Phospholipase C-ε Regulates Epidermal Morphogenesis in Caenorhabditis elegans
作者： Rafael P. Vázquez-Manrique , Anikó I. Nagy , James C. Legg , Olivia A. M. Bales , Sung Ly
DOI: 10.1371/JOURNAL.PGEN.1000043
关键词:
摘要: Migration of cells within epithelial sheets is an important feature embryogenesis and other biological processes. Previous work has demonstrated a role for inositol 1,4,5-trisphosphate (IP3)-mediated calcium signalling in the rearrangement epidermal (also known as hypodermal cells) during embryonic morphogenesis Caenorhabditis elegans. However mechanism by which IP3 production stimulated unknown. produced action phospholipase C (PLC). We therefore surveyed PLC family C. elegans using RNAi mutant strains, found that depletion PLC-1/PLC-e substantial lethality. used cell marker ajm-1::gfp to follow behaviour 96% arrested embryos have morphogenetic defects. These defects include defective ventral enclosure aberrant dorsal intercalation. Using time-lapse confocal microscopy we show migration cells, especially leading slower often fails plc-1(tm753) embryos. As consequence plc-1 loss function results ruptured with Gex phenotype (gut on exterior) lumpy larvae. Thus PLC-1 involved regulation morphogenesis. Genetic studies gain- loss-of-function alleles itr-1, gene encoding receptor elegans, demonstrate acts through ITR-1. double mutants deplete PLCs background, PLC-3/PLC-γ EGL-8/PLC-β can compensate reduced activity. Our places PLC-e into pathway controlling migration, thus establishing novel PLC-e.
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