A gene which encodes a predicted protein kinase can restore some functions of the ras gene in fission yeast.

Abstract

The ras1‐ mutation of the fission yeast Schizosaccharomyces pombe interferes with sexual differentiation by preventing conjugation and causing inefficient sporulation. From a gene library, we have isolated a gene, byr1+, which when in high copy number restores efficient sporulation to ras1‐ strains. byr1+ encodes a putative 340‐amino acid protein product, the sequence of which strongly suggests that it functions as a protein kinase. Gene disruption experiments show that loss of byr1+ function does not interfere with mitotic growth but it completely prevents both conjugation and sporulation. byr1 is thus another important gene in the sexual differentiation pathway and we believe that at least part of ras1 function is to act directly or indirectly through byr1 to modulate protein phosphorylation.

A gene encoding a protein with seven zinc finger domains acts on the sexual differentiation pathways of Schizosaccharomyces pombe.

“…Cells lacking sarl have a phenotype virtually indistinguishable from cells with activated raslvall7. byrl and byr2 were each found as multicopy suppressors of the sporulation defect of rasI null diploid cells, and both are predicted to encode serine/threonine kinases (Nadin-Davis and Nasim, 1988;Wang et al, 1991b). Overexpression of the byrl and byr2 genes only poorly suppress the conjugation defects of rasl-haploid cells (see RESULTS).…”

“…rasI null haploid strains fail to conjugate, and rasl null diploid strains fail to sporulate (Fukui et al, 1986). rasl null strains are more spherical in shape than the rod-shaped wild-type S. pombe strains (Nadin-Davis and Nasim, 1988). Cells expressing the activated mutant raslvall7 gene are partially defective in conjugation (Fukui et al, 1986;NadinDavis et al, 1986a).…”

The Schizosaccharomyces pombe mra1 gene, which is required for cell growth and mating, can suppress the mating inefficiency caused by a deficit in the Ras1 activity

“…Two protein kinase genes have been isolated as highcopy-number suppressors of the poor sporulation efficiency of ras1-defective cells (Nadin- Davis & Nasim 1988;Wang et al 1991). Their products, namely Byr1 (Nadin- Davis & Nasim 1988, 1990) and Byr2 (Wang et al 1991), are homologous to MAPKK (mitogen-activated protein kinase kinase) and MAPKKK (MAPKK kinase), respectively, and apparently function downstream of Ras1.…”

“…These kinases, together with Spk1, a MAP (mitogen-activated protein) kinase homologue identified in an entirely different screen (Toda et al 1991), constitute a cascade (Gotoh et al 1993;Neiman et al 1993). In addition to genetic and physiological evidence suggesting the interaction of Ras1 and this MAP kinase cascade (Nadin- Davis & Nasim 1988;Nadin-Davis & Nasim 1990;Wang et al 1991), evidence indicating physical contact between Ras1 and Byr2 has been obtained (Masuda et al 1995). Thus, Ras protein operates upstream of a MAP kinase cascade in S. pombe, as is the case in higher eukaryotes (Moodie et al 1993;Neiman et al 1993).…”

“…To address this question, we set out to isolate high-copy-number suppressors of the mating deficiency of a ras1 mutant. Three genes, namely byr1, byr2 and byr3, have been isolated as highcopy-number suppressors that can alleviate the sporulation deficiency of the ras1 disruptant (Nadin- Davis & Nasim 1988;Wang et al 1991;Xu et al 1992), but neither suppressor mutations nor high-copynumber suppressors that can recover the mating ability 304 Genes to Cells, (1996) 1, [303][304][305][306][307][308][309][310][311][312][313][314][315] # in the ras1 disruptant have been reported to date. We found that an alteration in the effector region of Ras1 causes less stringent mutant phenotypes than the disruption of ras1.…”