The role of small GTPases for exocyst localization and regulation of polar growth in Ustilago maydis

二态转换是许多病原真菌的一个特征。在植物病原菌Ustilago maydis的整个生活史中，它经历了从萌芽到丝状生长的形态发生转变。这种转换是由多等位基因b交配型基因座控制的，它编码一对同源结构域转录因子，命名为BE和BW。虽然已经鉴定了许多受该主控基因调控的基因，但b型交配型基因诱导丝状细胞生长的分子机制仍不清楚。我们正在研究Rho家族GTP结合蛋白rac1的功能，它在丝状细胞生长过程中扮演着分子开关的角色。我们发现b诱导的细丝形成涉及到对rac1特异的Rho-GFCDc24活性的刺激。依赖于RHO-环境基金的活性rac1重新招募到Bem1-支架三元复合体中，触发CDc24的破坏，从而构成一个负反馈循环。我们将分析这种自动调节在建立和维持菌丝顶端生长方面的作用。此外，还将研究活性rac1在细丝形成过程中的动态定位，以及鸟嘌呤核苷酸解离抑制剂Rdi1对rac1循环的作用。此外，我们还将分析与CDc24相互作用的Ras1是否刺激了CDc24的全球环境基金活性，从而可能参与了二态转换。

Dimorphic switching is a characteristic aspect of many pathogenic fungi. During its life cycle, the phytopathogenic fungus Ustilago maydis undergoes a morphogenetic transition between budding and filamentous growth. This switch is controlled by the multiallelic b mating-type locus, which encodes a pair of homeodomain transcription factors, named bE and bW. While many genes have been identified that are regulated by this master control locus, the molecular mechanism by which the b mating-type genes induce filamentous growth is still unknown. We are studying the function of the Rho family GTP binding protein Rac1, which acts as molecular switch during filamentous growth. We discovered that b-induced filament formation involves stimulation of the activity of the Rac1-specific Rho-GEF Cdc24. Rho-GEF dependent recruitment of active Rac1 into a Bem1-scaffolded ternary complex triggers destruction of Cdc24 and thus constitutes a negative feedback loop. We will analyze the role of this autoregulation for establishment and maintenance of hyphal tip growth. Furthermore, the dynamic localization of active Rac1 during filament formation and the role of Rac1 recycling by the guanine nucleotide dissociation inhibitor Rdi1 will be studied. In addition, we will analyze whether Ras1, which interacts with Cdc24, stimulates the GEF activity of Cdc24 and thus may participate in dimorphic switching.