Worm Breeder's Gazette 10(1): 112

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Pleotropic Suppression by Morpho-mabs

J. Hodgkin, A. Papp and V. Ambros

Mutations in two genes, mab-1 I and mab-11 I, have a conspicuous 
effect on morphogenesis of the male tail, leading to an abnormal 
swollen bursa (the 'Morpho-mab' phenotype).  Vulval morphogenesis is 
also affected, so that mab-1 and mab-11 hermaphrodites have an 
enlarged, protrusive vulva (the 'P-vul' phenotype).  Surprisingly, 
these mutations act as weak recessive suppressors of mutations in tra-
3 which cause partial masculinization of XX animals.  One hypomorphic 
mutation of tra-2 e1209 is also weakly suppressed, but strong (
putative null) alleles of tra-2 are not affected (WBG 9#2:94; 1987 
Meeting Abstr.  p.111).
Selection for reversion of lin-29 mutants, which have a retarded 
heterochronic hypodermal phenotype, led to the isolation of several 
unlinked suppressors that acted as recessive suppressors of one lin-29 
mutant, n546, but did not affect other lin-29 alleles (1987 Meeting 
Abstr.  p.  84; WBG contribution by A.P.  & V.A., this issue).  
Conversations at the 1987 Worm Meeting (also involving Michael Shen 
and Andrew Fire) suggested that some of the lin-29 suppressors might 
be morpho-mabs.  This is the case:  ma129 is an allele of mab-1 and 
ma123 is an allele of mab-11.  Both were isolated as n546 suppressors, 
but also suppress tra-2(e1209).  Conversely, the reference alleles of 
mab-1 and mab-11 (e1228 and e2008) act as good suppressors of n546.
Two other suppressors obtained by the n546 reversion also have a 
Morpho-mab phenotype and suppress e1209.  These identify new loci: 
ma117 maps to LGIV, near unc-5 and is assigned to mab-13 while ma116 
maps to LGV, near dpy-11 and is assigned to mab-14.  All mutations at 
these four loci (mab-1 (seven alleles), mab-11 (seven alleles), mab-13 (
two alleles), mab-14 (one allele)) appear to have much the same Morpho-
mab and P-vul phenotypes and (when tested) act equally well as 
suppressors of e1209 or n546 irrespective of how they were isolated.  
Mutations of mab-1 and mab-11 appear to be fairly frequent, and their 
phenotypes are recessive, but we do not know if they are simple loss-
of-function alleles.
These mutations behave as allele-specific suppressors for two 
apparently unrelated genes, which makes it possible that they are 
informational suppressors of some kind.  If this is so, then they may 
be encountered in the course of other reversion screens.  How the 
suppression is working is entirely unclear, but it may be significant 
that the suppressed tra-2 allele is hypomorphic (and tra-3 mutations 
can be regarded as honorary tra-2 hypomorphs).  Perhaps e1209 and n546 
both produce very unstable proteins, and the suppression occurs 
because protein degradation occurs more slowly in mab-1 etc.  Other 
possibilities can be envisaged.  None of these hypotheses provides a 
good explanation of the bursal and vulval abnormalities.
Other unexplained interactions have been encountered.  For example, 
mab-1 and mab-11 enhance, rather than suppress, the paralysed 
phenotype of unc-54 mutations such as e190 and e1300.  Enhancement 
effects have also been observed with certain tra-1 alleles (see WBG 
contribution by J.H., this issue).