Cell Reports

Report
Dendrite Injury Triggers
DLK-Independent Regeneration
Michelle C. Stone,1 Richard M. Albertson,1 Li Chen,1 and Melissa M. Rolls1,*
1Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA
*Correspondence: mur22@psu.edu
http://dx.doi.org/10.1016/j.celrep.2013.12.022
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-No Derivative Works
License, which permits non-commercial use, distribution, and reproduction in any medium, provided the original author and source are
credited.

SUMMARY

Axon injury triggers regeneration through activation

of a conserved kinase cascade, which includes the
dual leucine zipper kinase (DLK). Although dendrites
are damaged during stroke, traumatic brain injury,
and seizure, it is not known whether mature neurons
monitor dendrite injury and initiate regeneration. We
probed the response to dendrite damage using
model Drosophila neurons. Two larval neuron types
regrew dendrites in distinct ways after all dendrites
were removed. Dendrite regeneration was also
triggered by injury in adults. Next, we tested
whether dendrite injury was initiated with the same
machinery as axon injury. Surprisingly, DLK, JNK,
and fos were dispensable for dendrite regeneration.
Moreover, this MAP kinase pathway was not activated by injury to dendrites. Thus, neurons respond
to dendrite damage and initiate regeneration without
using the conserved DLK cascade that triggers axon
regeneration.
INTRODUCTION
Most neurons need both dendrites and axons to function. The
responses of neurons to axon injury are relatively well documented. After severe axon damage, distal regions of axons are
cleared by Wallerian degeneration (Coleman and Freeman,
2010; Wang et al., 2012), which is followed by reinitiation of
axon outgrowth. In mammals, both degeneration and regeneration are more efficient in peripheral than central neurons (Huebner and Strittmatter, 2009; Liu et al., 2011; Vargas and Barres,
2007). Axon injury triggers a cascade of signals that travel
back from the injury site to the cell body. Within minutes of the
initial trauma, a calcium wave travels back to the cell body
(Cho and Cavalli, 2012; Ghosh-Roy et al., 2010). Subsequently,
microtubule motor-based transport brings signaling molecules
between the site of injury and the cell body (Abe and Cavalli,
2008; Rishal and Fainzilber, 2010). This process may take hours
to days depending on the distance from the site of injury to the
cell body. Several key proteins take this motor-based route.
Among these, the mitogen-activated protein kinase kinase

kinase (MAPKKK) dual leucine zipper kinase (DLK) has been

shown to be required for efficient regeneration in worms, flies,
and mammals (Hammarlund et al., 2009; Shin et al., 2012; Xiong
et al., 2010; Yan et al., 2009) and thus seems to be a core
signaling element in the response to axon injury. A major transcriptional response is mounted downstream of DLK to allow
reinitiation of axon growth from the damaged cell.
Although key players in axon regeneration have been identified, it is not known whether neurons have signaling machinery
that senses dendrite damage, or if mature neurons can regenerate dendrites. Dendrites are particularly susceptible to damage by excitotoxicity and other environmental changes during
stroke, seizure, and traumatic brain injury (Gao and Chen,
2011; Greenwood and Connolly, 2007; Murphy et al., 2008;
Risher et al., 2010; Zeng et al., 2007). It is difficult to track dendrites from individual cells in mammals over time, so it has not
been possible to determine whether dendrite regeneration is
possible after damage using these models. Therefore, several
labs have turned to Drosophila dendritic arborization neurons
to ask whether dendrite injury triggers regeneration.
Dendritic arborization (da) neurons in Drosophila larvae are
highly polarized cells with dendrites that innervate the body
wall and axons that extend to the CNS (Grueber et al., 2002).
Although their dendrites are sensory, they share many features
with dendrites that house postsynaptic sites. For example,
minus-end-out microtubules are present in dendrites, but not
axons, of all types of mammalian and Drosophila neurons examined, including da neurons (Baas and Lin, 2011; Stone et al.,
2008).
Different types of da neurons exist in Drosophila larvae, and
they can be distinguished by arbor complexity and tiling behavior
(Grueber et al., 2002). Several studies have suggested that the
most complex of these neurons, the class IV cells, have some
capacity to respond to dendrite damage, although this becomes
more limited as larvae age (Song et al., 2012; Sugimura et al.,
2003). These studies also agree that the simplest da neurons,
the class I cells, are unable to reinitiate growth in response to
dendrite injury at any point during larval life and can only do
this during embryogenesis. Loss of sensory endings in zebrafish
skin also triggers robust reinnervation only very early in development (OBrien et al., 2009). Thus, the evidence so far suggests
that, even in the peripheral nervous system where regeneration
tends to be most exuberant, only some cells early in development can upregulate dendrite growth in response to injury.
Cell Reports 6, 247253, January 30, 2014 2014 The Authors 247

Figure 1. Dendrites Regrow Completely after They Are Removed from Larval Neurons
(A) An example of an uninjured ddaE neuron expressing mCD8-GFP and tracked during 4 days of larval life is shown.
(B) A ddaE neuron expressing mCD8-GFP had all dendrites removed at their base (arrows) and was then tracked for 4 days. At 5 hr, the cut dendrites have
degenerated.
(C) A ddaC neuron had its dendrites removed (arrows) and was then imaged over 4 days. Four hours after dendrite severing, degenerating remnants are seen. At
48 hr, new dendrites do not reach the edge of the normal territory (double arrows). By 96 hr, the new dendrites directly abut neighboring cells.
(D and E) Quantitation of branchpoint number in uninjured (D) ddaE neurons, and ddaE neurons after dendrite removal (E). Averages from nine cells are shown in
(D), and seven (5 and 96 hr) or eight (0 and 48 hr) cells are shown in (E).
Error bars show the SD. See also Figure S1.

However, all studies on responses of single cells to dendrite

injury have damaged only one dendrite. To fully test the idea
that only subsets of neurons at specific developmental stages
can initiate dendrite regeneration, we developed methods to
remove all dendrites from neurons and reasoned that the cells
would either die or regenerate.
RESULTS
Dendrite Injury Triggers Robust Regeneration in
Multiple Types of Dendritic Arborization Neurons
To test the idea that only subsets of neurons at specific developmental stages can initiate dendrite regeneration, we developed
methods to remove all dendrites from da neurons and reasoned
that the cells would either die or regenerate. The simplest da
neurons, including the ddaE cell, normally have very stable
dendrite arbors during larval life and do not add or remove
branches (Figures 1A and 1D; Sugimura et al., 2003). We thus
tested whether these neurons would die if all dendrites were
removed. We severed all dendrites from larval ddaE neurons in
whole animals with a pulsed UV laser. After dendrite removal,
248 Cell Reports 6, 247253, January 30, 2014 2014 The Authors

larvae were returned to food. We imaged the cells at 5 hr to

make sure dendrites were completely severed and then on subsequent days to determine if the cells would die. At 24 hr after
injury, the cells were still alive. Moreover, in most cases new processes could be seen to emerge from the cell body. By 48 hr, a
branched dendrite arbor was visible in almost half (16/34) of the
animals tested (Figures 1B and S1A). The remaining neurons
grew fine processes alongside the axon (Figure S1B). We speculate that in neurons with periaxonal growth, the new processes
could not reach the layer in which they normally arborize, which
is between the epidermal cells and basement membrane (Kim
et al., 2012); in many of them, the cell body was seen to float
deeper into the animal after the dendrites were cut. The remaining analysis will focus only on the cells that regrew processes
into the region normally occupied by dendrites rather than along
the axon. At 96 hr after dendrite injury, the area of the body wall
covered by the new processes was smaller than in cells without
injury. However, when we counted dendrite branchpoints, we
found that the complexity had reached a similar level to that
before injury (Figure 1E). These neurons, which are part of a circuit that is responsible for coordinated motion (Hughes and

Thomas, 2007) and do not normally tile the entire body wall
(Grueber et al., 2002), perhaps rely more on complexity of the
arbor rather than exact area of coverage to function. We
conclude that the ddaE neuron can regenerate a branched arbor
after dendrite removal, and that it regrows to the same branching
complexity as uninjured neurons.
To test whether other cell types could respond to dendrite
damage by growing new processes, we performed dendrite
removal on the class IV neuron ddaC. Class IV neurons tile the
entire body wall (Grueber et al., 2002) and receive information
about painful stimuli (Hwang et al., 2007). After dendrite removal,
new processes initiated growth by 24 hr. At 48 hr after injury, an
elaborate arbor covered the central part of the ddaC territory
(Figure 1C). By 96 hr after injury, the entire territory was covered
(Figure 1C). Out of 27 neurons tested, all except two followed this
pattern (pooled data from all genotypes used, Figure S1C). Thus,
unlike the ddaE neuron, the ddaC neuron regenerated to cover
its complete territory.
To determine whether the regrown processes were correctly
specified as dendrites, we analyzed microtubule polarity in
the new neurites that emerged after dendrite removal. The presence of minus-end-out microtubules distinguishes dendrites
from axons in Drosophila, C. elegans, and mammalian neurons
(Baas et al., 1988; Goodwin et al., 2012; Stone et al., 2008) and
is a good indicator of compartment identity. The new processes
that formed after dendrite removal in the ddaC neuron initially
had slightly mixed polarity. By 48 hr after injury, this had resolved
to about 90% minus-end-out microtubules, similar to uninjured
ddaC neurons (Figure S1D). This result suggests that the new
processes are dendrites and is in sharp contrast to dendrite
growth initiated by damage to the proximal axon. In both
mammals (Gomis-Ruth et al., 2008) and flies (Stone et al.,
2010), proximal axotomy causes a new axon to grow from a
dendrite. However, this new axon is easily distinguished from
the processes that regrow after dendrite injury; it leaves the
normal territory of the dendrites, is unbranched, and has plusend-out microtubule polarity (Stone et al., 2010). To further test
the identity of the regrown processes, we used two additional
methods. First, we used a marker, Apc2-GFP, that localizes to
dendrite branchpoints, the proximal axon, but not more distal
regions of the axon (Rolls et al., 2007; Stone et al., 2010). This
marker was expressed in ddaC neurons and analyzed after
dendrite removal. Both 48 and 96 hr after dendrite removal, it
could be seen to occupy branchpoints in regrown processes,
again suggesting these are specified as dendrites (Figure S1E).
Second, we tested the effect of dynein on dendrite regrowth.
Dynein is known to be required for dendrite development, and
ddaC neurons in which it is reduced generate short, bushy
arbors (Satoh et al., 2008; Zheng et al., 2008). In fact, because
of the arrangement of microtubules in Drosophila neurons, it is
predicted to be required for the bulk of transport from the cell
body into dendrites (Rolls, 2011). Consistent with a role for
dynein in transporting building blocks for dendrites, but not
axons, axonal regeneration proceeded normally when dynein
was reduced by RNAi (Figure S1F). Dendrite regrowth after
removal initiated normally, but dendrite arbors were small
and bushy (Figure S1F), recapitulating the phenotype observed
during dendrite development (Satoh et al., 2008; Zheng et al.,

2008). Thus, several different lines of evidence suggest that the

processes that regrow after dendrite removal are correctly specified as dendrites.
Because previous studies have suggested that larval neurons
have limited capacity to regenerate dendrites after a single dendritic injury (Song et al., 2012; Stone et al., 2010; Sugimura et al.,
2003), we removed single dendrites from the ddaE and ddaC
neurons. In analyzing the results, we kept in mind that after total
dendrite removal the ddaE neuron regenerated a dendrite arbor
with similar complexity, but not coverage, to control arbors, and
the ddaC neuron regenerated to cover the body wall. We therefore analyzed number of branchpoints for ddaE and visually
scored coverage for ddaC (Figures S2A and S2B). Using this
perspective, we found that removal of a single dendrite triggered
a similar response in both cells to removal of all dendrites; that is,
the ddaC neuron regrew until its territory was covered, and the
ddaE neuron added branchpoints to its remaining dendrite until
complexity was regained. We also tested whether the position of
the injury might affect the outcome and severed some dendrites
further from the cell body. Again, we observed robust regrowth
(Figure S2C).
Late Larval and Adult Neurons Retain the Capacity to
Regrow Dendrites
Previous studies suggested that the capacity of neurons to
respond to dendrite damage decreases during larval life (Song
et al., 2012; Sugimura et al., 2003). We therefore aged larvae
longer than in the published studies and tested whether neurons
could still respond to dendrite injury. We saw no difference in
regenerative capacity between young and old larvae (Figure S2D). We conclude that dendrite injury triggers a robust
regenerative growth response in larval Drosophila neurons irrespective of age, branching complexity, or whether one or all dendrites are removed.
The dendrite arbors of ddaE and ddaC function during larval
life and so are, at least in this sense, mature. During pupariation,
dendrites from both neurons are pruned and new arbors are
regrown into the adult body wall. ddaC and other class IV neurons, including vada, persist through adult life, whereas ddaE
undergoes apoptosis 35 days after adults emerge (Shimono
et al., 2009). To address the possibility that larval neurons have
some dendrite growth potential not present in adult neurons,
we tested whether dendrite removal in adults could also trigger
regenerative growth. We developed methods to mount living
young adult flies so that we could sever dendrites in intact animals. We chose to use the most anterior vada neuron for these
experiments because it could be visualized in the abdomen
using the ppk-Gal4 driver with relatively little overlap from dendrites of other neurons.
As in larval neurons, we severed a major dendrite near its base
and determined whether the cell would undergo apoptosis or
would reinitiate dendrite outgrowth. We could not repeatedly
remount the same adult for imaging; therefore, we analyzed
different cells at various times after injury. At 48 hr after
dendrite removal, five of six neurons had new processes sprouting near the cell body (Figure 2). At 96 or 120 hr after injury, 12
of 13 neurons had regrown complex, branched arbors into
their normal territory (Figure 2). Thus, adult neurons seem to
Cell Reports 6, 247253, January 30, 2014 2014 The Authors 249

Figure 2. Adult Neurons Reinitiate Dendrite Outgrowth after

Dendrite Injury
The major dendrite root in the anterior vada neuron in the adult abdomen was
severed with a laser at 0 hr (except in top row). Flies were then returned to food
vials and aged for 2, 4, or 5 days. They were then remounted and the same
neuron was imaged. In all cases, the cell remained alive and new dendrites had
sprouted.

retain the capacity to respond to dendrite injury and to regenerate dendrites.

The Conserved DLK Axon Regeneration Pathway Is Not
Involved in the Response to Dendrite Injury
In C. elegans, Drosophila and mammals, efficient axon regeneration requires signaling through the dual leucine zipper kinase
(DLK, or Wallenda [wnd] in flies) pathway (Hammarlund et al.,
2009; Shin et al., 2012; Xiong et al., 2010; Yan et al., 2009).
250 Cell Reports 6, 247253, January 30, 2014 2014 The Authors

DLK is a mitogen-activated protein kinase kinase kinase

(MAPKKK) that initiates a signal transduction cascade after
axon injury that includes cJun N-terminal kinase (JNK) in flies
(Xiong et al., 2010), and both JNK and the related MAPK, p38,
in C. elegans (Nix et al., 2011). In Drosophila, the AP-1 transcription factor fos is required for the transcriptional response to axon
injury downstream of DLK (Xiong et al., 2010), and in mammals
accumulation of the AP-1 transcription factor jun in the nucleus
after axon injury requires DLK (Shin et al., 2012). Thus, DLK is
believed to be at the core of a conserved signaling cascade
that initiates the cell body response to axon injury.
To determine whether dendrite regeneration requires this
conserved injury signaling pathway, we used RNAi and mutant
approaches to lower levels of DLK and assayed dendrite regeneration after complete dendrite removal in ddaC. As a control for
the effectiveness of the RNAi in the ddaC neuron, we assayed
axon regeneration. In control ddaC neurons, seven of seven
axons initiated regeneration from the axon stump (Figures 3A
and 3D). In contrast, only one of eight of the wnd (DLK) RNAi neurons or one of nine of the wnd1/wnd3 loss-of-function (Collins
et al., 2006) mutants showed any sign of axon outgrowth (Figures
3B and 3D). Thus, wnd reduction effectively blocked axon injury
signaling in the ddaC neuron. We then tested dendrite regeneration in the same genetic backgrounds. The ddaC neurons
with reduced wnd regrew dendrite arbors with similar efficiency
and timing to control neurons (Figures 3C, 3D, and S3A). We also
tested whether wnd was required for dendrite regeneration in
ddaE neurons and again found that dendrite regeneration was
robust when wnd was targeted by RNAi (Figure S3B). This result
suggests DLK signaling is not required for dendrite regeneration.
In the response to axon injury, DLK levels increase due to reduction in turnover by the ubiquitin ligase highwire (hiw) (Xiong et al.,
2010). Hiw also seems to regulate DLK during dendrite development (Wang et al., 2013). However, like DLK, reduction of hiw
impaired the response to axon injury, but not dendrite injury
(Figure S3D).
In Drosophila, downstream components of the DLK pathway
include the kinase JNK (called bsk in flies), and the AP-1 transcription factor fos. Dominant-negative forms of JNK (bskDN)
or fos (fosDN) block the response to axon injury in motor neurons
(Xiong et al., 2010) and block axon regeneration in dendritic
arborization neurons (Stone et al., 2010; data not shown). We
therefore expressed both of these transgenes in the ddaC and
ddaE neurons. In both genetic backgrounds in both cell types
cases, dendrites regrew in the majority of neurons (Figure 4).
Thus, downstream components of the axon injury signaling
pathway do not seem to be required for dendrite regeneration.
It is possible that although the DLK/JNK/fos pathway is not
required for dendrite regeneration, it could be activated in
parallel with another pathway that can compensate for its loss
during the injury response. We therefore wished to use a reporter
for pathway activation. JNK signaling is regulated in a negative
feedback loop by MAP kinase phosphatases (MKPs) that are
transcribed in response to activity of the pathway (Caunt and
Keyse, 2012). After motor axon injury, levels of the MKP puckered (puc) can be seen to increase when monitored with a
puc-bgal reporter (Xiong et al., 2010). We wished to use a puc
reporter that could be visualized in whole, living animals, so we

Figure 3. wnd Is Not Required for Dendrite

Regeneration
(AC) Axons (A and B) or dendrites (C) of ddaC
neurons were severed at 0 hr. Larvae were
remounted for imaging 45 hr later to check for
complete severing and then at 48 and 96 hr to
assay regeneration. Quantitation is shown in (D).
For axon injury, cells that were scored as
regrowing extended axon stumps as shown in (A),
and cells that were scored as not regrowing retained a clear stump as in (B). For dendrite injury,
regrowing cells all had robust dendrite arbors as in
(C). Statistical significance was calculated with a
Fishers exact test.

tested whether a puc-GFP protein trap (Morin et al., 2001) that

reports on JNK signaling in embryos (Taniguchi et al., 2007)
would increase in nuclear fluorescence after axon injury in the
ddaE neuron. In uninjured ddaE neurons, low levels of pucGFP fluorescence were seen in the nucleus. We used ddaE for
this experiment because a similar class I da neuron, ddaD, lies
next to it and can be used for comparison (Figure S4). By 24 hr
after axon injury, the amount of nuclear fluorescence in ddaE
compared to its uninjured ddaD neighbor had increased approximately 4-fold (Figure S4). We therefore used this as a reporter for
JNK signaling after dendrite injury. When we tracked puc-GFP
levels in ddaE neurons after dendrite removal, no increase in
fluorescence was observed (Figure S4). We conclude that the
DLK/JNK pathway is neither required for the response to
dendrite injury nor activated by it. Thus, dendrite injury triggers
regenerative growth without using the conserved axon injury
signal transduction cascade.
DISCUSSION
It has not previously been clear whether mature neurons have
a surveillance mechanism that allows them to respond to
dendrite injury. We demonstrate that dendrite removal triggers
robust reinitiation of dendrite outgrowth in multiple neuron
types, even after development of dendrite shape is complete.
Unlike previous studies that have examined the response to
removal of single dendrites, we find that dendrite regeneration
is not restricted to a specific developmental window, or to neurons with complex dendrite arbors. Instead, our data suggest
that dendrite regeneration may be a property of many neurons
throughout life. It is also interesting to note that different cell

types seem to complete dendrite regrowth in distinct ways. Not surprisingly,

neurons that respond to pain regrew
dendrites until their normal territory was
covered. Intriguingly, neurons responsible for proprioception regrew dendrites
until they had regained the normal number of dendrite branchpoints.
This difference in how regeneration is
completed can account for some of the
differences between our conclusions
and those made in previous studies.
Area of coverage was previously assayed as a key aspect of
all types of dendrite regeneration (Song et al., 2012; Sugimura
et al., 2003), and so the response of ddaE to removal of a
single dendrite was not noted even though an increase in
complexity of the remaining dendrite is clear in the published
data (Song et al., 2012). By performing complete dendrite
removal, we were able to get much more striking results to
demonstrate the ability of multiple cell types to respond to
dendrite injury.
Our data suggest that neurons possess at least two different
injury surveillance systems: (1) signaling through DLK informs
the cell body of axon injury, and (2) an independent signal is
responsible for informing the cell body of dendrite injury. A previous study suggested that the Akt kinase may be a shared
component of axon and dendrite regeneration (Song et al.,
2012). Perhaps Akt is generally required to promote cell growth
downstream of specific regulators that inform the cell of axon
or dendrite injury.
If the DLK pathway does not signal dendrite injury, what type
of surveillance machinery might monitor dendrites? It seems
likely that transcription changes are required to allow growth of
a new dendrite arbor. Perhaps a signal is generated at the site
of injury and transported back to the cell body in the same way
that has been proposed for axons (Abe and Cavalli, 2008; Rishal
and Fainzilber, 2010). In this case, however, the retrograde motor
should be a kinesin rather than dynein because microtubules
have minus-end-out orientation in Drosophila dendrites (Stone
et al., 2008). Alternately, a change in electrical signals arising
from dendrites could directly regulate transcription factors in
the cell body. It will be very interesting to explore different types
of injury signals in the future.
Cell Reports 6, 247253, January 30, 2014 2014 The Authors 251

allow us to probe its importance in mammalian models of nervous system trauma.

EXPERIMENTAL PROCEDURES
Labeling Identified Neurons in Drosophila Larvae and Adults
For most experiments, UAS-mCD8-GFP was expressed in neuronal subsets to
identify specific neurons in whole animals. UAS-EB1-GFP was used to analyze
microtubule polarity and dynamics. GFP markers were expressed in class I
neurons with 221-Gal4 and class IV neurons with either 477-Gal4 (larvae) or
ppk-Gal4 in adults. For more detailed information about genotypes, please
see the Supplemental Experimental Procedures.
Axon and Dendrite Injury
In both larvae and adults, individual axons or dendrites were severed at their
base with a pulsed UV laser (Micropoint, Andor Technology). In all cases,
whole living animals were mounted for laser surgery and were recovered to
normal growth conditions immediately after severing. Animals were remounted for imaging at later time points. Please see the Supplemental Experimental Procedures for more details about imaging conditions.
SUPPLEMENTAL INFORMATION
Supplemental Information includes Supplemental Experimental Procedures
and four figures and can be found with this article online at http://dx.doi.org/
10.1016/j.celrep.2013.12.022.
ACKNOWLEDGMENTS
We are very grateful to the Bloomington Drosophila Stock Center, the Vienna
Drosophila RNAi Center, and FlyTrap; all are invaluable resources. Catherine
Collins, Wesley Grueber, and Dirk Bohmann generously provided us with
Drosophila stocks. Tadashi Uemura provided helpful information for imaging
da neurons in adults. Michelle Nguyen kindly helped collect flies and embryos.
This work was funded by the NIH (R01 GM085115), and M.M.R. was a Pew
Scholar in the Biomedical Sciences.

Figure 4. Downstream Components of the DLK Pathway Are

Dispensable for Dendrite Regeneration
(A and B) Examples of ddaC (A) and ddaE (B) neurons expressing bskDN and
fosDN are shown at different times after dendrite removal. Arrows indicate
sites of severing at 0 hr.
(C) ddaC cells were scored as regrowing dendrite arbors or not. All cells that
regrew had robust arbors similar to those shown in (A).
(D) Quantitation of branchpoint number in ddaE neurons after dendrite removal
was performed as in Figure 1. The error bars show the SD. The ns are numbers
of cells analyzed for each genotype at each time point following severing and
are shown on the bars in the graph.

The ability of mature neurons to initiate new growth in

response to large-scale dendrite damage could play an important role in recovery from stroke, seizure, and TBI. Considerable neurite sprouting occurs during recovery from these
conditions (Nudo, 2006), and so it is possible that both axon
and dendrite outgrowth are triggered. If so, it seems likely
that they are triggered through separate signaling pathways
because DLK is required for injury-induced axon outgrowth,
but not injury-induced dendrite outgrowth. By establishing a
tractable genetic model for dendrite regeneration, we should
be able to identify key players in this process. Having a molecular handle on this uncharacterized type of regeneration will
252 Cell Reports 6, 247253, January 30, 2014 2014 The Authors

Received: November 29, 2012

Revised: September 20, 2013
Accepted: December 12, 2013
Published: January 9, 2014
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