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J. Cell Biol.,
Volume 140, Number 2, January 26, 1998 377-390
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544
kar9 was originally identified as a bilateral
karyogamy mutant, in which the two zygotic nuclei remained widely separated and the cytoplasmic microtubules were misoriented (Kurihara, L.J., C.T. Beh, M. Latterich, R. Schekman, and M.D. Rose. 1994. J. Cell Biol. 126:911-923.). We now report a general defect in
nuclear migration and microtubule orientation in kar9
mutants. KAR9 encodes a novel 74-kD protein that is
not essential for life. The kar9 mitotic defect was similar to mutations in dhc1/dyn1 (dynein heavy chain
gene), jnm1, and act5. kar9
dhc1, kar9 jnm1, and
kar9 act5 double mutants were synthetically lethal,
suggesting that these genes function in partially redundant pathways to carry out nuclear migration. A functional GFP-Kar9p fusion protein localized to a single
dot at the tip of the shmoo projection. In mitotic cells,
GFP-Kar9p localized to a cortical dot with both
mother-daughter asymmetry and cell cycle dependence.
In small-budded cells through anaphase, GFP-Kar9p
was found at the tip of the growing bud. In telophase
and G1 unbudded cells, no localization was observed. By indirect immunofluorescence, cytoplasmic microtubules intersected the GFP-Kar9p dot. Nocodazole experiments demonstrated that Kar9p's cortical localization was microtubule independent. We propose that
Kar9p is a component of a cortical adaptor complex
that orients cytoplasmic microtubules.
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