Odf2-deficient mother centrioles lack distal/subdistal appendages and the ability to generate primary cilia
Odf2-deficient mother centrioles lack distal/subdistal appendages and the ability to generate primary cilia
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DOI：
10.1038/ncb1251
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发表时间：
2005-05-01
影响因子：
21.3
通讯作者：
Tsukita, S
中科院分区：
文献类型：
--
作者：
Ishikawa, H;Kubo, A;Tsukita, S
外致密纤维2（ODF 2;也称为cenexin）最初被确定为精子尾部细胞骨架的主要成分，但后来被证明是一种一般的支架蛋白，特异性地定位于母体中心粒的远端/近远端附件（1，2）。在这里，我们表明，Odf 2基因的两个等位基因被删除时，在小鼠F9细胞中的Odf 2表达被抑制。出乎意料的是，Odf 2（-/-）细胞的细胞周期似乎不受影响。免疫荧光和超薄切片电子显微镜显示，在Odf 2（-/-）细胞，远端/近远端附属物从母亲中心粒消失，使其难以区分母亲从女儿中心粒。然而，在Odf 2（-/-）细胞中，初级纤毛的形成被完全抑制，尽管类似于25%的野生型F9细胞在稳态细胞周期下纤毛化。Odf 2（-/-）F9细胞中初级纤毛的丧失可以通过外源性Odf 2表达来挽救。这些研究结果表明，Odf 2是必不可少的远端/近远端附属物的形成和初级纤毛的产生，但不是其他细胞周期相关的中心粒功能。
Outer dense fibre 2 (Odf2; also known as cenexin) was initially identified as a main component of the sperm tail cytoskeleton, but was later shown to be a general scaffold protein that is specifically localized at the distal/subdistal appendages of mother centrioles(1,2). Here we show that Odf2 expression is suppressed in mouse F9 cells when both alleles of Odf2 genes are deleted. Unexpectedly, the cell cycle of Odf2(-/-) cells does not seem to be affected. Immunofluorescence and ultrathin-section electron microscopy reveals that in Odf2(-/-) cells, distal/subdistal appendages disappear from mother centrioles, making it difficult to distinguish mother from daughter centrioles. In Odf2(-/-) cells, however, the formation of primary cilia is completely suppressed, although similar to 25% of wild-type F9 cells are ciliated under the steady-state cell cycle. The loss of primary cilia in Odf2(-/-) F9 cells can be rescued by exogenous Odf2 expression. These findings indicate that Odf2 is indispensable for the formation of distal/subdistal appendages and the generation of primary cilia, but not for other cell-cycle-related centriolar functions.