Phospholipase C-epsilon regulates epidermal morphogenesis in Caenorhabditis elegans.

Phospholipase C-epsilon regulates epidermal morphogenesis in Caenorhabditis elegans.

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Migration of cells within epithelial sheets is an important feature of embryogenesis and other biological processes.Previous work has demonstrated a role for inositol 1,4,5-trisphosphate (IP(3))-mediated calcium signalling in the rearrangement of epidermal cells (also known as hypodermal cells) during embryonic morphogenesis #grooming-organiser in Caenorhabditis elegans.However the mechanism by which IP(3) production is stimulated is unknown.IP(3) is produced by the action of phospholipase C (PLC).

We therefore surveyed the PLC family of C.elegans using RNAi and mutant strains, and found that depletion of PLC-1/PLC-epsilon produced substantial embryonic lethality.We used the epithelial cell marker ajm-1::gfp to follow the behaviour of epidermal cells and found that 96% of the arrested embryos have morphogenetic defects.These defects include defective ventral enclosure and aberrant dorsal intercalation.

Using time-lapse confocal microscopy we show that the migration of the ventral epidermal cells, especially of the leading cells, is slower and often fails in plc-1(tm753) embryos.As a consequence plc-1 loss of function results in ruptured embryos with a Gex phenotype (gut COLLAGEN PLUS on exterior) and lumpy larvae.Thus PLC-1 is involved in the regulation of morphogenesis.Genetic studies using gain- and loss-of-function alleles of itr-1, the gene encoding the IP(3) receptor in C.

elegans, demonstrate that PLC-1 acts through ITR-1.Using RNAi and double mutants to deplete the other PLCs in a plc-1 background, we show that PLC-3/PLC-gamma and EGL-8/PLC-beta can compensate for reduced PLC-1 activity.Our work places PLC-epsilon into a pathway controlling epidermal cell migration, thus establishing a novel role for PLC-epsilon.