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The Ustilago maydis a2 Mating-Type Locus Genes lga2 and rga2 Compromise Pathogenicity in the Absence of the Mitochondrial p32 Family Protein Mrb1

机译:在没有线粒体p32家族蛋白Mrb1的情况下,Ustilago maydis a2交配型基因lga2和rga2会损害致病性。

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摘要

The Ustilago maydis mrb1 gene specifies a mitochondrial matrix protein with significant similarity to mitochondrial p32 family proteins known from human and many other eukaryotic species. Compatible mrb1 mutant strains were able to mate and form dikaryotic hyphae; however, proliferation within infected tissue and the ability to induce tumor development of infected maize (Zea mays) plants were drastically impaired. Surprisingly, manifestation of the mrb1 mutant phenotype selectively depended on the a2 mating type locus. The a2 locus contains, in addition to pheromone signaling components, the genes lga2 and rga2 of unknown function. Deletion of lga2 in an a2Δmrb1 strain fully restored pathogenicity, whereas pathogenicity was partially regained in an a2Δmrb1Δrga2 strain, implicating a concerted action between Lga2 and Rga2 in compromising pathogenicity in Δmrb1 strains. Lga2 and Rga2 localized to mitochondria and Mrb1 interacted with Rga2 in the yeast two-hybrid system. Conditional expression of lga2 in haploid cells reduced vegetative growth, conferred mitochondrial fragmentation and mitochondrial DNA degradation, and interfered with respiratory activity. The consequences of lga2 overexpression depended on the expression strength and were greatly exacerbated in Δmrb1 mutants. We propose that Lga2 interferes with mitochondrial fusion and that Mrb1 controls this activity, emphasizing a critical link between mitochondrial morphology and pathogenicity.
机译:Ustilago maydis mrb1基因指定了一种线粒体基质蛋白,与人类和许多其他真核生物已知的线粒体p32家族蛋白具有显着相似性。兼容的mrb1突变菌株能够交配并形成双核菌丝。但是,受感染组织内的增殖以及诱导受感染玉米(Zea mays)植物肿瘤发展的能力大大受损。出人意料的是,mrb1突变表型的表现选择性地取决于a2交配型基因座。除了信息素信号传导成分外,a2基因座还包含未知功能的基因lga2和rga2。在a2Δmrb1菌株中lga2的缺失完全恢复了致病性,而在a2Δmrb1Δrga2菌株中部分恢复了致病性,这暗示了Lga2和Rga2之间的协同作用会损害Δmrb1菌株的致病性。 Lga2和Rga2定位于线粒体,Mrb1在酵母双杂交系统中与Rga2相互作用。 lga2在单倍体细胞中的有条件表达会减少营养生长,导致线粒体断裂和线粒体DNA降解,并干扰呼吸活动。 lga2过表达的结果取决于表达强度,并且在Δmrb1突变体中大大加剧。我们建议Lga2干扰线粒体融合,Mrb1控制这一活动,强调线粒体形态与致病性之间的关键联系。

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