COP9 signalosome subunits 4 and 5 regulate multiple pleiotropic pathways in<i>Drosophila melanogaster</i>
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- Efrat Oron
- Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel
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- Mattias Mannervik
- Department of Developmental Biology, Wenner-Gren Institute, Stockholm University, S-106 91 Stockholm, Sweden
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- Sigal Rencus
- Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Tel Aviv 69978, Israel
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- Orit Harari-Steinberg
- Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel
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- Shira Neuman-Silberberg
- Molecular Genetics of Development, Faculty of Health Sciences, Ben-Gurian University of the Neger, Beer-Sheva 84105, Israel
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- Daniel Segal
- Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Tel Aviv 69978, Israel
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- Daniel A. Chamovitz
- Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel
書誌事項
- 公開日
- 2002-10-01
- DOI
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- 10.1242/dev.129.19.4399
- 公開者
- The Company of Biologists
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説明
<jats:p>The COP9 signalosome (CSN) is an essential eight-subunit repressor of light-regulated development in Arabidopsis. This complex has also been identified in animals, though its developmental role remains obscure. CSN subunits have been implicated in various cellular processes, suggesting a possible role for the CSN as an integrator of multiple signaling pathways. In order to elucidate the function of the CSN in animals, a Drosophila model system has previously been established. Gel-filtration analysis with antibodies against CSN subunits 4, 5 and 7 revealed that these proteins act as a complex in Drosophila that is similar in size to the plant and mammalian complexes. Null mutations in either one of two subunits, CSN4 or CSN5, are larval lethal. Successful embryogenesis appears to be a consequence of maternal contribution of the complex. Biochemical analysis indicates that the different subunits are found in both CSN-dependent and CSN-independent forms, and that these forms are differentially affected by the mutations. Phenotypic characterization of these two mutants indicates that they show both shared and unique phenotypes, which suggest specific roles for each subunit. Both mutants have defective oocyte and embryo patterning, and defects in response to DNA damage, while csn5 mutants develop melanotic tumors and csn4 mutants have phenotypes reminiscent of defects in ecdysone signaling.</jats:p>
収録刊行物
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- Development
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Development 129 (19), 4399-4409, 2002-10-01
The Company of Biologists
