An eIF4E-binding protein regulates katanin protein levels in C. elegans embryos

Wei Li, Leah R. DeBella, Tugba Guven-Ozkan, Rueyling Lin, Lesilee S. Rose

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

In Caenorhabditis elegans, the MEI-1-katanin microtubule-severing complex is required for meiosis, but must be down-regulated during the transition to embryogenesis to prevent defects in mitosis. A cullin-dependent degradation pathway for MEI-1 protein has been well documented. In this paper, we report that translational repression may also play a role in MEI-1 down-regulation. Reduction of spn-2 function results in spindle orientation defects due to ectopic MEI-1 expression during embryonic mitosis. MEL-26, which is both required for MEI-1 degradation and is itself a target of the cullin degradation pathway, is present at normal levels in spn-2 mutant embryos, suggesting that the degradation pathway is functional. Cloning of spn-2 reveals that it encodes an eIF4E-binding protein that localizes to the cytoplasm and to ribonucleoprotein particles called P granules. SPN-2 binds to the RNA-binding protein OMA-1, which in turn binds to the mei-1 3′ untranslated region. Thus, our results suggest that SPN-2 functions as an eIF4E-binding protein to negatively regulate translation of mei-1.

Original languageEnglish (US)
Pages (from-to)33-42
Number of pages10
JournalJournal of Cell Biology
Volume187
Issue number1
DOIs
StatePublished - Oct 5 2009

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ASJC Scopus subject areas

  • Cell Biology

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