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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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Extra copies of TPM1 and TPM2 can suppress the temperature-sensitive growth defect in mdm20Δ cells. (A) MDM20+  (JSY999) or isogenic mdm20Δ (JSY1065) strains harboring  pRS426, pRS426-MDM20, or pRS426-TPM1 plasmids were serially diluted and spotted on SD minus uracil (SD − Ura) solid medium and grown at 37°C for 3 d. (B) MDM20+ (JSY999) or  isogenic mdm20Δ (JSY1065) strains harboring pRS416, pRS416- MDM20, or GAL1-TPM2 plasmids were serially diluted and  spotted on SGal minus uracil (SGal − Ura) solid medium and  grown at 37°C for 3 d.
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Figure 4: Extra copies of TPM1 and TPM2 can suppress the temperature-sensitive growth defect in mdm20Δ cells. (A) MDM20+ (JSY999) or isogenic mdm20Δ (JSY1065) strains harboring pRS426, pRS426-MDM20, or pRS426-TPM1 plasmids were serially diluted and spotted on SD minus uracil (SD − Ura) solid medium and grown at 37°C for 3 d. (B) MDM20+ (JSY999) or isogenic mdm20Δ (JSY1065) strains harboring pRS416, pRS416- MDM20, or GAL1-TPM2 plasmids were serially diluted and spotted on SGal minus uracil (SGal − Ura) solid medium and grown at 37°C for 3 d.

Mentions: The MDM20 gene was isolated by complementing the temperature-sensitive growth defect of the mdm20-1 mutant allele (see Materials and Methods). Integrative mapping studies indicated that the cloned DNA contained the wild-type MDM20 gene. Transposon mutagenesis (Sedgwick and Morgan, 1994) and DNA sequence analysis revealed that a 3.2-kb fragment (Fig. 3 A) was sufficient to rescue both the temperature-sensitive growth defect (Fig. 4) and the mitochondrial inheritance defect (not shown) in the mdm20 mutant strain.


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)

Extra copies of TPM1 and TPM2 can suppress the temperature-sensitive growth defect in mdm20Δ cells. (A) MDM20+  (JSY999) or isogenic mdm20Δ (JSY1065) strains harboring  pRS426, pRS426-MDM20, or pRS426-TPM1 plasmids were serially diluted and spotted on SD minus uracil (SD − Ura) solid medium and grown at 37°C for 3 d. (B) MDM20+ (JSY999) or  isogenic mdm20Δ (JSY1065) strains harboring pRS416, pRS416- MDM20, or GAL1-TPM2 plasmids were serially diluted and  spotted on SGal minus uracil (SGal − Ura) solid medium and  grown at 37°C for 3 d.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 4: Extra copies of TPM1 and TPM2 can suppress the temperature-sensitive growth defect in mdm20Δ cells. (A) MDM20+ (JSY999) or isogenic mdm20Δ (JSY1065) strains harboring pRS426, pRS426-MDM20, or pRS426-TPM1 plasmids were serially diluted and spotted on SD minus uracil (SD − Ura) solid medium and grown at 37°C for 3 d. (B) MDM20+ (JSY999) or isogenic mdm20Δ (JSY1065) strains harboring pRS416, pRS416- MDM20, or GAL1-TPM2 plasmids were serially diluted and spotted on SGal minus uracil (SGal − Ura) solid medium and grown at 37°C for 3 d.
Mentions: The MDM20 gene was isolated by complementing the temperature-sensitive growth defect of the mdm20-1 mutant allele (see Materials and Methods). Integrative mapping studies indicated that the cloned DNA contained the wild-type MDM20 gene. Transposon mutagenesis (Sedgwick and Morgan, 1994) and DNA sequence analysis revealed that a 3.2-kb fragment (Fig. 3 A) was sufficient to rescue both the temperature-sensitive growth defect (Fig. 4) and the mitochondrial inheritance defect (not shown) in the mdm20 mutant strain.

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