Jorurnal : Hauling tail

Published online 7 April 2008
doi:10.1083/jcb.1811iti4
The Journal of Cell Biology, Vol. 181, No. 1, 3-
© The Rockefeller University Press, 0021-9525 $30.00

Hauling tail

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During budding, glowing mitochondria remain stuck in the parent cell if Myo2's tail is mutated (bottom).

Solving a long-standing mystery, Altmann et al. have discovered that mitochondria get around a yeast cell in style. The organelles ride on the tail of a myosin molecule known as Myo2.

Mitochondria are always on the move. They change positions within the cell, come together to fuse, and split apart. During cell division or budding, they migrate into the daughter cell. The organelles scoot along actin filaments, but what powers them has stumped scientists. Prime candidates are myosin motors, which attach to actin and tow vacuoles and other organelles. But the evidence for the myosins' involvement in mitochondrial movement is mixed. Yeast strains with mutations in certain myosin genes show no abnormalities in mitochondrial structure or distribution. However, researchers have detected hesitant mitochondria in yeast with a mutant form of the myosin Myo2.

To clarify Myo2's contribution, Altmann et al. turned to yeast cells in which the level of Myo2 can be reduced by treating the cells with the antibiotic, doxycycline. The organelles normally link up to form a network. But in cells grown with the antibiotic, they clumped or curled into rings, suggesting disrupted movement. Altmann et al. found that isolated mitochondria lacking functional Myo2 cannot bind to actin filaments. The team then tested whether Myo2's tail, which carries vacuoles and other organelles, also hauls mitochondria. In yeast with mutations in the Myo2 tail, the researchers observed mitochondrial clumping. When a cell with one of these tail mutants sprouted a bud, few mitochondria moved in, Altmann et al. found. They conclude that mitochondria travel by boarding Myo2's tail. Up next: determining how Myo2 attaches to the mitochondrial surface.

Reference:

Altmann, K., et al. 2008. J. Cell Biol. 181:119–130.[Abstract/Free Full Text]