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Anthropology

9.09.05

Evolution- non-directional Change through time- no goal

Darwin:
Upper middle class; theology
Loved Natural Science
Erasmus- Grandfather
MS Beagle- 1831-1836. A boat, for a voyage. Darwin may have been invited to be the
captain’s companion. Darwin was allowed to go on the trip.
He carried a book by Lyle…
Galapagos Islands- off NW coast of Ecuador
Finches.
He started studying birds.

Darwin’s- evolution- descent with modification

Progeny (offspring)
Darwinian evolution: Simple, elegant
Simple: components
a. Variation- essential component
b. B. Natural selection- pressures that determine: whether or not they will survive
Reproduction success
Examples of pressures: food source, environment,

Obvious pressures:

Disease
Food supply
Climate
Predators

Less obvious pressures:

Territory
(Birds, bears, raccoon)

Ability to adapt to new territory.

Adaptive advantage
Reproduce at expense of others
Reproductive success- survival of fittest a little misleading..
Whether you leave offspring who survive
If your offspring, you are successful in terms of evolution.
Why? - variability for continuing change
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NO MECHANISM TO PREVENT MAXIMUM REPRODUCTION CAPACITY

NO GUARD AGAINST EXTINCTION EITHER

EXTINCTION ACTUALLY THE RULE
LESS THAN .1% OF ALL SPECIES THAT EVER LIVED ARE ALIVE TODAY!

Interaction between pre-existing variation and natural selection (reproductive success)

promotes non-direction change thru time.

Selection operates n variability

What will be passed down?
Lyles’s influence on Darwin.
Malthus’s influence
Populations- checks and balances in nature
Food supplies cannot keep up with reproduction of populations- doubling can occur ever
25 years.
Impulse to multiply- checked b fierce struggle for existence in nature.

(Bands of hypoplasia illustrate an interruption in growth and development. Harris lines-

little white bands at the top and the bottom of the tibia. Also known as tranverse lines
where the most growth takes place. In his eye organ he has little white holes called cribra
orbitalia. Iron core diet.)

MALTUS DEMONSTRATED TO DARWIN:

SELECTION- operates on individual
EVOLUTION- operates on population
MEANING: small changes that accumulate and change gene frequency of characteristics
eventually change populations.
Through time speciation: can change.

COMPONENTS OF DARWIN’S THEORY (IN TEXT)

1. Offspring production- faster than food.
2. All living things vary.
3. More born than can survive; fierce struggle.
4. Those with favorable traits survive.
5. Environmental context determines if trait is beneficial.
6. Over long periods- successful variations produce great differences- result- new
species.
7. Traits are inherited (passed down).

Non-directional change through time is really a change in the gene frequency from one
generation to the next.
Darwin- did not understand source of change or mechanism.

Peppered Moth-England.
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Moth Story Represent three things:

1) Industrial Melanism
Change in gene frequency due to environmental impact
2) Adaptation to environment
3) Natural selection

Genetics and Human Variation

Genetics is 5-6 billion ppl live on earth today

- biological communication between generations
- Focus of heredity and variation
- Recipe

Germ Cells- Gametes

Females- ovum (ova)
Males- Sperm
Zygote- initial cell of offspring

Cell- basic to all forms of life

Cytology- study of the cell

Two kinds of cells involved in heredity

1. Somatic- “soma”
2. Sex cells (gametes)

Cell contains:
A. Cytoplasm
B. Nucleus

Nucleus contains:
DNA- deoxyribonucleic acid
RNA- ribonucleic acid

James Watson and Francis Crick

1st Published- 1953

Nobel Prize- 1962

Who else was instrumental to figuring DNA configuration? Rosalind Franklin..died 1958

Nature of cells is to divide

Chromosome (Chroma) consists of these things:
Arm
Centro mere
Arm
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Humans- 46 chromosomes in each somatic cell

- 23 pairs

Autosomes- 1st 22 pairs

Sex chromosomes- 23rd pair Chimps have 48 chromosomes

Some characteristics on the x isn’t present on the y.

DNA and RNA transfer heredity into action

DNA- double helix

Cell Division:
Mitosis- somatic cells

1. Chromosomes double- becomes 92 chromatids still held together by Centro mere.

Mitosis continued…
2. Position along equator of nucleus.. single file
3. Move in opposite directions
4. Result- 2 daughter cells identical to original diploid number.
46 chromosomes in each somatic cell.

Meiosis- gametes
-takes place in gonads
Males= testes
Females= ovaries
- also called Reduction/Division
- necessary for bisexual reproduction
- Must end up with only 23 chromosomes (haploid) instead of 46 in somatic cells.
Mature gamete has how many chromosomes? 23.
Sex cell- 23 from one .. 23 from the other….

Steps of Meiosis

1. Chromosomes double
2. Line up in pairs (instead of sincle file like Mitosis)
3. 1st divison- 23 doubled chromosomes in each cell
4. Line up in single file and divide again
– males- 4 cells (gametes)
-females- 4 ova but only 1 is viable
-polar bodies

Mitosis vs. Meiosis

Fertilization occurs- intial cell of the offspring (zygote)

Gene- segment of chromosome that codes for a particular protein
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On chromosome- gene has specific position- locus (address)

Thousands, perhaps millions of “loci”
Gene at particular locus codes for same heredity characteristic as gene at that location on
matching chromosome
Homologus pairs- true for first 22 pair (autosomes)

23rd pair (sex chromosomes) are different

Y is smaller than the X
Male= one X and one Y
Female= Two x’s
Female can give only an X
Male determines sexof offspring

From where does variation come??

1. Mutation (only true source of change of variation
2. During meiosis, doubled chromosomes line up in pairs before first division- line
up differently every time they line up.
3. Also- crossing over and recombination-
4. No two sex cells will be the same.

9/14/05

Remember- nucleus is focal point for heredity

In nucleus- DNA and RNA

DNA- four bases called nucleic acids

Adenine
Thymine
Guanine
Cytosine

RNA- four bases

Adenine
Uracil
Guanine
Cytosine

Note: In TNA you have Uracil rather than Thmine.

Base Pairing Rule- certain bases pair (or “bond”) with only cerain other bases:

C with G
G with C
A with T
T with A
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DNA bases combine with sugar and phosphate residues to form “nucleotides”
DNA chain composed of nucleotides.
Nucleotides composed to phosphate and sugar.

Nucleotides linked to other nucleotides on the DNA ladder by hydrogen bonds- long
chains of nucleotides

When chromosomes are duplicating, what you really see:

DNA duplicating
DNA strand opens up down middle like zipper
Corresponding DNA nucleotides attracted to each side
Wander in and bond

Result: Two new strands- each with one half of the old
Semi- conservative model

So, - duplication has taken place- how does information get out of nucleus

In steps RNA-RNA nucleotides- also in nucleus

RNA takes the chemical codes out the nucleus and into the cytoplasm

DNA is template- Cannot, should not leave nucleus

Up to RNA to get out of nucleus with instructions to build proteins.
How- free RNA nucleotides in nucleus (pretty crowded in there)
Particular protein (synthesized), DNA chain opens up at very specific spot.

Free RNA nucleotides- attracted to sensing side; temporarily bond to the DNA
nucleotides in a specific sequence

Information complete, RNA detaches from DNA strand. DNA strand closes up

RNA strand can leave the nucleus.

RNA is this case is “Messenger” RNA

Migrates into cytoplasm (FNA strand same as sense strand)
In cytoplasm, “code” which RNA carries is converted into a protein
How?
Organelles- ribosome’s- move along strand of messenger RNA reading the code
Ribosome’s- called “protein factories”
Every three bases= “codon” (also called a triplet)- represents one of the 20 amino acids
that are building blocks of protein

Ex: UUU- Phenylalanine

UUA- leucine
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In comes another kind of RNA which is waiting out in cytoplasm.

tRNA (transfer RNA)
tRNA carries a cargo- fore and aft
Fore- anticodon or complementary code
Aft- amino acid
tRNA “docks” with ribosome, leaves amino acid
Polypeptide chains.

Added Note: Ribosome’s multiple readings if need be

Once t RNA deposits its cargo(amino acid), it detaches from ribosomal chain.
Chemical codes for starting and stopping the formation of proteins.
IMPORTANT- the kind of protein created depends solely on the DNA CODE-

Important to note: Even small mutations can have dramatic impact-

Ex. Point Mutation

Hemoglobin- type of molecule in red blood cells

Carries oxygen from lungs to tissue; carbon dioxide from tissue to lungs

Hemoglobin made up of protein chains

One Type- beta chain
146 amino acids in beta chain (438)
(Remember: every three bases equal an amino acid)

Mutation can occur in only ONE base to produce sickle cell anemia
Blacks; Greek islanders
Child- mutate gene from both parents- full brown case
If bad (called deleterious), why still present?
Only one sickling gene can provide adaptive advantage.
Full blown case of sickle cell:
Major circulatory problems
Destruction of red blood cells
Enlarged heart; clogged vessels; bleeding from joints

Sickling hemoglobin- substitution at “Point 6” in 438 bases

“A” instead of “T”
Code: “CAC” instead of “CTC”
Wrong amino acid brought in: Valine instead of glutamic acid
DNA faithful- will produce replicate of exactly what code says
Over and Over again

Specifics help us understand

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Genotype- sum total of all hereditary material from both parents

Phenotype- physical express of that information

Noted earlier- Phenotypes can be greatly altered by environment

Diet
Exposure to sun
Chemicals

Important to remember: What we are is an interaction b/w heredity and……

So what about genetics?

Gregor Mendel
Austrian monk
Loved math
Used pea plants as models
WHY? Distinguishing characteristics:
Color, height, shape of seed, etc.

Published in 1866- ignored! Work rediscovered around turn of century.

Accomplished two impartant things:

Helped to eliminate idea of pangenesis

(children- blend of parents)

Discovered laws of inheritance

Mendel’s 2 “rules” or “laws”

1. Law of segregation- genes occur in pairs; pair members separate during cell
formation (meiosis)
2. Law of independent assortment- separation of one pair of genes does not
influence the separation of other pairs of genes (member of one pair of
chromosomes that enters a sex cell is unrelated to which member- male or female-
of any other pair of chromosomes enters that cell).

Mendel- very lucky- characteristics he followed on different chromosomes

Mendelian traits- discreet of discontinuous traits- traits that are governed by only one
locus.

Continuous traits are different- hair color; height (multiple loci)

Mendel planted peas- carefully observed

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Came up with “pure bred” stock- those yellow only produced yellow; those wrinkled
only produced wrinkled.

Then- he crossed them- green with yellow; smooth with wrinkled; tall with short.

Followed through many generations and counted results

Result: 1st generation- (1st Filial) all smooth; all yellow all tall

2nd filial- key- traits not lost.

Terms: dominant vs. recessive- some traits dominate over others.

Not so much “dominance” as effect; a dominant allele affects the expression of a

recessive one.

Dominant written in upper case (D); recessive lower case (d)

Terms: Punnett square- predict combinations of particular traits (dominant vs. recessive)
in next generation

BB (Homozygous dominant) B- allele- alternative form of gene

Bb (heterozygous) b- allele- alternative from of gene
Bb (homozygous recessive)
Genotypic ratio (on right square) 1:2:1 Phenotypic ratio: 3:1

Mid 1800s- scientists in Mendels’s time did not understand

Math was his key; others not viewing things the way he did
By 1900’s mendel’s idea were “rediscovered”
By 1940s- “population” studies taking place
Population Genetics studies
So: By 1900’s, scientists knew:
1. Characteristics genetically controlled
2. Characteristics affect an organism’s survival
3. Genes are responsible for mmorphology
4. Frequencies will increase if characteristic is desirable; decrease

5 different modes of mendelian inheritance

1. Autosomal dominant trait
2. Autosomal recessive trait
3. Y- linked
4. X- linked dominant
5. X-linked recessive

Population- group of individuals that mate among themselves

Subdivision of a species
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Gene Pool- sum total of all genes (alleles)

Hardy- Weinberg- early 1900s- predict gene frequency if present distribution known-
ABO blood system

H-W Equilibrium- no appreciable change in gene frequency- no selection going on

2 prerequisites for equilibrium

1. Infinitely large population
2. Random mating- Beards!!

9/19/05

In humans, social rules determine with whom you mate!

In actuality four forces keep population out of H-W Eq.

1. Gene Flow(migration
2. Random genetic drift
3. Mutation
4. Natural Science

1. Gene Flow- movement of genes b/w populations

Increases variability in a group
Decreases variability b/w groups
Example- Hawaii, Japan

2. Random Genetic Drift- statistical randomness in passage of alleles from one generation
to next.

Only “lucky” gametes are fertilized.

Large populations more accurately reflect true frequency of certain characteristics.

Random genetic drift- represents “random” factor in evolution

Example- car accident- random happening

IN large groups- loss balanced out

Small groups- greater impact to gene pool

Could produce “founder effect”

Example- Pinelop Atoll- coral reef island- south seas typhoon 1775- all but 20 killled

Population back up to several thousand

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High frequency- chromatopsia- rare worldwide (recessive trait- cataracts,

shortsightedness)

Oral tradition explanation versus reality

Mwahuele- chief
Isoaphahu- cat god
Only certain genes get through- genetic bottleneck
Founder Effect
Yanomamo (villages split- small gene pool)
Universal taboo against incest
Inbreeding- promotes expression of deleterious genes- threatens group’s survival

3. Mutation- Mutations are evolutionary important ONLY if they can be passed from
one generation to the next.

Sickle cell anemia- Hemoglobin beta chain- alleles co dominant

HbN/HbN- Homozygous Normal- Malaria
HbS/HbS- Homozygous for sickling- very ill probably die
HbS/HbN- Heterozygous (one normal allele; one sickling)
In areas of world where malaria is prevalent- heterozygous has adaptive advantage
Plasmodium (parasite cannot live in sickling homozygous or heterozygous blood)
Balanced polymorphism- multiple forms of same gene present in a population at an
appreciable rate (usually 5% or more)

Mutations (cont’d)

In ancient times, mutations at birth were signs of impending wars or famine

More than 60 kinds of birth defects recorded on clay tablets from Babylonia

Dwarfs often regarded as highly prized curiosities- treated well; dwarf tossing

Cyclops- ancient myths

Acholdroplastic dwarfism- Dominant mutation

If present in the genotype, it will be expressed in the phenotype.

Dominant Autosomal Mutation

Acondroplastic dwarfism- dominant mutation

Normal intelligence; body proportions are not normal

Long bones shortened
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Mutation occurs is one gene in every 10,000 people

If present in genotype, it will be expressed

N(NA)= NA/N
N(N)= N/N 1 in 2 chance for normal growth

NA(NA)= NA/NA 1 in 4 chance for normal growth

NA(N)= NA/N
N(NA)= NA/N
N(N)= N/N

Problems with some mutations- don’t show up at birth

Huntington’s chorea- dominant mutation- onset- during young adulthood- often after
childbearing years have already started
Dominant mutation
Neurological condition- nerve

Marfan’s syndrome- Abe Lincoln

Sex-linked mutations: Carried on X and not on Y

If recessive, takes a double dose for female; recessive or dominant in male, he gets it.

Whatever mother is carrying: hemophilia-

EX.
Queen Victoria carried hemphilia- Passed to many royal families in Europe especially

Alexandria marries Czar Nicholas II- Russia- several children

Alexis- hemophilia- very ill

Alexandria influenced by Rasputin- in turn, influenced Czar

Russian Revolution- 1917

Royal Family murdered in 1918

In 1980’s- Anna Anderson- Anastasia?
Royal family Exhumed
Dr. Williams Maples- Forensic Anthropologist
DNA
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Problems with mutations in predicting some of them is that they can be hidden in the
heterozygous individual.
Can some kinds of mutation be predicted in future generations?

Hiroshima

Rad- absorbed radiation change

20-25- break a chromosome
Average lethal- 50 rads
Chest x-ray- .003 rad; cosmic radiation- 1/20 per year
Ground radiation- 1/12 rad per year
Hiroshima survivors-200 rads; prediction- 1 lethal mutation
Per offspring- has not happened.

4. Natural Selection: those forces that operate on an individual that determines

survival

Sickle Cell
ABO Blood Group:
Antigen Systems (ABO,Rh, others) – ABO- blood type
Antigen- macromolecules in red blood cells
For our purposes, like soildiers who create antibodies
Reactions to forerign invasions
ABO system

If parents give two A’s, child is A

If parents give two B’s, child is B
If parents give 1A, 1B- child is AB
If parents give 1A, 1O- child is A
If parents give 1B, 1O- child is B
If parents give 2 O’s- child is O
“O” is recessive, “O” simple means lack of agglutinating protein

Agglutination discovered around turn of 19th century when trying to do blood

transfusions- if blood transfusions- if blood not compatible, persons can die.

A cannot receive B
B cannot

10.3.2005.

Ageing and sexing- best bone is the hip bone

Auricular- changes throughout our lifetime
Sacrum
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Hipbone
Pubic bone-changes just like the auricular surface. .

Sciatic notch assist in sexing male has narrow notch (acute angle), Female has wider(90
degree angle) notch.

Sub pubic angle much broader in a male than a female.

Males in general are larger. Females generally smaller than males.

The skull helps determine sex…

Male square chin, supra orbital tourus , sloping forhead, blunt border on the ear orbit..
large
Female- pointed chin, smooth forehead, sharper border on the eye orbit

Race:
Use the skull for that.
Whites- dropeed eye orbital, narrow nasal area, staraighter face
Blacks- square eye orbitals, more prominent region
Asians- intermediate b/t the too.

Dental records help identify someone

Positive ID using one tooth.

Perimortem- happens during time of death

Post mortem trauma- happens after death

Blunt force trauma to the head.. makes it all messy

Post mortem interval-