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Functional Characterization of a New Member of the Cdk9 Family in Aspergillus nidulans

机译:构巢曲霉Cdk9家族的新成员的功能表征。

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摘要

Cdk9-like kinases in complex with T-type cyclins are essential components of the eukaryotic transcription elongation machinery. The full spectrum of Cdk9/cyclin T targets, as well as the specific consequences of phosphorylations, is still largely undefined. We identify and characterize here a Cdk9 kinase (PtkA) in the filamentous ascomycete Aspergillus nidulans. Deletion of ptkA had a lethal effect in later stages of vegetative growth and completely impeded asexual development. Overexpression of ptkA affected directionality of polarized growth and the initiation of new branching sites. A green fluorescent protein-tagged PtkA version localized inside the nucleus during interphase, supporting a role of PtkA in transcription elongation, as observed in other organisms. We also identified a putative cyclin T homolog, PchA, in the A. nidulans genome and confirmed its interaction with PtkA in vivo. Surprisingly, the Pcl-like cyclin PclA, previously described to be involved in asexual development, was also found to interact with PtkA, indicating a possible role of PtkA in linking transcriptional activity with development and/or morphogenesis in A. nidulans. This is the first report of a Cdk9 kinase interacting with a Pcl-like cyclin, revealing interesting new aspects about the involvement of this Cdk-subfamily in differential gene expression.
机译:与T型细胞周期蛋白复合的Cdk9样激酶是真核转录延伸机制的重要组成部分。 Cdk9 / cyclin T靶标的全谱以及磷酸化的特定结果在很大程度上仍不确定。我们在这里鉴定和表征丝状子囊菌构巢曲霉中的Cdk9激酶(PtkA)。 ptkA的删除在营养生长的后期具有致命作用,并完全阻碍了无性恋的发展。 ptkA的过表达影响极化生长的方向性和新分支站点的启动。如在其他生物中观察到的,在相间期期间,绿色荧光蛋白标记的PtkA版本位于细胞核内,支持PtkA在转录伸长中的作用。我们还确定了构巢曲霉基因组中假定的细胞周期蛋白T同源物PchA,并证实了其与PtkA在体内的相互作用。出乎意料的是,还发现先前描述为参与无性发育的Pcl样细胞周期蛋白PclA与PtkA相互作用,表明PtkA可能在构巢曲霉中将转录活性与发育和/或形态发生联系起来。这是Cdk9激酶与Pcl样细胞周期蛋白相互作用的首次报道,揭示了有关该Cdk亚家族参与差异基因表达的有趣新方面。

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