Cyanidioschyzon merolae aurora kinase phosphorylates evolutionarily conserved sites on its target to regulate mitochondrial division
Cyanidioschyzon merolae aurora kinase phosphorylates evolutionarily conserved sites on its target to regulate mitochondrial division
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Cyanidioschyzon merolae 极光激酶磷酸化其靶标上的进化保守位点以调节线粒体分裂
DOI：
10.1038/s42003-019-0714-x
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发表时间：
2019
影响因子：
5.9
通讯作者：
Matsunaga Sachihiro
中科院分区：
文献类型：
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作者：
Kato Shoichi;Okamura Erika;Matsunaga Tomoko M.;Nakayama Minami;Kawanishi Yuki;Ichinose Takako;Iwane Atsuko H.;Sakamoto Takuya;Imoto Yuuta;Ohnuma Mio;Nomura Yuko;Nakagami Hirofumi;Kuroiwa Haruko;Kuroiwa Tsuneyoshi;Matsunaga Sachihiro
细胞器是一种细胞器，它是从内共生中衍生出来的。虽然宿主细胞对线粒体生长的调节对于线粒体的维持是必要的，但尚不清楚这种调节机制是如何获得的。为了解决这个问题，我们研究了原始的单细胞红藻Cyanidioschyzon merolae，它具有最简单的真核基因组和一个单一的染色体。在这里，我们表明，C。merolaeAurora激酶直系同源物CmAUR通过线粒体分裂环组分的磷酸化调节线粒体分裂。其中一个成分，Drp1直系同源物CmDnm1，至少有四个位点被CmAUR磷酸化。在真核生物中保守的磷酸化位点的耗尽诱导了缺陷，例如细胞一侧的线粒体分布。考虑到人极光激酶在体外磷酸化Drp1的观察，我们认为，磷酸化调节是保守的，从最简单的真核生物到哺乳动物，并获得内共生的原始阶段。
The mitochondrion is an organelle that was derived from an endosymbiosis. Although regulation of mitochondrial growth by the host cell is necessary for the maintenance of mitochondria, it is unclear how this regulatory mechanism was acquired. To address this, we studied the primitive unicellular red algaCyanidioschyzon merolae, which has the simplest eukaryotic genome and a single mitochondrion. Here we show that theC. merolaeAurora kinase ortholog CmAUR regulates mitochondrial division through phosphorylation of mitochondrial division ring components. One of the components, the Drp1 ortholog CmDnm1, has at least four sites phosphorylated by CmAUR. Depletion of the phosphorylation site conserved among eukaryotes induced defects such as mitochondrial distribution on one side of the cell. Taken together with the observation that human Aurora kinase phosphorylates Drp1 in vitro, we suggest that the phosphoregulation is conserved from the simplest eukaryotes to mammals, and was acquired at the primitive stage of endosymbiosis.