Document Type
Article
Date
8-29-1991
Keywords
Amino acid sequence, Caenorhabditis elegans Proteins, Cell division, Caenorhabditis/embryology, Caenorhabditis/genetics, Germ cells, Membrane proteins, Molecular sequence data, Mutation, Phenotype, Vulva/embryology, Vulva growth and development
Language
English
Disciplines
Biology
Description/Abstract
The glp-1 and lin-12 genes encode homologous transmembrane proteins that may act as receptors for cell interactions during development. The glp-1 product is required for induction of germ-line proliferation and for embryogenesis. By contrast, lin-12 mediates somatic cell interactions, including those between the precursor cells that form the vulval hypodermis (VPCs). Here we analyse an unusual allele of glp-1, glp-1(q35), which displays a semidominant multivulva phenotype (Muv), as well as the typical recessive, loss-of-function Glp phenotypes (sterility and embryonic lethality). We find that the effects of glp-1(q35) on VPC development mimic those of dominant lin-12 mutations, even in the absence of lin-12 activity. The glp-1(q35) gene bears a nonsense mutation predicted to eliminate the 122 C-terminal amino acids, including a ProGluSerThr (PEST) sequence thought to destabilize proteins. We suggest that the carboxy terminus bears a negative regulatory domain which normally inactivates glp-1 in the VPCs. We propose that inappropriate glp-1(q35) activity can substitute for lin-12 to determine vulval fate, perhaps by driving the VPCs to proliferate.
Recommended Citation
Mango, Susan E.; Maine, Eleanor M.; and Kimble, Judith, "Carboxy-Terminal Truncation Activates glp-1 Protein to Specify Vulval Fates in Caenorhabditis elegans" (1991). Biology - All Scholarship. 14.
https://surface.syr.edu/bio/14
Source
Local input
Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.
