Maternal effect lethal mutations in
gut-2 and
gut-4 lead to very similar embryonic defects including a very penetrant failure to produce differentiated gut cells and pharyngeal muscle cells, a failure of E cells to elongate their cell-cycle at the 26-cell stage of embryogenesis and a failure to gastrulate. Embryos arrest development with an approximately wild-type number of cells and differentiated hypodermal, body-wall muscle and neuronal tissues. Laser ablation of early blastomeres in embryos from mutant mothers indicate that E and MS produce hypodermal, body-wall muscle and neuronal cells. These tissues are normally produced by the C blastomere; however, the number of neuronal cells derived from the mutant E and MS blastomeres suggests that they do not take on precisely a C-like fate. Deletion mutations of
gut-2 have a slow-growing, sterile phenotype and are thus stronger than the maternal effect lethal mutations. Cloning of
gut-2 and of
gut-4 has revealed that both of these genes encode proteins with similarity to Sm-like proteins, which are related to core spliceosomal snRNP proteins. A functional GUT-2::HA protein is localized to nuclei and is expressed in most cells, including the germline. The lesions in two
gut-2 alleles and four
gut-4 alleles have been analyzed; all six mutations affect the same conserved glycine residue in the GUT-2 and GUT-4 proteins. Thus the maternal effect lethal mutations are special alleles of these genes. It is possible that these special alleles affect a particular function of
gut-2 and
gut-4 leading to the observed defects in E- and MS-derived cell fate. Alternatively, these special alleles may reduce the efficiency of general splicing so that the production of mature mRNA is reduced for a few transcripts whose levels are critical for specifying the fates of these cells.