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The yeast gene, MDM20, is necessary for mitochondrial inheritance and organization of the actin cytoskeleton.

Hermann GJ, King EJ, Shaw JM - J. Cell Biol. (1997)

Bottom Line: Together, these results provide compelling evidence that mitochondrial inheritance in yeast is an actin-mediated process.Although MDM20 and TPM1 are both required for the formation and/or stabilization of actin cables, mutations in these genes disrupt mitochondrial inheritance and nuclear segregation to different extents.Thus, Mdm20p and Tpm1p may act in vivo to establish molecular and functional heterogeneity of the actin cytoskeleton.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Utah, Salt Lake City 84112, USA.

ABSTRACT
In Saccharomyces cerevisiae, the growing bud inherits a portion of the mitochondrial network from the mother cell soon after it emerges. Although this polarized transport of mitochondria is thought to require functions of the cytoskeleton, there are conflicting reports concerning the nature of the cytoskeletal element involved. Here we report the isolation of a yeast mutant, mdm20, in which both mitochondrial inheritance and actin cables (bundles of actin filaments) are disrupted. The MDM20 gene encodes a 93-kD polypeptide with no homology to other characterized proteins. Extra copies of TPM1, a gene encoding the actin filament-binding protein tropomyosin, suppress mitochondrial inheritance defects and partially restore actin cables in mdm20 delta cells. Synthetic lethality is also observed between mdm20 and tpm1 mutant strains. Overexpression of a second yeast tropomyosin, Tpm2p, rescues mutant phenotypes in the mdm20 strain to a lesser extent. Together, these results provide compelling evidence that mitochondrial inheritance in yeast is an actin-mediated process. MDM20 and TPM1 also exhibit the same pattern of genetic interactions; mutations in MDM20 are synthetically lethal with mutations in BEM2 and MYO2 but not SAC6. Although MDM20 and TPM1 are both required for the formation and/or stabilization of actin cables, mutations in these genes disrupt mitochondrial inheritance and nuclear segregation to different extents. Thus, Mdm20p and Tpm1p may act in vivo to establish molecular and functional heterogeneity of the actin cytoskeleton.

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Cells lacking MDM20 have normal mitochondrial morphology but do not segregate mitochondria into buds at 37°C.  DIC images (A and C) and DiOC6 mitochondrial staining (B and  D) of MDM20+ (JSY999) (A and B) and mdm20Δ (JSY1065) (C  and D) cells grown at 37°C for 3 h. Bar, 5 μm.
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Figure 2: Cells lacking MDM20 have normal mitochondrial morphology but do not segregate mitochondria into buds at 37°C. DIC images (A and C) and DiOC6 mitochondrial staining (B and D) of MDM20+ (JSY999) (A and B) and mdm20Δ (JSY1065) (C and D) cells grown at 37°C for 3 h. Bar, 5 μm.

Mentions: Wild-type strains grown at 25° or 37°C (Fig. 2, A and B) segregate a portion of the mitochondrial network into buds almost as soon as they can be detected on the surface of the mother cell. In contrast, mdm20 mutants retained their branched mitochondrial networks but produced large buds that lack this organelle (Fig. 2, C and D). This mitochondrial inheritance defect was observed at the permissive temperature and became more pronounced at 37°C (Table II). Both transmission EM and DAPI staining of mitochondrial genomes confirmed that mitochondria were absent from mdm20 buds (data not shown). In addition, organelles labeled with a mitochondrially targeted form of the green fluorescent protein (kindly provided by R. Jensen) also failed to be transported into buds in the mdm20 strain (data not shown). Although the mdm20 mutation caused a striking mitochondrial inheritance defect, it did not severely affect metabolic functions of mitochondria since they could still be efficiently labeled with the potential-dependent dye DiOC6, which only stains actively respiring organelles (Pringle et al., 1989).


The yeast gene, MDM20, is necessary for mitochondrial inheritance and organization of the actin cytoskeleton.

Hermann GJ, King EJ, Shaw JM - J. Cell Biol. (1997)

Cells lacking MDM20 have normal mitochondrial morphology but do not segregate mitochondria into buds at 37°C.  DIC images (A and C) and DiOC6 mitochondrial staining (B and  D) of MDM20+ (JSY999) (A and B) and mdm20Δ (JSY1065) (C  and D) cells grown at 37°C for 3 h. Bar, 5 μm.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2139847&req=5

Figure 2: Cells lacking MDM20 have normal mitochondrial morphology but do not segregate mitochondria into buds at 37°C. DIC images (A and C) and DiOC6 mitochondrial staining (B and D) of MDM20+ (JSY999) (A and B) and mdm20Δ (JSY1065) (C and D) cells grown at 37°C for 3 h. Bar, 5 μm.
Mentions: Wild-type strains grown at 25° or 37°C (Fig. 2, A and B) segregate a portion of the mitochondrial network into buds almost as soon as they can be detected on the surface of the mother cell. In contrast, mdm20 mutants retained their branched mitochondrial networks but produced large buds that lack this organelle (Fig. 2, C and D). This mitochondrial inheritance defect was observed at the permissive temperature and became more pronounced at 37°C (Table II). Both transmission EM and DAPI staining of mitochondrial genomes confirmed that mitochondria were absent from mdm20 buds (data not shown). In addition, organelles labeled with a mitochondrially targeted form of the green fluorescent protein (kindly provided by R. Jensen) also failed to be transported into buds in the mdm20 strain (data not shown). Although the mdm20 mutation caused a striking mitochondrial inheritance defect, it did not severely affect metabolic functions of mitochondria since they could still be efficiently labeled with the potential-dependent dye DiOC6, which only stains actively respiring organelles (Pringle et al., 1989).

Bottom Line: Together, these results provide compelling evidence that mitochondrial inheritance in yeast is an actin-mediated process.Although MDM20 and TPM1 are both required for the formation and/or stabilization of actin cables, mutations in these genes disrupt mitochondrial inheritance and nuclear segregation to different extents.Thus, Mdm20p and Tpm1p may act in vivo to establish molecular and functional heterogeneity of the actin cytoskeleton.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, University of Utah, Salt Lake City 84112, USA.

ABSTRACT
In Saccharomyces cerevisiae, the growing bud inherits a portion of the mitochondrial network from the mother cell soon after it emerges. Although this polarized transport of mitochondria is thought to require functions of the cytoskeleton, there are conflicting reports concerning the nature of the cytoskeletal element involved. Here we report the isolation of a yeast mutant, mdm20, in which both mitochondrial inheritance and actin cables (bundles of actin filaments) are disrupted. The MDM20 gene encodes a 93-kD polypeptide with no homology to other characterized proteins. Extra copies of TPM1, a gene encoding the actin filament-binding protein tropomyosin, suppress mitochondrial inheritance defects and partially restore actin cables in mdm20 delta cells. Synthetic lethality is also observed between mdm20 and tpm1 mutant strains. Overexpression of a second yeast tropomyosin, Tpm2p, rescues mutant phenotypes in the mdm20 strain to a lesser extent. Together, these results provide compelling evidence that mitochondrial inheritance in yeast is an actin-mediated process. MDM20 and TPM1 also exhibit the same pattern of genetic interactions; mutations in MDM20 are synthetically lethal with mutations in BEM2 and MYO2 but not SAC6. Although MDM20 and TPM1 are both required for the formation and/or stabilization of actin cables, mutations in these genes disrupt mitochondrial inheritance and nuclear segregation to different extents. Thus, Mdm20p and Tpm1p may act in vivo to establish molecular and functional heterogeneity of the actin cytoskeleton.

Show MeSH
Related in: MedlinePlus