C. elegans RBX‐2‐CUL‐5‐ and RBX‐1‐CUL‐2‐based complexes are redundant for oogenesis and activation of the MAP kinase MPK‐1

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Abstract
Cul5‐based complex is a member of ECS (Elongin B/C‐Cul2/Cul5‐SOCS‐box protein) ubiquitin ligase family. The cellular function of the Cul5‐based complex is poorly understood. In this study, we found that oocyte septum formation and egg production did not occur in either cul‐5‐ or rbx‐2‐depleted cul‐2 homozygotes, although control cul‐2 homozygotes laid approximately 50 eggs. These phenotypes are reminiscent of those caused by the MAP kinase mpk‐1 depletion. In fact, activation of MPK‐1 was significantly inhibited in cul‐5‐depleted cul‐2 mutant and cul‐2‐depleted cul‐5 mutant. Yeast two‐hybrid analysis and RNAi‐knockdown experiments suggest that oocyte maturation from pachytene exit and MPK‐1 activation are redundantly controlled by the RBX‐2‐CUL‐5‐ and RBX‐1‐CUL‐2‐based complexes.