纤毛或真核细胞的鞭毛是细胞表面的一种突起结构，主要由细胞微管组成。除参与细胞的运动外，纤毛可以接受及传导外界的信号从而调控动物的生理及动物的发育与生殖。纤毛在组装上的缺陷可导致多种疾病，如肾囊肿，内脏转位，不育，失明，精神迟滞、肥胖乃至癌症。研究纤毛长度的调控可以更加深刻的认识纤毛组装的分子机理。目前关于纤毛长度的模型有“平衡点模型”，该模型认为细胞不存在一种“感知系统”感知纤毛的长度。还有一种模型认为细胞内可能存在一种感知纤毛长度的系统而参与纤毛长度的调控，但是，一直缺乏强有力的实验证据支持。生命科学院潘俊敏教授实验室研究发现一种蛋白质的激酶CALK的磷酸化状态和纤毛的长度相关。CALK在鞭毛组装的初期呈现磷酸化状态，发现鞭毛长度达到一半时发生去磷酸化。这些实验证据表明，细胞可能确实存在一种纤毛长度的感知系统。新的研究成果使人们对纤毛长度的调控具有一个全新的认识。
该研究成果3月31日在《Current Biology》上在线发表。值得一提的是，潘俊敏教授实验室自2006年成立以来，2009年在PNAS上发表关于鞭毛研究的重要成果，这次在国际顶尖学术期刊《Current Biology》上的研究成果代表了这个领域最重要的进展。这两项研究工作都是由博士研究生完成。（生物谷Bioon.com）
生物谷推荐原文出处：
Current Biology, 31 March 2011 doi:10.1016/j.cub.2011.02.046
The Phosphorylation State of an Aurora-Like Kinase Marks the Length of Growing Flagella in Chlamydomonas
Minna Luo, Muqing Cao, Yinan Kan, Guihua Li, William Snell, Junmin Pan
Highlights
Aurora-like protein kinase CALK is dephosphorylated during flagellar assembly
Cells translate flagellar length into a protein posttranslational modification
Chlamydomonas detects absolute, not relative, flagellar length
Summary
Flagella and cilia are structurally polarized organelles whose lengths are precisely defined, and alterations in length are related to several human disorders [1,2]. Intraflagellar transport (IFT) and protein signaling molecules are implicated in specifying flagellar and ciliary length [3,4,5,6], but evidence has been lacking for a flagellum and cilium length sensor that could participate in active length control or establishment of structural polarity. Previously, we showed that the phosphorylation state of the aurora-like protein kinase CALK in Chlamydomonas is a marker of the absence of flagella. Here we show that CALK phosphorylation state is also a marker for flagellar length. CALK is phosphorylated in cells without flagella, and during flagellar assembly it becomes dephosphorylated. Dephosphorylation is not simply a consequence of initiation of flagellar assembly or of time after experimentally induced flagellar loss, but instead requires flagella to be assembled to a threshold length. Analysis of cells with flagella of varying lengths shows that the threshold length for CALK dephosphorylation is 6 m (half length). Studies with short and long flagellar mutants indicate that cells detect absolute rather than relative flagellar length. Our results demonstrate that cells possess a mechanism for translating flagellar length into a posttranslational modification of a known flagellar regulatory protein.
