Open AccessPolarized epidermal growth factor secretion ensures robust vulval cell fate specification in Caenorhabditis elegans
Author(s) -
Louisa Mereu,
Matthias K. Morf,
Silvan Spiri,
Peter L. Gutiérrez,
Juan M. Escobar-Restrepo,
Michael Daube,
Michael Walser,
Alex Hajnal
Publication year - 2020
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.15
H-Index - 36
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.175760
Subject(s) - biology , caenorhabditis elegans , epidermal growth factor , secretion , mapk/erk pathway , ectopic expression , microbiology and biotechnology , cell polarity , signal transduction , polarity (international relations) , receptor , epidermal growth factor receptor , cell , gene , genetics , endocrinology
The anchor cell (AC) in C. elegans secretes an epidermal growth factor (EGF) homolog that induces adjacent vulval precursor cells (VPCs) to differentiate. The EGF receptor in the nearest VPC sequesters the limiting EGF amounts released by the AC to prevent EGF from spreading to distal VPCs. Here, we show that not only EGFR localization in the VPCs but also EGF polarity in the AC is necessary for robust fate specification. The AC secretes EGF in a directional manner towards the nearest VPC. Loss of AC polarity causes signal spreading and, when combined with MAPK pathway hyperactivation, the ectopic induction of distal VPCs. In a screen for genes preventing distal VPC induction, we identified sra-9 and nlp-26 as genes specifically required for polarized EGF secretion. sra-9(lf) and nlp-26(lf) mutants exhibit errors in vulval fate specification, reduced precision in VPC to AC alignment and increased variability in MAPK activation. sra-9 encodes a seven-pass transmembrane receptor acting in the AC and nlp-26 a neuropeptide-like protein expressed in the VPCs. SRA-9 and NLP-26 may transduce a feedback signal to channel EGF secretion towards the nearest VPC.