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TRAPPII is required for cleavage furrow ingression and localization of Rab11 in dividing male meiotic cells ofDrosophila
Author(s) -
Carmen C. Robinett,
Maria Grazia Giansanti,
Maurizio Gatti,
Margaret T. Fuller
Publication year - 2009
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.054536
Subject(s) - cytokinesis , biology , ingression , cleavage furrow , microbiology and biotechnology , cytoplasm , meiosis , cleavage (geology) , septin , chromosome segregation , genetics , gene , cell , cell division , chromosome , paleontology , fracture (geology)
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.

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