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M-Phase Phosphoprotein 9 regulates ciliogenesis by modulating CP110-CEP97 complex localization at the mother centriole.
Nature Communications ( IF 14.7 ) Pub Date : 2018-10-30 , DOI: 10.1038/s41467-018-06990-9 Ning Huang , Donghui Zhang , Fangyuan Li , Peiyuan Chai , Song Wang , Junlin Teng , Jianguo Chen
Nature Communications ( IF 14.7 ) Pub Date : 2018-10-30 , DOI: 10.1038/s41467-018-06990-9 Ning Huang , Donghui Zhang , Fangyuan Li , Peiyuan Chai , Song Wang , Junlin Teng , Jianguo Chen
The primary cilium is elongated from the mother centriole and has diverse signaling roles during development and disease. The CP110-CEP97 complex functions as a negative regulator of ciliogenesis, although the mechanisms regulating its mother centriole localization are poorly understood. Here we show that M-Phase Phosphoprotein 9 (MPP9) is recruited by Kinesin Family Member 24 (KIF24) to the distal end of mother centriole where it forms a ring-like structure and recruits CP110-CEP97 by directly binding CEP97. Loss of MPP9 causes abnormal primary cilia formation in growing cells and mouse kidneys. After phosphorylation by Tau Tubulin Kinase 2 (TTBK2) at the beginning of ciliogenesis, MPP9 is targeted for degradation via the ubiquitin-proteasome system, which facilitates the removal of CP110 and CEP97 from the distal end of the mother centriole. Thus, MPP9 acts as a regulator of ciliogenesis by regulating the localization of CP110-CEP97 at the mother centriole.
中文翻译:
M相磷酸蛋白9通过调节CP110-CEP97复合体在母体中央的定位来调节纤毛发生。
初级纤毛从母中心延长,在发育和疾病过程中具有多种信号传导作用。CP110-CEP97复合体可作为纤毛发生的负调节剂,尽管对其母体中心粒定位的调节机制知之甚少。在这里,我们显示M-相磷酸蛋白9(MPP9)由Kinesin家族成员24(KIF24)募集到母亲中心的远端,在那里它形成环状结构,并通过直接结合CEP97募集CP110-CEP97。MPP9的丢失会在生长中的细胞和小鼠肾脏中引起异常的初级纤毛形成。在纤毛形成开始时,由Tau Tubulin Kinase 2(TTBK2)磷酸化后,MPP9被靶向通过遍在蛋白-蛋白酶体系统降解,这有助于从母体远端去除CP110和CEP97。
更新日期:2018-10-31
中文翻译:
M相磷酸蛋白9通过调节CP110-CEP97复合体在母体中央的定位来调节纤毛发生。
初级纤毛从母中心延长,在发育和疾病过程中具有多种信号传导作用。CP110-CEP97复合体可作为纤毛发生的负调节剂,尽管对其母体中心粒定位的调节机制知之甚少。在这里,我们显示M-相磷酸蛋白9(MPP9)由Kinesin家族成员24(KIF24)募集到母亲中心的远端,在那里它形成环状结构,并通过直接结合CEP97募集CP110-CEP97。MPP9的丢失会在生长中的细胞和小鼠肾脏中引起异常的初级纤毛形成。在纤毛形成开始时,由Tau Tubulin Kinase 2(TTBK2)磷酸化后,MPP9被靶向通过遍在蛋白-蛋白酶体系统降解,这有助于从母体远端去除CP110和CEP97。