Leveleki Leonora, Mahlert Michael, Sandrock Björn, Bölker Michael
Philipps-Universität Marburg, Fachbereich Biologie, 35032 Marburg, Germany.
Mol Microbiol. 2004 Oct;54(2):396-406. doi: 10.1111/j.1365-2958.2004.04296.x.
The phytopathogenic basidiomycete Ustilago maydis displays a dimorphic switch between budding growth of haploid cells and filamentous growth of the dikaryon. In a screen for mutants affected in morphogenesis and cytokinesis, we identified the serine/threonine protein kinase Cla4, a member of the family of p21-activated kinases (PAKs). Cells, in which cla4 has been deleted, are viable but they are unable to bud properly. Instead, cla4 mutant cells grow as branched septate hyphae and divide by contraction and fission at septal cross walls. Delocalized deposition of chitinous cell wall material along the cell surface is observed in cla4 mutant cells. Deletion of the Cdc42/Rac1 interaction domain (CRIB) results in a constitutive active Cla4 kinase, whose expression is lethal for the cell. cla4 mutant cells are unable to induce pathogenic development in plants and to display filamentous growth in a mating reaction, although they are still able to secrete pheromone and to undergo cell fusion with wild-type cells. We propose that Cla4 is involved in the regulation of cell polarity during budding and filamentation.
植物病原担子菌玉蜀黍黑粉菌（Ustilago maydis）在单倍体细胞的出芽生长和双核体的丝状生长之间表现出二态性转换。在一项针对形态发生和胞质分裂受影响的突变体的筛选中，我们鉴定出丝氨酸/苏氨酸蛋白激酶Cla4，它是p21激活激酶（PAK）家族的成员。cla4基因被缺失的细胞是有活力的，但它们不能正常出芽。相反，cla4突变体细胞以分支的有隔菌丝形式生长，并通过在隔膜横壁处收缩和分裂进行分裂。在cla4突变体细胞中观察到几丁质细胞壁物质沿细胞表面的异位沉积。Cdc42/Rac1相互作用结构域（CRIB）的缺失导致组成型活性Cla4激酶的产生，其表达对细胞是致命的。cla4突变体细胞无法在植物中诱导致病发育，也无法在交配反应中表现出丝状生长，尽管它们仍然能够分泌信息素并与野生型细胞进行细胞融合。我们提出Cla4参与出芽和丝状生长过程中细胞极性的调节。
