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Polo-like kinase phosphorylation of bilobe-resident TbCentrin2 facilitates flagellar inheritance in Trypanosoma brucei

机译:TbCentrin2居民的马球状激酶磷酸化促进布鲁氏锥虫鞭毛遗传

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摘要

In the protist parasite Trypanosoma brucei, the single Polo-like kinase (TbPLK) controls the inheritance of a suite of organelles that help position the parasite's single flagellum. These include the basal bodies, the bilobe, and the flagellar attachment zone (FAZ). TbCentrin2 was previously shown to be a target for TbPLK in vitro, and this is extended in this study to in vivo studies, highlighting a crucial role for serine 54 in the N-terminal domain. Duplication of the bilobe correlates with the presence of TbPLK and phospho-TbCentrin2, identified using phosphospecific antiserum. Mutation of S54 leads to slow growth (S54A) or no growth (S54D), the latter suggesting that dephosphorylation is needed to complete bilobe duplication and subsequent downstream events necessary for flagellum inheritance.
机译:在原生寄生虫布鲁氏锥虫中,单个Polo样激酶(TbPLK)控制着一系列细胞器的遗传,这些细胞器有助于定位寄生虫的单个鞭毛。这些包括基体,胆囊和鞭毛附着区(FAZ)。 TbCentrin2以前被证明是体外TbPLK的靶标,并且在本研究中扩展到了体内研究,突显了丝氨酸54在N端结构域中的关键作用。胆红素的重复与TbPLK和磷酸化TbCentrin2的存在有关,这是用磷酸特异性抗血清鉴定的。 S54的突变导致生长缓慢(S54A)或无生长(S54D),后者表明需要去磷酸化才能完成bilobe复制以及鞭毛遗传所必需的后续下游事件。

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