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Department of Biology, University of Utah, Salt Lake City, Utah 84112
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
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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