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- Title
MAP Kinase Signaling Antagonizes PAR-1 Function During Polarization of the Early Caenorhabditis elegans Embryo.
- Authors
Spilker, Annina C.; Rabiotta, Alexia; Zbinden, Caroline; Labbé, Jean-Claude; Gotta, Monica
- Abstract
PAR proteins (partitioning defective) are major regulators of cell polarity and asymmetric cell division. One of the par genes, par-1, encodes a Ser/Thr kinase that is conserved from yeast to mammals. In Caenorhabditis elegans, par-1 governs asymmetric cell division by ensuring the polar distribution of cell fate determinants. However the precise mechanisms by which PAR-1 regulates asymmetric cell division in C. elegans remain to be elucidated. We performed a genomewide RNAi screen and identified six genes that specifically suppress the embryonic lethal phenotype associated with mutations in par-1. One of these suppressors is mpk-1, the C. elegans homolog of the conserved mitogen activated protein (MAP) kinase ERK. Loss of function of mpk-1 restored embryonic viability, asynchronous cell divisions, the asymmetric distribution of cell fate specification markers, and the distribution of PAR-1 protein in par-1 mutant embryos, indicating that this genetic interaction is functionally relevant for embryonic development. Furthermore, disrupting the function of other components of the MAPK signaling pathway resulted in suppression of par-1 embryonic lethality. Our data therefore indicates that MAP kinase signaling antagonizes PAR-1 signaling during early C. elegans embiyonic polarization.
- Subjects
MITOGEN-activated protein kinases; CAENORHABDITIS elegans; CELL proliferation; CELL polarity; CELL division; GENOTYPE-environment interaction
- Publication
Genetics, 2009, Vol 183, Issue 3, p965
- ISSN
0016-6731
- Publication type
Article
- DOI
10.1534/genetics.109.106716