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Roles of septins in prospore membrane morphogenesis and spore wall assembly in Saccharomyces cerevisiae

机译:隔膜在酿酒酵母中的膜结构和孢子壁组装中的作用。

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摘要

The highly conserved family of septin proteins has important functions in cytokinesis in mitotically proliferating cells. A different form of cytokinesis occurs during gametogenesis in Saccharomyces cerevisiae, in which four haploid meiotic products become encased by prospore membrane (PSMs) and specialized, stress-resistant spore walls. Septins are known to localize in a series of structures near the growing PSM, but previous studies noted only mild sporulation defects upon septin mutation. We report that directed PSM extension fails in many septin-mutant cells, and, for those that do succeed, walls are abnormal, leading to increased susceptibility to heating, freezing, and digestion by the Drosophila gut. Septin mutants mislocalize the leading-edge protein (LEP) complex required for normal PSM and wall biogenesis, and ectopic expression of the LEP protein Ssp1 perturbs mitotic septin localization and function, suggesting a functional interaction. Strikingly, extra copies of septin CDC10 rescue sporulation and LEP localization in cells lacking Sma1, a phospholipase D–associated protein dispensable for initiation of PSM assembly and PSM curvature but required for PSM extension. These findings point to key septin functions in directing efficient membrane and cell wall synthesis during budding yeast gametogenesis.
机译:高度保守的Septin蛋白家族在有丝分裂增殖细胞的胞质分裂中具有重要功能。酿酒酵母在配子发生过程中会发生不同形式的胞质分裂,其中四个单倍体减数分裂产物被孢子膜(PSM)和专门的抗压力孢子壁包裹。已知Septins位于生长中的PSM附近的一系列结构中,但先前的研究表明,Septin突变后仅出现轻度的孢子形成缺陷。我们报道定向PSM扩展在许多septin突变细胞中失败,并且对于那些成功的细胞,壁异常,导致对果蝇肠道加热,冷冻和消化的敏感性增加。 Septin突变体将正常PSM和壁生物发生所需的前沿蛋白(LEP)复合体错位,并且LEP蛋白Ssp1的异位表达干扰有丝分裂性Septin的定位和功能,提示功能相互作用。令人惊讶的是,多余的Septin CDC10拷贝可以在缺乏Sma1的细胞中拯救孢子形成和LEP定位,Sma1是一种磷脂酶D相关蛋白,可用于启动PSM组装和PSM弯曲,但需要PSM延伸。这些发现指出了在发芽的酵母配子发生过程中指导有效的膜和细胞壁合成的关键Septin功能。

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