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A more recent version of this article appeared on September 1, 2004
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Submitted on January 20, 2004
Revised on June 2, 2004
Accepted on June 8, 2004
Department of Anatomy and Cell Biology, Columbia University College of Physicians and Surgeons, New York, NY 10032
Monitoring Editor: Thomas Fox
Two actin-dependent force generators contribute to mitochondrial inheritance: Arp2/3 complex and the myosin V, Myo2p (together with its Rab-like binding partner, Ypt11p). We found that deletion of YPT11, reduction of the length of the Myo2p lever arm (myo2-
6IQ), or deletion of MYO4 (the other yeast myosin V), had no effect on mitochondrial morphology, colocalization of mitochondria with actin cables, or the velocity of bud-directed mitochondrial movement. In contrast, retention of mitochondria in the bud was compromised in YPT11 and MYO2 mutants. Retention of mitochondria in the bud tip of wild-type cells results in a 60% decrease in mitochondrial movement in buds compared with mother cells. In ypt11
mutants, however, the level of mitochondrial motility in buds was similar to that observed in mother cells. Moreover, the myo2-66 mutant, which carries a temperature sensitive mutation in the Myo2p motor domain, exhibited a 55% decrease in accumulation of mitochondria in the bud tip, and an increase in accumulation of mitochondria at the retention site in the mother cell after shift to restrictive temperatures. Finally, destabilization of actin cables and the resulting delocalization of Myo2p from the bud tip had no significant effect on the accumulation of mitochondria in the bud tip.
Corresponding author. E-mail: lap5{at}columbia.edu
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