Common and distinct genetic properties of ESCRT-II components in Drosophila.

Common and distinct genetic properties of ESCRT-II components in Drosophila.
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果蝇中ESCRT-II成分的常见和独特的遗传特性。

DOI:
10.1371/journal.pone.0004165
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发表时间:
2009
期刊:
影响因子:
3.7
通讯作者:
Bergmann A
Bergmann A
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Herz HM;Woodfield SE;Chen Z;Bolduc C;Bergmann A

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Genetic studies in yeast have identified class E vps genes that form the ESCRT complexes required for protein sorting at the early endosome. In Drosophila, mutations of the ESCRT-II component vps25 cause endosomal defects leading to accumulation of Notch protein and increased Notch pathway activity. These endosomal and signaling defects are thought to account for several phenotypes. Depending on the developmental context, two different types of overgrowth can be detected. Tissue predominantly mutant for vps25 displays neoplastic tumor characteristics. In contrast, vps25 mutant clones in a wild-type background trigger hyperplastic overgrowth in a non-autonomous manner. In addition, vps25 mutant clones also promote apoptotic resistance in a non-autonomous manner. Here, we genetically characterize the remaining ESCRT-II components vps22 and vps36. Like vps25, mutants of vps22 and vps36 display endosomal defects, accumulate Notch protein and – when the tissue is predominantly mutant – show neoplastic tumor characteristics. However, despite these common phenotypes, they have distinct non-autonomous phenotypes. While vps22 mutations cause strong non-autonomous overgrowth, they do not affect apoptotic resistance. In contrast, vps36 mutations increase apoptotic resistance, but have little effect on non-autonomous proliferation. Further characterization reveals that although all ESCRT-II mutants accumulate Notch protein, only vps22 and vps25 mutations trigger Notch activity. The ESCRT-II components vps22, vps25 and vps36 display common and distinct genetic properties. Our data redefine the role of Notch for hyperplastic and neoplastic overgrowth in these mutants. While Notch is required for hyperplastic growth, it appears to be dispensable for neoplastic transformation.
DOI: 10.1016/s0092-8674(00)81111-3
发表时间: 1996-05-03
期刊: CELL
影响因子: 64.5
作者:
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通讯作者: Cohen, SN
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发表时间: 1991-01-01
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发表时间: 2003-12-01
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影响因子: 64.8
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