A novel MAP kinase regulates flagellar length in Chlamydomonas

A novel MAP kinase regulates flagellar length in Chlamydomonas
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DOI:
10.1016/s0960-9822(03)00415-9
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发表时间:
2003-07-01
期刊:
影响因子:
9.2
通讯作者:
Lefebvre, PA
Lefebvre, PA
中科院分区:
生物学1区
文献类型:
--
作者:
Berman, SA;Wilson, NF;Lefebvre, PA

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关于真核生物中细胞器大小控制的分子基础知之甚少。双鞭毛藻莱茵衣藻的细胞积极地将其鞭毛保持在精确的长度。失去鞭毛长度控制的衣藻突变体已被分离出来,并用于证明动态过程使鞭毛保持在适当的长度 [1, 2]。迄今为止,尚未在任何真核生物中鉴定出控制鞭毛长度所需的蛋白质。在这里,我们证明了一种新型 MAP 激酶对于增强莱茵衣藻野生型鞭毛长度至关重要。 LF4 [2](一种编码与功能未知的哺乳动物 MAP 激酶 MOK [3] 具有广泛氨基酸序列同一性的蛋白质的基因)的无效突变体无法调节其鞭毛的长度。 LF4 蛋白 (LF4p) 定位于鞭毛,体外酶测定证实该蛋白是 MAP 激酶。 If4 细胞的长鞭毛表型通过克隆的 LF4 基因转化得以恢复。新型 MAP 激酶有助于加强鞭毛长度控制的证明表明,先前未识别的信号转导途径控制着莱茵衣藻的细胞器大小。
Little is known about the molecular basis of organelle size control in eukaryotes. Cells of the biflagellate alga Chlamydomonas reinhardtii actively maintain their flagella at a precise length. Chlamydomonas mutants that lose control of flagellar length have been isolated and used to demonstrate that a dynamic process keeps flagella at an appropriate length [1, 2]. To date, none of the proteins required for flagellar length control have been identified in any eukaryotic organism. Here, we show that a novel MAP kinase is crucial to enforcing wild-type flagellar length in C. reinhardtii. Null mutants of LF4 [2], a gene encoding a protein with extensive amino acid sequence identity to a mammalian MAP kinase of unknown function, MOK [3], are unable to regulate the length of their flagella. The LF4 protein (LF4p) is localized to the flagella, and in vitro enzyme assays confirm that the protein is a MAP kinase. The long-flagella phenotype of If4 cells is rescued by transformation with the cloned LF4 gene. The demonstration that a novel MAP kinase helps enforce flagellar length control indicates that a previously unidentified signal transduction pathway controls organelle size in C. reinhardtii.