Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.
J Cell Sci. 2009 Dec 15;122(Pt 24):4526-34. doi: 10.1242/jcs.054536. Epub 2009 Nov 24.
Although membrane addition is crucial for cytokinesis in many animal cell types, the specific mechanisms supporting cleavage furrow ingression are not yet understood. Mutations in the gene brunelleschi (bru), which encodes the Drosophila ortholog of the yeast Trs120p subunit of TRAPPII, cause failure of furrow ingression in male meiotic cells. In non-dividing cells, Brunelleschi protein fused to GFP is dispersed throughout the cytoplasm and enriched at Golgi organelles, similarly to another Drosophila TRAPPII subunit, dBet3. Localization of the membrane-trafficking GTPase Rab11 to the cleavage furrow requires wild-type function of bru, and genetic interactions between bru and Rab11 increase the failure of meiotic cytokinesis and cause synthetic lethality. bru also genetically interacts with four wheel drive (fwd), which encodes a PI4Kbeta, such that double mutants exhibit enhanced failure of male meiotic cytokinesis. These results suggest that Bru cooperates with Rab11 and PI4Kbeta to regulate the efficiency of membrane addition to the cleavage furrow, thus promoting cytokinesis in Drosophila male meiotic cells.
尽管在许多动物细胞类型中,膜的添加对于胞质分裂至关重要,但支持分裂沟内陷的具体机制尚不清楚。编码酵母 TRAPPII 中 Trs120p 亚基的果蝇同源物 brunelleschi(bru)基因突变会导致雄性减数分裂细胞的分裂沟内陷失败。在非分裂细胞中,与 GFP 融合的 Brunelleschi 蛋白弥散在细胞质中,并在高尔基体细胞器中富集,这与另一个果蝇 TRAPPII 亚基 dBet3 相似。膜运输 GTPase Rab11 定位于分裂沟需要 bru 的野生型功能,并且 bru 和 Rab11 之间的遗传相互作用增加了减数分裂胞质分裂的失败,并导致合成致死。bru 还与四轮驱动(fwd)基因发生遗传相互作用,该基因编码 PI4Kbeta,因此双突变体表现出雄性减数分裂胞质分裂失败的增强。这些结果表明,Bru 与 Rab11 和 PI4Kbeta 合作调节分裂沟中膜的添加效率,从而促进果蝇雄性减数分裂细胞的胞质分裂。