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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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Mitochondrial inheritance during mitotic cell division.  Mitochondria are localized near the cortex of unbudded and budding cells. Early in the cell cycle (S phase) a portion of the maternal mitochondrial network extends into the developing bud. As  the bud grows (S phase to G2 phase), mitochondria continue to  accumulate in the daughter cell. At cytokinesis (M phase/G1 phase  boundary), the mitochondrial content of the daughter cell is often  greater than that of the mother cell.
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Figure 1: Mitochondrial inheritance during mitotic cell division. Mitochondria are localized near the cortex of unbudded and budding cells. Early in the cell cycle (S phase) a portion of the maternal mitochondrial network extends into the developing bud. As the bud grows (S phase to G2 phase), mitochondria continue to accumulate in the daughter cell. At cytokinesis (M phase/G1 phase boundary), the mitochondrial content of the daughter cell is often greater than that of the mother cell.

Mentions: In the budding yeast Saccharomyces cerevisiae, respiring mitochondria form an elaborate network of tubular membranes located near the cell periphery (Hoffman and Avers, 1973). Very early in the cell cycle (early S phase), a portion of this mitochondrial network is transported from the mother cell into the growing bud (Fig. 1) (Stevens, 1981). Recent genetic studies have identified a few proteins that control mitochondrial morphology and distribution in cells and mitochondrial transmission during cell division. These include Mdm10p and Mmm1p, two proteins of the outer mitochondrial membrane required for the maintenance of normal organelle morphology (Sogo and Yaffe, 1994, mdm [mitochondrial distribution and morphology]; Burgess et al., 1994, mmm [maintenance of mitochondrial morphology]; Mdm2p/Ole1p, a fatty acid desaturase that may regulate the level of unsaturated fatty acids in the mitochondrial membrane (Stukey et al., 1989, 1990; Stewart and Yaffe, 1991, ole [oleic acid requiring]); and Mdm1p, a protein with characteristics of the mammalian intermediate filament–like proteins keratin and vimentin (McConnell and Yaffe, 1992, 1993). In addition, there are several proteins that are required for the normal maintenance or segregation of mitochondrial DNA. Mgm1p is a member of the dynamin family of GTP binding proteins (Jones and Fangman, 1992; Guan et al., 1993; Backer, 1995; mgm [mitochondrial genome maintenance]); ILV5 encodes a protein that plays an as yet unidentified role in mitochondrial genome maintenance (Zelenaya-Troitskaya et al., 1995; ilv [isoleucine-plus-valine requiring]); and Abf2p is an HMG1-like DNA binding protein (Diffley and Stillman, 1991, 1992; abf [ARS binding factor]). Studies are in progress in a number of laboratories to determine how the activities of these proteins control the behavior of the mitochondrial compartment and the replication and segregation of the mitochondrial genome.


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)

Mitochondrial inheritance during mitotic cell division.  Mitochondria are localized near the cortex of unbudded and budding cells. Early in the cell cycle (S phase) a portion of the maternal mitochondrial network extends into the developing bud. As  the bud grows (S phase to G2 phase), mitochondria continue to  accumulate in the daughter cell. At cytokinesis (M phase/G1 phase  boundary), the mitochondrial content of the daughter cell is often  greater than that of the mother cell.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 1: Mitochondrial inheritance during mitotic cell division. Mitochondria are localized near the cortex of unbudded and budding cells. Early in the cell cycle (S phase) a portion of the maternal mitochondrial network extends into the developing bud. As the bud grows (S phase to G2 phase), mitochondria continue to accumulate in the daughter cell. At cytokinesis (M phase/G1 phase boundary), the mitochondrial content of the daughter cell is often greater than that of the mother cell.
Mentions: In the budding yeast Saccharomyces cerevisiae, respiring mitochondria form an elaborate network of tubular membranes located near the cell periphery (Hoffman and Avers, 1973). Very early in the cell cycle (early S phase), a portion of this mitochondrial network is transported from the mother cell into the growing bud (Fig. 1) (Stevens, 1981). Recent genetic studies have identified a few proteins that control mitochondrial morphology and distribution in cells and mitochondrial transmission during cell division. These include Mdm10p and Mmm1p, two proteins of the outer mitochondrial membrane required for the maintenance of normal organelle morphology (Sogo and Yaffe, 1994, mdm [mitochondrial distribution and morphology]; Burgess et al., 1994, mmm [maintenance of mitochondrial morphology]; Mdm2p/Ole1p, a fatty acid desaturase that may regulate the level of unsaturated fatty acids in the mitochondrial membrane (Stukey et al., 1989, 1990; Stewart and Yaffe, 1991, ole [oleic acid requiring]); and Mdm1p, a protein with characteristics of the mammalian intermediate filament–like proteins keratin and vimentin (McConnell and Yaffe, 1992, 1993). In addition, there are several proteins that are required for the normal maintenance or segregation of mitochondrial DNA. Mgm1p is a member of the dynamin family of GTP binding proteins (Jones and Fangman, 1992; Guan et al., 1993; Backer, 1995; mgm [mitochondrial genome maintenance]); ILV5 encodes a protein that plays an as yet unidentified role in mitochondrial genome maintenance (Zelenaya-Troitskaya et al., 1995; ilv [isoleucine-plus-valine requiring]); and Abf2p is an HMG1-like DNA binding protein (Diffley and Stillman, 1991, 1992; abf [ARS binding factor]). Studies are in progress in a number of laboratories to determine how the activities of these proteins control the behavior of the mitochondrial compartment and the replication and segregation of the mitochondrial genome.

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