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Curr Biol. 2012 Jan 10;22(1):1-11. doi: 10.1016/j.cub.2011.12.009. Epub 2011 Dec 22.

Semaphorin and Eph receptor signaling guide a series of cell movements for ventral enclosure in C. elegans.

Author information

1
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5S 1A8, Canada.

Abstract

BACKGROUND:

In the last stage of the Caenorhabditis elegans body wall closure, an open pocket in the epidermis is closed by the migration of marginal epidermal P/pocket cells to the ventral midline. The cellular and molecular mechanisms of this closure remain unknown.

RESULTS:

Cells within the pocket align to form a bridge for migration of contralateral P cell pair P9/10 L,R (and neighboring P cells) to the midline. Bridge formation involves rearrangement of five sister pairs of PLX-2/plexin and VAB-1/Eph receptor expressing "plexin band" cells, of which three pairs form a scaffold for bridge assembly and two pairs form the bridge. Bridge formation requires VAB-1 kinase-dependent extension of presumptive bridge cells over scaffold cells toward the ventral midline. An unassembled vab-1 null mutant bridge obstructs P cell migration, which is largely overcome by plexin band expression of VAB-1 or VAB-1(delC) (a kinase deletion of VAB-1). VAB-1 also functions redundantly with MAB-20/semaphorin to prevent perdurant gaps between sister plexin band cells that block P cell migration.

CONCLUSIONS:

The Eph receptor mediates cellular extensions required for bridge formation, independently facilitates P cell migration to the midline, and functions redundantly with PLX-2/plexin to prevent gaps in the bridge used for P9/10 cell migration in body wall closure.

PMID:
22197242
PMCID:
PMC4306670
DOI:
10.1016/j.cub.2011.12.009
[Indexed for MEDLINE]
Free PMC Article

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