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Development 129, 4399-4409 (2002)
© 2002 The Company of Biologists Limited

COP9 signalosome subunits 4 and 5 regulate multiple pleiotropic pathways in Drosophila melanogaster

Efrat Oron1,*, Mattias Mannervik2, Sigal Rencus3,*, Orit Harari-Steinberg1, Shira Neuman-Silberberg4, Daniel Segal3,{dagger} and Daniel A. Chamovitz1,{dagger}

1 Department of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel
2 Department of Developmental Biology, Wenner-Gren Institute, Stockholm University, S-106 91 Stockholm, Sweden
3 Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Tel Aviv 69978, Israel
4 Molecular Genetics of Development, Faculty of Health Sciences, Ben-Gurian University of the Neger, Beer-Sheva 84105, Israel
* These authors contributed equally to this manuscript

{dagger}Authors for correspondence (e-mail: dannyc{at}tauex.tau.ac.il and dsegal{at}post.tau.ac.il)

Accepted 17 June 2002

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.

Key words: COP9 signalosome, Maternal effect, Embryo development, Oogenesis, Drosophila




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© The Company of Biologists Ltd 2002