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The yeast dynamin-like protein, Mgm1p, functions on the mitochondrial outer membrane to mediate mitochondrial inheritance.

Shepard KA, Yaffe MP - J. Cell Biol. (1999)

Bottom Line: It also caused aberrant mitochondrial distribution and morphology when expressed at high levels in cells that also contained a wild-type copy of the gene.Mgm1p was localized to the mitochondrial outer membrane and fractionated as a component of a high molecular weight complex.These results indicate that Mgm1p is a mitochondrial inheritance and morphology component that functions on the mitochondrial surface.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of California, San Diego, La Jolla, California 92093-0347, USA.

ABSTRACT
The mdm17 mutation causes temperature-dependent defects in mitochondrial inheritance, mitochondrial morphology, and the maintenance of mitochondrial DNA in the yeast Saccharomyces cerevisiae. Defects in mitochondrial transmission to daughter buds and changes in mitochondrial morphology were apparent within 30 min after shifting cells to 37 degrees C, while loss of the mitochondrial genome occurred after 4-24 h at the elevated temperature. The mdm17 lesion mapped to MGM1, a gene encoding a dynamin-like GTPase previously implicated in mitochondrial genome maintenance, and the cloned MGM1 gene complements all of the mdm17 mutant phenotypes. Cells with an mgm1- mutation displayed aberrant mitochondrial inheritance and morphology. A version of mgm1 mutated in a conserved residue in the putative GTP-binding site was unable to complement any of the mutant defects. It also caused aberrant mitochondrial distribution and morphology when expressed at high levels in cells that also contained a wild-type copy of the gene. Mgm1p was localized to the mitochondrial outer membrane and fractionated as a component of a high molecular weight complex. These results indicate that Mgm1p is a mitochondrial inheritance and morphology component that functions on the mitochondrial surface.

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mgm1- cells display defects in mitochondrial inheritance as well as aberrant mitochondrial morphology. mgm1-  cells (MYY974) were grown in YPD at 23°C, fixed, and processed for indirect immunofluorescence. Mitochondria were visualized as described for Fig. 2. Staining of microtubules using an  antitubulin antibody demonstrates accessibility of buds to antibodies. Two representative cells are shown. Bar, 2 μm.
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Figure 3: mgm1- cells display defects in mitochondrial inheritance as well as aberrant mitochondrial morphology. mgm1- cells (MYY974) were grown in YPD at 23°C, fixed, and processed for indirect immunofluorescence. Mitochondria were visualized as described for Fig. 2. Staining of microtubules using an antitubulin antibody demonstrates accessibility of buds to antibodies. Two representative cells are shown. Bar, 2 μm.

Mentions: Previous studies reported that mgm1 mutant cells readily lost mitochondrial DNA and contained aggregated mitochondria but showed normal mitochondrial distribution to buds (Guan et al., 1993). This latter property differs from the phenotype of the mdm17 mutant, where a large fraction of cells exhibited buds devoid of mitochondria. Accordingly, the phenotype of a mutant in mgm1 generated in the same strain background as the mdm17 mutant was examined. Indirect immunofluorescence microscopy revealed many mgm1- cells with buds devoid of mitochondria, even in cells cultured at 23°C (Fig. 3). As previously described (Guan et al., 1993), mitochondria in the mgm1- strain were extensively aggregated.


The yeast dynamin-like protein, Mgm1p, functions on the mitochondrial outer membrane to mediate mitochondrial inheritance.

Shepard KA, Yaffe MP - J. Cell Biol. (1999)

mgm1- cells display defects in mitochondrial inheritance as well as aberrant mitochondrial morphology. mgm1-  cells (MYY974) were grown in YPD at 23°C, fixed, and processed for indirect immunofluorescence. Mitochondria were visualized as described for Fig. 2. Staining of microtubules using an  antitubulin antibody demonstrates accessibility of buds to antibodies. Two representative cells are shown. Bar, 2 μm.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2132935&req=5

Figure 3: mgm1- cells display defects in mitochondrial inheritance as well as aberrant mitochondrial morphology. mgm1- cells (MYY974) were grown in YPD at 23°C, fixed, and processed for indirect immunofluorescence. Mitochondria were visualized as described for Fig. 2. Staining of microtubules using an antitubulin antibody demonstrates accessibility of buds to antibodies. Two representative cells are shown. Bar, 2 μm.
Mentions: Previous studies reported that mgm1 mutant cells readily lost mitochondrial DNA and contained aggregated mitochondria but showed normal mitochondrial distribution to buds (Guan et al., 1993). This latter property differs from the phenotype of the mdm17 mutant, where a large fraction of cells exhibited buds devoid of mitochondria. Accordingly, the phenotype of a mutant in mgm1 generated in the same strain background as the mdm17 mutant was examined. Indirect immunofluorescence microscopy revealed many mgm1- cells with buds devoid of mitochondria, even in cells cultured at 23°C (Fig. 3). As previously described (Guan et al., 1993), mitochondria in the mgm1- strain were extensively aggregated.

Bottom Line: It also caused aberrant mitochondrial distribution and morphology when expressed at high levels in cells that also contained a wild-type copy of the gene.Mgm1p was localized to the mitochondrial outer membrane and fractionated as a component of a high molecular weight complex.These results indicate that Mgm1p is a mitochondrial inheritance and morphology component that functions on the mitochondrial surface.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of California, San Diego, La Jolla, California 92093-0347, USA.

ABSTRACT
The mdm17 mutation causes temperature-dependent defects in mitochondrial inheritance, mitochondrial morphology, and the maintenance of mitochondrial DNA in the yeast Saccharomyces cerevisiae. Defects in mitochondrial transmission to daughter buds and changes in mitochondrial morphology were apparent within 30 min after shifting cells to 37 degrees C, while loss of the mitochondrial genome occurred after 4-24 h at the elevated temperature. The mdm17 lesion mapped to MGM1, a gene encoding a dynamin-like GTPase previously implicated in mitochondrial genome maintenance, and the cloned MGM1 gene complements all of the mdm17 mutant phenotypes. Cells with an mgm1- mutation displayed aberrant mitochondrial inheritance and morphology. A version of mgm1 mutated in a conserved residue in the putative GTP-binding site was unable to complement any of the mutant defects. It also caused aberrant mitochondrial distribution and morphology when expressed at high levels in cells that also contained a wild-type copy of the gene. Mgm1p was localized to the mitochondrial outer membrane and fractionated as a component of a high molecular weight complex. These results indicate that Mgm1p is a mitochondrial inheritance and morphology component that functions on the mitochondrial surface.

Show MeSH
Related in: MedlinePlus