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The developmental age of muscle cells in vitro correlated with muscle arm development.
The new alleles represent partial loss-of-function mutants that specifically disrupt muscle arm development.
Interestingly, the muscle arm development was similarly affected in lin-12 e2621), lin-12 e2621hat the musuggestingevelopmenthatghtheequire the positive transcriptional feedback of the LIN-12/Notch pathway.
If vm2 postsynaptic differentiation and muscle arm development are independent of presynaptic components, we asked whether the surrounding vulval epithelial cells that physically contact vm2 provide guidance for vm2 specification and muscle arm development.
We hypothesized that the late egg-laying defect could be caused by the defects of vm2 muscle arm development.
We found that postsynaptic muscle arm development in egg-laying circuit is mediated by LIN-12/Notch-dependent cell specification.
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Therefore, the ability to form muscle arms during development dictates the choice of vm2, but not its sister cell vm1, to become the postsynaptic partner of the egg-laying motor neurons.
However, the data do document an interesting muscle differentiation program that precedes postsynaptic differentiation and the participation of the muscle cell in synapse development through muscle arm formation.
We also agree with the reviewers that we are studying a "muscle differentiation program that precedes postsynaptic differentiation and the participation of the muscle cell in synapse development through muscle arm formation".
The mosaic rescue analyses argue that lin-12 functions cell-autonomously in vm2 to specify vm2 postsynaptic development through regulating muscle arm formation.
The HSN presynaptic development occurs before vm2 muscle arm formation and is independent of vulval muscles.
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