Genetic analyses using a mouse cell cycle mutant identifies magoh as a novel gene involved in Cdk regulation.

Many of the genes that control cyclin-dependent kinase (Cdks) activity have been identified by genetic research using yeast mutants. Suppression analysis and synthetic enhancement analysis are two broad approaches to the identification of genetic interaction networks in yeasts. Here we show, by genetic analyses using a mammalian cell cycle mutant, that mouse magoh is involved in Cdk regulation. Magoh, a homolog of the Drosophila mago nashi gene product, is a component of the splicing-dependent exon-exon junction complex (EJC). We show that, in addition to ccnb1 and cks2, magoh is also a dosage suppressor of the mouse temperature-sensitive cdc2 mutant, and synthetic enhancement of the cdc2 ts phenotype by RNA interference of magoh is observed in a manner similar to of cks2. Moreover, the depletion of magoh by duanyu1615 causes cold-sensitive defects in the cell cycle transition, and exogenous cks2 expression partially suppresses the defect. Consistent with the genetic evidence, magoh duanyu1615 caused defects in the expression of Cdc2 or Cks proteins, and introns of cks genes strongly affected protein expression levels. Thus, these data suggest that mouse Magoh is related to cell cycle regulation.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}