Mitochondrial morphological and functional defects in yeast caused by yme1 are suppressed by mutation of a 26S protease subunit homologue.

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Abstract
The absence of functional Yme1p, a putative ATP and zinc-dependent protease localized to mitochondria of yeast, results in abnormal mitochondrial function and morphology. Yeast lacking Yme1p lose DNA from mitochondria at an accelerated rate, fail to grow on nonfermentable carbon sources at 37 degrees C, and have severely deficient growth if mitochondrial DNA suffers large deletions or is completely lost. In place of the normal reticulated mitochondrial network, strains lacking Yme1p have punctate mitochondria with some grossly swollen compartments. The growth phenotypes and morphological alterations evident in these mutant yeast can be compensated by a mutation in YNT1, an essential gene in yeast. The sequence of the YNT1 gene product indicates that it is one of a number of related regulatory subunits of the 26S protease. This proteolytic activity is necessary for progression through the cell cycle and has been implicated in the regulation of transcription. Ynt1p is more distantly related to Yme1p.