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Vol. 9, Issue 4, 917-930, April 1998
Department of Biology, University of Utah, Salt Lake City, Utah
84112
In wild-type yeast mitochondrial inheritance occurs early in the
cell cycle concomitant with bud emergence. Cells lacking the
PTC1 gene initially produce buds without a mitochondrial
compartment; however, these buds later receive part of the
mitochondrial network from the mother cell. Thus, the loss of
PTC1 causes a delay, but not a complete
block, in mitochondrial transport. PTC1 encodes a
serine/threonine phosphatase in the high-osmolarity glycerol response
(HOG) pathway. The mitochondrial inheritance delay in the
ptc1 mutant is not attributable to changes in
intracellular glycerol concentrations or defects in the organization of
the actin cytoskeleton. Moreover, epistasis experiments with
ptc1
and mutations in HOG pathway kinases reveal that
PTC1 is not acting through the HOG pathway to control
the timing of mitochondrial inheritance. Instead, PTC1
may be acting either directly or through a different signaling pathway
to affect the mitochondrial transport machinery in the cell. These
studies indicate that the timing of mitochondrial transport in
wild-type cells is genetically controlled and provide new evidence that
mitochondrial inheritance does not depend on a physical link between
the mitochondrial network and the incipient bud site.
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