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A mutant for the yeast scERV1 gene displays a new defect in mitochondrial morphology and distribution
Author(s) -
Becher Dietmar,
Kricke Jörn,
Stein Georg,
Lisowsky Thomas
Publication year - 1999
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/(sici)1097-0061(19990915)15:12<1171::aid-yea443>3.0.co;2-t
Subject(s) - biology , mitochondrion , mutant , microbiology and biotechnology , gene product , mitochondrial biogenesis , gene , inner mitochondrial membrane , mitochondrial fusion , cytosol , intermembrane space , phenotype , bacterial outer membrane , mitochondrial dna , genetics , biochemistry , gene expression , enzyme , escherichia coli
Abstract The yeast scERV1 gene is the best characterized representative of a new gene family found in different lower and higher eukaryotes. The gene product is essential for the yeast cell and has a complex influence on different aspects of mitochondrial biogenesis. The homologous mammalian ALR ( A ugmenter of L iver R egeneration) genes from man, mouse and rat are important at different developmental stages of the organism as, for example, in spermatogenesis and liver regeneration. In this study the influence of scERV1 on the morphology of mitochondria and its submitochondrial localization are investigated. A temperature‐sensitive mutant of the gene was stained with a mitochondria‐specific dye and fluorescence was inspected at the permissive and restrictive temperature. A new phenotype for morphological defects of mitochondria was identified. Already at the permissive temperature mitochondrial vesicles accumulate at defined positions in the cell. After shift to the restrictive temperature, morphological changes, and finally complete loss of mitochondrial structures, are observed. Ultrastructural studies confirm these findings and demonstrate the loss of the mitochondrial inner membrane and at the final stage a drastic reduction or complete absence of mitochondria from the cell. GFP fusion experiments with the scERV1 gene and subcellular localization by fractionation experiments identify the gene product inside mitoplasts and the cytosol. Re‐investigation of the mutant phenotype demonstrates that after longer incubation of the mutant at the restrictive temperature an irreversible defect of the cells, even on glucose complete medium, is found that is in accordance with a complete loss or irreversible damage of mitochondria. Copyright © 1999 John Wiley & Sons, Ltd.