Pazour G J, Wilkerson C G, Witman G B
Department of Cell Biology, University of Massachusetts Medical Center (UMMC), Worcester Foundation Campus, Shrewsbury, Massachusetts 01545, USA.
J Cell Biol. 1998 May 18;141(4):979-92. doi: 10.1083/jcb.141.4.979.
Several enzymes, including cytoplasmic and flagellar outer arm dynein, share an Mr 8,000 light chain termed LC8. The function of this chain is unknown, but it is highly conserved between a wide variety of organisms. We have identified deletion alleles of the gene (fla14) encoding this protein in Chlamydomonas reinhardtii. These mutants have short, immotile flagella with deficiencies in radial spokes, in the inner and outer arms, and in the beak-like projections in the B tubule of the outer doublet microtubules. Most dramatically, the space between the doublet microtubules and the flagellar membrane contains an unusually high number of rafts, the particles translocated by intraflagellar transport (IFT) (Kozminski, K.G., P.L. Beech, and J.L. Rosenbaum. 1995. J. Cell Biol. 131:1517-1527). IFT is a rapid bidirectional movement of rafts under the flagellar membrane along axonemal microtubules. Anterograde IFT is dependent on a kinesin whereas the motor for retrograde IFT is unknown. Anterograde IFT is normal in the LC8 mutants but retrograde IFT is absent; this undoubtedly accounts for the accumulation of rafts in the flagellum. This is the first mutation shown to specifically affect retrograde IFT; the fact that LC8 loss affects retrograde IFT strongly suggests that cytoplasmic dynein is the motor that drives this process. Concomitant with the accumulation of rafts, LC8 mutants accumulate proteins that are components of the 15-16S IFT complexes (Cole, D.G., D.R. Deiner, A.L. Himelblau, P.L. Beech, J.C. Fuster, and J.L. Rosenbaum. 1998. J. Cell Biol. 141:993-1008), confirming that these complexes are subunits of the rafts. Polystyrene microbeads are still translocated on the surface of the flagella of LC8 mutants, indicating that the motor for flagellar surface motility is different than the motor for retrograde IFT.
包括细胞质动力蛋白和鞭毛外周臂动力蛋白在内的几种酶,都共享一种分子量为8000的轻链,称为LC8。该轻链的功能尚不清楚,但在多种生物体中高度保守。我们已经在莱茵衣藻中鉴定出编码这种蛋白质的基因(fla14)的缺失等位基因。这些突变体具有短的、不能运动的鞭毛,在径向辐条、内外臂以及外双联微管B微管中的喙状突起存在缺陷。最显著的是,双联微管和鞭毛膜之间的空间含有异常大量的筏,这些筏是通过鞭毛内运输(IFT)转运的颗粒(Kozminski,K.G.,P.L. Beech和J.L. Rosenbaum. 1995. J. Cell Biol. 131:1517 - 1527)。IFT是筏在鞭毛膜下沿轴丝微管的快速双向运动。顺行IFT依赖于驱动蛋白,而逆行IFT的动力蛋白未知。LC8突变体中的顺行IFT正常,但逆行IFT缺失;这无疑解释了鞭毛中筏的积累。这是第一个被证明特异性影响逆行IFT的突变;LC8缺失影响逆行IFT这一事实强烈表明细胞质动力蛋白是驱动这一过程的动力蛋白。与筏的积累同时发生的是,LC8突变体积累了作为15 - 16S IFT复合体成分的蛋白质(Cole,D.G.,D.R. Deiner,A.L. Himelblau,P.L. Beech,J.C. Fuster和J.L. Rosenbaum. 1998. J. Cell Biol. 141:993 - 1008),证实这些复合体是筏的亚基。聚苯乙烯微珠仍能在LC8突变体的鞭毛表面转运,表明鞭毛表面运动的动力蛋白与逆行IFT的动力蛋白不同。