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• W2796804546 abstract "Abstract The notoriety of the small GTPase Ras as the most mutated oncoprotein has led to a well-characterized signaling network largely conserved across metazoans. Yet the role of its close relative Rap1 (Ras Proximal), which shares 100% identity between their core effector binding sequences, remains unclear. A long-standing controversy in the field is whether Rap1 also functions to activate the canonical Ras effector, the S/T kinase Raf. We used the developmentally simpler Caenorhabditis elegans , which lacks the extensive paralog redundancy of vertebrates, to examine the role of RAP-1 in two distinct LET-60/Ras-dependent cell fate patterning events: induction of 1˚ vulval precursor cell (VPC) fate and of the excretory duct cell. Fluorescently tagged endogenous RAP-1 is localized to plasma membranes and is expressed ubiquitously, with even expression levels across the VPCs. RAP-1 and its activating GEF PXF-1 function cell autonomously and are necessary for maximal induction of 1˚ VPCs. Critically, mutationally activated endogenous RAP-1 is sufficient both to induce ectopic 1˚s and duplicate excretory duct cells. Like endogenous RAP-1, before induction GFP expression from the pxf-1 promoter is uniform across VPCs. However, unlike endogenous RAP-1, after induction GFP expression is increased in presumptive 1˚s and decreased in presumptive 2˚s. We conclude that RAP-1 is a positive regulator that promotes Ras-dependent inductive fate decisions. We hypothesize that PXF-1 activation of RAP-1 serves as a minor parallel input into the major LET-60/Ras signal through LIN-45/Raf." @default.
• W2796804546 created "2018-04-24" @default.
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• W2796804546 date "2018-04-09" @default.
• W2796804546 modified "2023-09-27" @default.
• W2796804546 title "C. elegans RAP-1 reinforces LET-60/Ras induction of cell fate" @default.
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• W2796804546 doi "https://doi.org/10.1101/297812" @default.
• W2796804546 hasPublicationYear "2018" @default.
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