Fantes P A
J Bacteriol. 1981 May;146(2):746-54. doi: 10.1128/jb.146.2.746-754.1981.
Previously known cell size (wee) mutations of fission yeast suppress the mitotic block caused by a defective cdc25 allele. Some 700 revertants of cdc25-22 were obtained after ultraviolet mutagenesis and selection at the restrictive temperature. Most revertants carried the original cdc25 lesion plus a mutation in or very close to the wee1 gene. Two partial wee1 mutations of a new type were found among the revertants. Two new wee mutations mapping at the cdc2 gene (cdc2-w mutants) were also obtained. The various mutations were examined for their effects on cell division size, their efficiency as cdc25 suppressors, and their dominance relations. Full wee1 mutations were found to suppress cdc25 lesions very efficiently, whereas partial wee1 mutations were poor suppressors. The cdc25 suppression ability of cdc2-w mutations was allele specific for cdc2, suggesting bifunctionality of the gene product. The wee1 mutations were recessive for cdc25 suppression; cdc2-w mutations were dominant. A model is proposed for the genetic control of mitotic timing and cell division size, in which the cdc2+ product is needed and is rate limiting for mitosis. The cdc2+ activity is inhibited by the wee1+ product, whereas the cdc25+ product relieves this inhibition.
裂殖酵母先前已知的细胞大小(wee)突变可抑制由有缺陷的cdc25等位基因引起的有丝分裂阻滞。在紫外线诱变并在限制温度下筛选后,获得了约700个cdc25-22的回复突变体。大多数回复突变体携带原始的cdc25损伤以及wee1基因内或其附近的一个突变。在回复突变体中发现了两种新型的部分wee1突变。还获得了两个定位于cdc2基因的新的wee突变(cdc2-w突变体)。研究了各种突变对细胞分裂大小的影响、它们作为cdc25抑制子的效率以及它们的显性关系。发现完全的wee1突变能非常有效地抑制cdc25损伤,而部分wee1突变则是较差的抑制子。cdc2-w突变对cdc25的抑制能力具有等位基因特异性,表明该基因产物具有双功能性。wee1突变对于cdc25抑制是隐性的;cdc2-w突变是显性的。提出了一个有丝分裂时间和细胞分裂大小的遗传控制模型,其中cdc2+产物是有丝分裂所必需的且是限速的。cdc2+活性受到wee1+产物的抑制,而cdc25+产物则解除这种抑制。