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.
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).