mei-1 and
mei-2 are specifically required for the C. elegans female meiotic spindle formation. MEI-1 and MEI-2 show homology to the two subunits of the microtubule-severing protein, katanin, and disassemble interphase microtubules when co-expressed in Hela cell. 1 In the wild-type embryo, MEI-1 and MEI-2 localize to meiotic spindle but disappear before the onset of the first mitotic cleavage. However, a
mei-1 gain-of-function ( gf ) mutant results in ectopic localization of the proteins into the mitotic spindles and abnormal mitotic spindle formation. This mimics defects observed when embryos are treated with nocodazole, suggesting an ectopic spindle microtubule-destabilizing activity in mitosis. 2 We isolated three extragenic suppressors of
mei-1 ( gf ). All genetically behave as activators of
mei-1 and
mei-2 function but are phenotypically wild-type by themselves. One of the suppressors,
sb26 , has a missense mutation in the b -tubulin gene,
tbb-2 . The amino acid change is in the carboxyl terminus, which has been shown to be required for the microtubule severing activity of sea urchin katanin. 3 Genetic interactions suggest that
tbb-2 (
sb26 ) behaves as a gf suppressor that impairs the microtubule-severing activity of MEI-1 and MEI-2. TBB-2 specific antisera stain microtubule structures through out the worm life cycle. By using RNA interference and indirect immunoflurescence, we showed that
tbb-2 and another b -tubulin gene,
tbb-1 , function redundantly during early development. The two other extragenic suppressors of
mei-1 ( gf ) are possibly allelic and map to the vicinity of an a -tubulin gene. Our work demonstrates genetic evidence that katanin requires specific interaction with spindle microtubules. 1. Srayko, M., Buster, D.W., Bazirgan O.A., McNally, F.J. and Mains, P.E. (2000). Genes Dev. 14, 1072-1084. 2. Strome, S. and Wood, W.B. (1983). Cell 35, 15-25. 3. McNally, F.J. and Vale, R.D. (1993). Cell 75, 419-429.