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© The Rockefeller University Press, 0021-9525/1999//1165 $5.00
The Journal of Cell Biology, Volume 145, Number 6, , 1999 1165-1175

Article

p24 Proteins and Quality Control of LIN-12 and GLP-1 Trafficking in Caenorhabditis elegans



Chenhui Wen* and Iva Greenwald*,{ddagger}

* Department of Biochemistry and Molecular Biophysics, {ddagger} Howard Hughes Medical Institute, Columbia University, College of Physicians and Surgeons, New York, New York 10032

Mutations in the Caenorhabditis elegans sel-9 gene elevate the activity of lin-12 and glp-1, which encode members of the LIN-12/NOTCH family of receptors. Sequence analysis indicates SEL-9 is one of several C. elegans p24 proteins. Allele-specific genetic interactions suggest that reducing sel-9 activity increases the activity of mutations altering the extracellular domains of LIN-12 or GLP-1. Reducing sel-9 activity restores the trafficking to the plasma membrane of a mutant GLP-1 protein that would otherwise accumulate within the cell. Our results suggest a role for SEL-9 and other p24 proteins in the negative regulation of transport of LIN-12 and GLP-1 to the cell surface, and favor a role for p24 proteins in a quality control mechanism for endoplasmic reticulum–Golgi transport.

Key Words: LIN-12 • SEL-9 • Notch • p24 • Emp24p

Abbreviations used in this paper: AC, anchor cell; ds, double-stranded; Egl, Egg-laying defective; Muv, Multivulva; RNAi, RNA-mediated interference; VU, ventral uterine precursor cell.

The initial phase of this work was supported by National Institutes of Health grant GM37602 (to I. Greenwald). I. Greenwald is an Associate Investigator of the Howard Hughes Medical Institute.


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