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Caenorhabditis elegans UBX cofactors for CDC‐48/p97 control spermatogenesis
Author(s) -
Sasagawa Yohei,
Yamanaka Kunitoshi,
SaitoSasagawa Yuko,
Ogura Teru
Publication year - 2010
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2010.01454.x
Subject(s) - ultrabithorax , biology , caenorhabditis elegans , microbiology and biotechnology , gene knockdown , aaa proteins , ubiquitin , phenotype , genetics , gene , biochemistry , atpase , enzyme , homeotic gene
UBX (ubiquitin regulatory X) domain–containing proteins act as cofactors for CDC‐48/p97. CDC‐48/p97 is essential for various cellular processes including retro‐translocation in endoplasmic reticulum–associated degradation, homotypic membrane fusion, nuclear envelope assembly, degradation of ubiquitylated proteins, and cell cycle progression. CDC‐48/p97‐dependent processes are determined by differential binding of cofactors including UBX proteins, but the cellular functions of UBX proteins have not yet been elucidated, especially in multicellular organisms. Therefore, we investigated the functions of UBX family members using Caenorhabditis elegans , which expresses six UBX proteins, UBXN‐1 to UBXN‐6. All six UBXN proteins directly interacted with CDC‐48.1 and CDC‐48.2, and simultaneous knockdown of the expression of three genes, ubxn‐1, ubxn‐2 and ubxn‐3 , induced embryonic lethal and sterile phenotypes, but knockdown of either one or two did not. The sterile worms had a feminized germ‐line phenotype, producing oocytes but no sperm. UBXN‐1, UBXN‐2 and UBXN‐3 colocalized with CDC‐48 in spermatocytes but not mature sperm. TRA‐1A, which is a key factor in the sex determination pathway and inhibits spermatogenesis, accumulated in worms in which UBXN‐1, UBXN‐2 and UBXN‐3 had been simultaneously knocked down. Taken together, these results suggest that UBXN‐1, UBXN‐2 and UBXN‐3 are redundant cofactors for CDC‐48/p97 and control spermatogenesis via the degradation of TRA‐1A.