Piperno G, Mead K, Shestak W
Department of Cell Biology and Anatomy, Mount Sinai Medical School, New York 10029.
J Cell Biol. 1992 Sep;118(6):1455-63. doi: 10.1083/jcb.118.6.1455.
We provide indirect evidence that six axonemal proteins here referred to as "dynein regulatory complex" (drc) are located in close proximity with the inner dynein arms I2 and I3. Subsets of drc subunits are missing from five second-site suppressors, pf2, pf3, suppf3, suppf4, and suppf5, that restore flagellar motility but not radial spoke structure of radial spoke mutants. The absence of drc components is correlated with a deficiency of all four heavy chains of inner arms I2 and I3 from axonemes of suppressors pf2, pf3, suppf3, and suppf5. Similarly, inner arm subunits actin, p28, and caltractin/centrin, or subsets of them, are deficient in pf2, pf3, and suppf5. Recombinant strains carrying one of the mutations pf2, pf3, or suppf5 and the inner arm mutation ida4 are more defective for I2 inner arm heavy chains than the parent strains. This evidence indicates that at least one subunit of the drc affects the assembly of and interacts with the inner arms I2.
我们提供了间接证据，表明这里称为“动力蛋白调节复合体”（drc）的六种轴丝蛋白与内动力蛋白臂I2和I3紧密相邻。在五个第二位点抑制子pf2、pf3、suppf3、suppf4和suppf5中，drc亚基的子集缺失，这些抑制子可恢复鞭毛运动，但不能恢复辐条突变体的辐条结构。drc成分的缺失与抑制子pf2、pf3、suppf3和suppf5的轴丝中I2和I3内臂的所有四条重链的缺乏相关。同样，内臂亚基肌动蛋白、p28和钙牵蛋白/中心蛋白或它们的子集在pf2、pf3和suppf5中也缺乏。携带pf2、pf3或suppf5突变之一和内臂突变ida4的重组菌株，其I2内臂重链的缺陷比亲本菌株更严重。这一证据表明，drc的至少一个亚基影响I2内臂的组装并与其相互作用。
