From owner-celegans@net.bio.net Thu Dec 12 22:00:00 1996
Path: biosci!CMGM.STANFORD.EDU!lackner
From: lackner@CMGM.STANFORD.EDU ("Mark R. Lackner")
Newsgroups: bionet.celegans
Subject: regarding ts mutations
Date: 13 Dec 1996 11:29:18 -0800
Organization: Stanford University
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Message-ID: <32B1AE98.4299@cmgm.stanford.edu>
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Dear Erik,

	In the course of studying the C. elegans MAP kinase mpk-1, I have
characterized two ts mutations. Neither of them appear to conform to the
general rules. In the first case the same lesion was found in two
independent alleles, mpk-1(ga110) and mpk-1(oz140). The mutation is
predicted to cause a trp to amber stop substitution that would lop off
the last 25 amino acids of a 376 amino acid protein. The ts phenotype is
fairly subtle. All worms are sterile at all temperatures.  However, at
20 degrees worms exhibit only a weak vulval phenotype (partial
underinduction of P6.p in ~60% of worms), whereas at 25 degrees a severe
vulval phenotype is seen (~80% of worms are completely vulvaless). These
alleles are smg-1 suppressible, so it's also possible that the ts nature
of the alleles reflects on some temperature sensitivity of the smg
system. Is smg suppression a temperature dependent process? 

	The second case, mpk-1(ga111), is a bit more dramatic. At 20 degrees
worms homozygous for this allele appear basically wild type, while at 25
degrees 100% of them are sterile. The mutation is predicted to cause a
valine to glycine substitution near the predicted substrate binding
site. The residue is conserved in all MAP kinases and is embedded in the
sequence SANVLHRD.

Regards,

Mark Lackner

.