Department of Cell and Developmental Biology, Pasteur Institute-Cenci Bolognetti Foundation, University of Rome, Rome, Italy.
FEMS Yeast Res. 2011 Feb;11(1):60-71. doi: 10.1111/j.1567-1364.2010.00690.x. Epub 2010 Nov 9.
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.
蛋白酶体盖亚基 Rpn11 对于维持酿酒酵母中正确的细胞周期和线粒体形态至关重要。在本文中，我们表明 rpn11-m1 突变体具有一种特殊的细胞周期缺陷，类似于在 FEAR 途径中延迟 Cdc14 蛋白磷酸酶从核仁中释放的突变体。我们分析了 rpn11-m1 的表型，发现 Cdc14 的过表达可以抑制 rpn11-m1 的所有缺陷，包括线粒体缺陷。Cdc14 对 rpn11-m1 线粒体形态缺陷的抑制揭示了线粒体和细胞周期事件之间未被表征的联系。有趣的是，Cdc14 的过表达也部分恢复了缺乏一种属于将线粒体锚定在肌动蛋白细胞骨架所需复合物的线粒体蛋白的Δmmm2 菌株中的管状网络。总之，我们的发现首次表明细胞周期和线粒体形态之间存在交叉对话。
