THE PHENOTYPE OF MES-2, MES-3, MES-4 AND MES-6, MATERNAL-EFFECT GENESREQUIRED FOR SURVIVAL OF THE GERMLINE IN CAENORHABDITIS-ELEGANS, IS SENSITIVE TO CHROMOSOME DOSAGE

Mutations in mes-2, mes-3, mes-4, and mes-6 result in maternal-effect sterility: hermaphrodite offspring of mes/mes mothers are sterile beca use of underproliferation and death of the germ cells, as well as an a bsence of gametes. Mutant germ cells do not undergo programmed cell de ath, but instead undergo a necrotic-type death, and their general poor health apparently prevents surviving germ cells from forming gametes. Male offspring of mes mothers display a significantly less severe ger mline phenotype than their hermaphrodite siblings, and males are often fertile, This differential response of hermaphrodite and male offspri ng to the absence of mes(+) product is a result of their different X c hromosome compositions; regardless of their sexual phenotype, XX worms display a more severe germline phenotype than XO worms, and XXX worms display the most severe phenotype. The sensitivity of the mutant phen otype to chromosome dosage, along with the similarity of two MES prote ins to chromatin-associated regulators of gene expression in Drosophil a, suggest that the essential role of the mes genes is in control of g ene expression in the germline. An additional, nonessential role of th e mes genes in the soma is suggested by the surprising finding that mu tations in the mes genes, like mutations in dosage compensation genes, feminize animals whose male sexual identity is somewhat ambiguous. We hypothesize that the mes genes encode maternally supplied regulators of chromatin structure and gene expression in the germline and perhaps in somatic cells of the early embryo, and that at least some of their targets are on the X chromosomes.