Biology Reference
In-Depth Information
CCAP, Burs-
a
and Burs-
b
at around 10-12 h after puparium formation,
and continue to express the peptides up to the pharate adult stage. Surpris-
ingly, of all CCAP neurons, the 12 late CCAP neurons are sufficient
for completing eclosion in all animals. When the authors ablated all CCAP
neurons up until to the mid-L3 stage, and then allowed for the late CCAP
neurons to differentiate at pupariation, all animals eclosed successfully,
suggesting that the late CCAP neurons exert an essential role during pupal
development. In contrast, ablation of all CCAP neurons including the late
CCAP neurons until after pupal ecdysis resulted in 100% failure of eclosion.
Likewise, when the late CCAP neurons were ablated after pupal ecdysis, that
is after they are required, all the animals eclosed with normal timing. The
only defect that was not rescued by the presence of late CCAP neurons
was wing inflation, which was consistent with the earlier finding that wing
inflation requires the presence of a subset of the CCAP-IN neurons, which
were also ablated in this experiment (
Davis, O'Keefe, Primrose, &Hodgetts,
2007
). Interestingly, when the authors used a stochastic ablation approach,
they found that the two subclasses of late CCAP neurons, the CCAP-ENs
and the CCAP-PLs, correlate with distinct phenotypes, and are there-
fore functionally separable. Specifically, they showed that the six late
CCAP-ENs correlated with a failure to properly execute leg extension,
while the CCAP-PL neurons corresponded to head eversion defects, both
commonly observed phenotypes in mutants with defects
in prepupal
development.
The authors were curious as to how the delayed appearance of the late
CCAP neurons was controlled. When they tracked postembryonic neuro-
blast lineages using BrdU, they never observed BrdU incorporation into
late CCAP neurons, suggesting these neurons derive from different cells.
Next, they followed early CCAP neurons by genetically marking these cells,
but they did not find late CCAP neurons expressing this marker, indicating
that the late CCAP neurons did not derive from their early cousins either.
These negative data prompted them to test the idea that the late CCAP
neurons are embryonic in origin, but stay undifferentiated until pupariation.
Indeed, through the elegant use of a series of genetic markers, the authors
demonstrated that the CCAP neurons are born in the embryonic segments
T3-A9, and that an unidentified mechanism delayed the differentiation of
the CCAPs in segments A5-A9, i.e. the late CCAP neurons.
Puparium formation is triggered by a large pulse of ecdysone at the end of
the third instar, which is followed by a smaller pulse
10-12 h later that cau-
ses head eversion and pupal ecdysis. This raised the possibility that the large
peak of ecdysone at the end of larval development triggers the onset of late
