to every individual
Southern Blotting is the method used for:
1) GENETIC FINGERPRINTING; the differences in DNA between humans is found in the non-coding
DNA, which is repetitive
The probability of two organisms having the same fingerprints is very low; about 1 in 10 9
2) To identify restriction fragments containing a particular gene
3) GENETIC SCREENING
Genetic fingerprinting is used for:
1) Crime investigation
2) Determine family relationships
3) Prevent undesirable breeding
4) Determine relationships between ancient humans
5) Establish evolutionary relationships with other species
6) Measure genetic diversity within a population
Why genetic fingerprinting takes long if the sample is small:
PCR is required to provide amplification of the DNA
Some plants can be made as a pesticide by incorporating the pesticide into genome of plant to allow
plant to produce toxin, this called genetically modifying crops. (PS Dont get confused, this isnt
Selective Breeding)
Advantages of making Genetically Modified Crops against pests:
1) More effective than other methods
2) Less use of insecticide
3) Prevent spread of disease
4) Economic benefit to farmer
5) Possible cheaper food
Disadvantages of making Genetically Modified Crops against pests:
1) Plasmid may enter another species
2) May sterilise other species
3) Disruption of food chain
4) Poison may harm other organisms
5) Consumer may consider product as unnatural
6) Unknown side-effects unknown
7) Risk to biodiversity
8) Risk to local farmers
For and against of doing genetic engineering to clone cells from human embryos:
FOR:
1) Embryo can develop into any type of tissue
2) Easier to use embryo cells than to extract cells from a person
3) Cells would replicate in patient during mitosis
4) Permanent cure
5) Likely to be safer than implants from animals as animals may contain new viruses
6) Only body cells implanted, therefore germ line would not be affected
AGAINST:
1) Long term side effects are unknown

2) Embryo has potential for development to person therefore could be regarded as murder
Completely irrelevant point you should remember: When substance comes out in faeces, we say it has
not been absorbed, but when a substance comes out in
urine, we say it has been absorbed but not used for growth.
REMEMBER: Lysosomes are substances that break down tissue

SYNOPTIC ESSAY TOPICS


Structure of Glucose

How heart beat is initiated and coordinated

Formation of disaccharide from 2


monosaccahrides using condensation
(removing water)
Formation of 2 monosaccahrides from a
disaccharide using hydrolysis (adding water)
Starch Digestion
Lactose Intolerance
Formation of dipeptide from 2 amino acids
using condensation (removing water)
Formation of 2 amino acids from dipeptide
using hydrolysis (adding water)
Structure of amino acid
Stages of globular protein primary,
secondary, tertiary, quaternary
Enzyme-substrate complexes
Effect on temperature/pH/substrate
concentration on Enzyme
Competitive and Non-competitive inhibitors
Test for starch, lipids, reducing sugars, nonreducing sugars, protein
Organelles of a cell and their functions
Process of ultracentrifugation
Magnification
TEM and SEM
Structure of partially permeable membrane of
cell
Structure of the 2 Lipids, Triglycerides and
Phospholipids i.e. how they are made of
fatty acids and glycerol molecule
Function of cell membrane
Extrinsic proteins and Intrinsic proteins and
their involvement with facilitated diffusion
What is Lipid diffusion through Phospholipid
bilayer
What is osmosis
What is active transport and how its related
to carrier proteins only
How products of starch are absorbed by
epithelial cells, role of epithelial cells and
adaptations
Organelles of prokaryotic cell and its
differences from eukaryotic cell
Cholera
Oral Rehydration Therapy
What is ventilation
Inspiration and Expiration
Essential features of gas exchange and how
the lung is adapted for gas exchange
Pulmonary Tuberculosis
Pulmonary Fibrosis
Asthma
Emphysema

What are pathogens


How valves in heart maintain one way flow of
blood
Physical barriers against pathogens
Phagocytosis
Cell-Mediated response
Humoral response and how it involves a primary
and secondary response
Antigens and antigenic variability
Antigen-Antibody complex (remember
antibodies are made by B-Lymphocytes)
What are Monoclonal Antibodies
Process of Vaccination and ethical issues
concerning it
Causes of variation (mutations, meiosis, fusion
of gametes, environmental influences) and
diversity index
Sampling (involves bias, chance, sample size,
etc.)
Structure of DNA and how it is related to its
function
Homologous chromosomes (structure and
function) and alleles (what it is and where its
found)
Triplet Code
Process of Meiosis and how it provides variation
Vertical Gene Transmission and Horizontal
(conjugation) Gene Transmission and how
antibiotics work
Selective Breeding, Genetic Bottleneck and
Founder Effect and how they reduce genetic
diversity
Thrombosis
Structure of Haemoglobin
Role of Haemoglobin (readily associate with O 2
at a gas exchange site and readily disassociate
at respiration site)
Bohr Effect
Diseases associated with Haemoglobin
Properties and components of Starch, Glycogen
and Cellulose
Genetic comparison, Amino Acid sequence
comparison and Immunological comparison to
compare species
Taxonomy and use of Hierarchy
Courtship behaviour and its importance
Structure of leaf Palisade Cell and its adaptation
for Photosynthesis
Semi Conservative DNA Replication
Process of gas exchange in insects
Counter-current system in fishes
How fish maintain continuous flow of water over

Risk factors of Chronic Obstructive Pulmonary


Disease like smoking, genetic make-up, air
pollution
How Atrial systole and Ventricular systole take
place, i.e. heart cycle
Atheroma and how it causes heart attack
Features of transport system
Structure of blood vessels (arteries,
arterioles, capillaries, veins) and how each
one is related to its function
Formation of tissue fluid and its return to
circulatory system
Movements of water through roots
(Apoplastic pathway and Symplastic
pathway), absorption of water through roots
Transpiration and factors affecting it
(movement of water out of leaf)
Biotic and Abiotic Factors
Limiting factors of Photosynthesis
Greenhouses and what they do inside them
Biological and Chemical pesticides
Using transect, interrupted belt-transect,
continuous belt transect, point transect and
line transect for measuring abundance
Mark Release Capture, how you do it and
things you ensure whilst doing it
Population changes (demographic transition)
and why they take place
Interspecific and Intraspecific competition
Transfer of energy through ecosystem and
how farmers take measures to increase this,
NP = GP RL
Why ATP is a good source of energy and its
importance
ATP synthesis from ADP and Pi
Light Dependent Reaction and everything it
involves
Light Independent Reaction (CALVIN CYCLE)
and everything it involves
Glycolysis and Link Reaction
Krebs Cycle
Electron Transport Chain
Anaerobic Respiration and its implications
Carbon Cycle
Nitrogen Cycle
Eutrophication
Deforestation and Conservation, ethical
arguments for conservation and against
deforestation
Process of succession and role of
decomposers
Monohybrid Inheritance (homozygous and
heterozygous) and its influence on genetic
disease like Haemophilia

gills
Mitosis (Interphase, Prophase, Metaphase,
Anaphase, Telophase) and components of each
stage
Small surface area to volume ratio and large
surface area to volume ratio and their
implications
Structure of a plant leaf and its adaptation for
gas exchange
Structure of Myofibril
Process of Sliding Filament Theory
Comparison of hormonal system with nervous
system
Plant growth factors
Process of Transcription and all that it involves
and its importance in protein synthesis
Process of Translation and all that it involves and
its importance in protein synthesis
Comparison of RNA with DNA and mRNA with
tRNA
Types of mutations
Process of controlling cell division
Process of controlling the expression of a gene
(SiRNA, Oestrogen and Transcriptional Factors)
Isolation (use of Restriction Endonucleases and
Reverse Transcriptase)
In Vivo Insertion (use of DNA Ligase)
In Vivo Transformation (use of Ca2+ ions)
In Vivo Identification (4 types of gene markers)
In Vivo Growth
In Vitro PCR
Process of locating genes using DNA Probes
What is gene therapy, how could it be done and
is it effective
Process of finding the base sequence of a gene
using Gel Electrophoresis
Genetic screening and its implications
Process of Genetic Fingerprinting
Genetically modified crops, pros and cons
Using embryos in genetic modification, pros and
ethical arguments
Importance of refractory period
Synaptic Transmission
Structure of neurone and process of action
potential

Write any extra topics you need to learn


here:

Hardy-Weinberg Principle and equation


Stabilising selection and Directional selection
Process of Speciation
Nervous System and the basis of how it
works (stimulus ... Effector)
Process of controlling Heart Rate (negative
feedback)
Process of regulating body temperature
(negative feedback)
Process of regulating glucose concentration
(negative feedback)
Process of menstrual cycle (negative and
positive feedback)
Pacinian Corpuscle and Rods/Cones (Retinal
Convergence)
Reflex Arc and its importance