Reference: Esposito M, et al. (2011) Analysis of the rpn11-m1 proteasomal mutant reveals connection between cell cycle and mitochondrial biogenesis. FEMS Yeast Res 11(1):60-71

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Abstract


The proteasomal lid subunit Rpn11 is essential for maintaining a correct cell cycle and mitochondrial morphology in Saccharomyces cerevisiae. In this paper, we show that the rpn11-m1 mutant has a peculiar cell cycle defect reminiscent of mutants defective in the FEAR pathway that delay the release of the Cdc14 protein phosphatase from the nucleolus. We analyzed the rpn11-m1 phenotypes and found that overexpression of Cdc14 suppresses all the rpn11-m1 defects, including the mitochondrial ones. Suppression by Cdc14 of the rpn11-m1 mitochondrial morphology defect reveals an uncharacterized connection between mitochondrial and cell cycle events. Interestingly, the overexpression of Cdc14 also partially restores the tubular network in an Δmmm2 strain, which lacks a mitochondrial protein belonging to the complex necessary to anchor the mitochondrion to the actin cytoskeleton. Altogether our findings indicate, for the first time, a cross-talk between the cell cycle and mitochondrial morphology.

Reference Type
Journal Article | Research Support, Non-U.S. Gov't
Authors
Esposito M, Piatti S, Hofmann L, Frontali L, Delahodde A, Rinaldi T
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