Rho5 is the yeast homolog of the human small GTPase Rac1. We characterized the genes encoding Rho5 and the subunits of its dimeric activating guanine-nucleotide-exchange factor (GEF), Dck1 and Lmo1, in the yeast Kluyveromyces lactis. Rapid translocation of the three GFP-tagged components to mitochondria upon oxidative stress and carbon starvation indicate a similar function of KlRho5 in energy metabolism and mitochondrial dynamics as described for its Saccharomyces cerevisiae homolog. Accordingly, Klrho5 deletion mutants are hyper-resistant towards hydrogen peroxide. Moreover, synthetic lethalities of rho5 deletions with key components in nutrient sensing, such as sch9 and gpr1, are not conserved in K. lactis. Instead, Klrho5 deletion mutants display morphological defects with strengthened lateral cell walls and protruding bud scars. The latter result from aberrant cytokinesis, as observed by following the budding process in vivo and by transmission electron microscopy of the bud neck region. This phenotype can be suppressed by KlCDC42G12V, which encodes a hyper-active variant. Data from live-cell fluorescence microscopy support the notion that KlRho5 interferes with the actin moiety of the contractile actomyosin ring, with consequences different from those previously reported for mutants lacking myosin.

中文翻译：

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小 GTPase KlRho5 响应氧化应激并影响胞质分裂。

Rho5 是人类小 GTPase Rac1 的酵母同源物。我们在酵母乳酸克鲁维酵母中表征了编码 Rho5 的基因及其二聚体激活鸟嘌呤核苷酸交换因子 (GEF)、Dck1 和 Lmo1 的亚基。三个 GFP 标记的成分在氧化应激和碳饥饿时快速易位到线粒体表明 KlRho5 在能量代谢和线粒体动力学中的类似功能，如其酿酒酵母同源物所述。因此，Klrho5 缺失突变体对过氧化氢具有超强抗性。此外，具有营养传感关键成分的 rho5 缺失的合成致死率，如 sch9 和 gpr1，在 K. lactis 中并不保守。相反，Klrho5 缺失突变体表现出形态缺陷，具有加强的横向细胞壁和突出的芽痕。后者是异常胞质分裂的结果，如通过体内出芽过程和芽颈区域的透射电子显微镜观察到的。这种表型可以被 KlCDC42G12V 抑制，它编码一个过度活跃的变体。来自活细胞荧光显微镜的数据支持 KlRho5 干扰收缩肌球蛋白环的肌动蛋白部分的观点，其后果与先前报道的缺乏肌球蛋白的突变体不同。