Schmidt Martin, Varma Archana, Drgon Tomás, Bowers Blair, Cabib Enrico
National Institute of Diabetes and Digestive and Kidney Diseases, Laboratory of Biochemistry and Genetics, Bethesda, Maryland 20892, USA.
Mol Biol Cell. 2003 May;14(5):2128-41. doi: 10.1091/mbc.e02-08-0547. Epub 2003 Feb 6.
CLA4, encoding a protein kinase of the PAK type, and CDC11, encoding a septin, were isolated in a screen for synthetic lethality with CHS3, which encodes the chitin synthase III catalytic moiety. Although Ste20p shares some essential function with Cla4p, it did not show synthetic lethality with Chs3p. cla4 and cdc11 mutants exhibited similar morphological and septin localization defects, including aberrant and ectopic septa. Myo1p, which requires septins for localization, formed abnormally wide rings in cla4 mutants. In cultures started with unbudded cells, an inhibitor of Chs3p activity, nikkomycin Z, aggravated the abnormalities of cla4 and cdc11 mutants and gave rise to enlarged necks at the mother-bud junction, leading to cell death. It is concluded that Cla4p is required for the correct localization and/or assembly of the septin ring and that both the septin ring and the Chs3p-requiring chitin ring at the mother-bud neck cooperate in maintaining the neck constricted throughout the cell cycle, a vital function in budding yeast.
CLA4编码一种PAK类型的蛋白激酶,CDC11编码一种septin蛋白,它们是在与CHS3(编码几丁质合酶III催化部分)的合成致死筛选中分离得到的。尽管Ste20p与Cla4p具有一些基本功能,但它与Chs3p没有表现出合成致死性。cla4和cdc11突变体表现出相似的形态和septin定位缺陷,包括异常和异位隔膜。Myo1p的定位需要septin,在cla4突变体中形成异常宽的环。在用未出芽细胞开始的培养物中,Chs3p活性抑制剂尼可霉素Z加剧了cla4和cdc11突变体的异常,并在母-芽连接处产生扩大的颈部,导致细胞死亡。得出的结论是,Cla4p是septin环正确定位和/或组装所必需的,并且母-芽颈部的septin环和需要Chs3p的几丁质环在整个细胞周期中协同维持颈部收缩,这是芽殖酵母中的一项重要功能。