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Originally published as Genetics Published Articles Ahead of Print on March 21, 2005.

Genetics, Vol. 170, 115-126, May 2005, Copyright © 2005
doi:10.1534/genetics.104.030106

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Mutations of a Redundant {alpha}-Tubulin Gene Affect Caenorhabditis elegans Early Embryonic Cleavage via MEI-1/Katanin-Dependent and -Independent Pathways

Chenggang Lu and Paul E. Mains1

Genes and Development Research Group, Department of Biochemistry and Molecular Biology, University of Calgary, Calgary, Alberta T2N 4N1, Canada

1 Corresponding author: Genes and Development Research Group, Department of Biochemistry and Molecular Biology, 3330 Hospital Dr. NW, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
E-mail: mains{at}ucalgary.ca

The C. elegans zygote supports both meiosis and mitosis within a common cytoplasm. The meiotic spindle is small and is located anteriorly, whereas the first mitotic spindle fills the zygote. The C. elegans microtubule-severing complex, katanin, is encoded by the mei-1 and mei-2 genes and is solely required for oocyte meiotic spindle formation; ectopic mitotic katanin activity disrupts mitotic spindles. Here we characterize two mutations that rescue the lethality caused by ectopic MEI-1/MEI-2. Both mutations are gain-of-function alleles of tba-2 {alpha}-tubulin. These tba-2 alleles do not prevent MEI-1/MEI-2 microtubule localization but do interfere with its activity. TBA-1 and TBA-2 are redundant for viability, but when katanin activity is limiting, TBA-2 is preferred over TBA-1 by katanin. This is similar to what we previously reported for the ß-tubulins. Removing both preferred {alpha}- and ß-isoforms results in normal development, suggesting that the katanin isoform preferences are not absolute. We conclude that while the C. elegans embryo expresses redundant {alpha}- and ß-tubulin isoforms, they nevertheless have subtle functional specializations. Finally, we identified a dominant tba-2 allele that disrupts both meiotic and mitotic spindle formation independently of MEI-1/MEI-2 activity. Genetic studies suggest that this tba-2 mutation has a "poisonous" effect on microtubule function.






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