| Abstract: | During C. elegans development, EGF signal from the anchor cell (AC) induces the roughly six equipotent vulval precursor cells (VPCs) to assume the pattern 3˚-3˚-2˚-1˚-2˚-3˚ of cell fates. The VPC closest to the AC is induced via the Ras-Raf-MEK-ERK MAP kinase cascade to assume 1˚ fate. Presumptive 1˚ cells express DSL ligands to induce the two neighboring cells via the Notch receptor to assume 2˚ fate. In contrast, 3˚ fate is typically referred to as the "ground" or "uninduced" cell fate; 3˚ cells divide once and fuse with the surrounding epithelium. We observed that MIG-15, a MAP4 kinase, plays a role in VPC patterning. Upon genetic perturbation of MIG-15 function, we observed an increase in ectopic 1˚ as well as ectopic 2˚ cells. This is also true for RAP-2, a protein shown in various systems to activate MIG-15. Both RAP-2 and MIG-15 are necessary for full expression of a marker expressed in 3° cells. Endogenous CRISPR tags of MIG-15 and RAP-2 revealed ubiquitous expression with cytosolic and cell-membrane localization of both genes respectively. Our work positions us to explore signals that promote "ground" developmental state and perhaps informs the relationship between cancers and stromal cells. The electronic version of this dissertation is accessible from https://hdl.handle.net/1969.1/198706 |
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