Female meiotic spindle formation requires two meiosis-specific components, MEI-1 and MEI-2, which are similar to the
p60 (severing) and
p80 (localization) subunits, respectively, of the sea urchin microtubule-severing complex katanin. In addition to their sequence similarities to katanin, MEI-1 and MEI-2 disassemble interphase microtubules when coexpressed in Hela cells.1 In wild-type embryos, MEI-1 and MEI-2 localize exclusively to the female meiotic spindle. MEI-1 and MEI-2 likely regulate the length of meiotic spindle fibres to maintain the unique morphology of the small anteriorly-located, barrel-shaped meiotic spindle, but MEI-1/MEI-2 must be inactivated prior to mitosis. Here we report analysis of three extragenic suppressors of a
mei-1(gf) mutant that results in ectopic microtubule-severing activity during mitosis. These suppressors show semi-dominant suppression of the
mei-1(gf) defects, but are phenotypically wild type by themselves. One suppressor is a missense allele of the -tubulin gene,
tbb-2 (C36E8.5). The other two are missense alleles of an -tubulin gene,
tba-2 (C47B2.3). All three suppressors genetically behave as if they generally inhibit microtubule severing: they suppress the mitotic phenotype resulting from ectopic
mei-1 activity while enhancing meiotic defects seen when MEI-1 severing activity is compromised during meiosis. Although functional redundancies were seen with and -tubulins during worm development (our data, Philips et al. and Wright et al.), our experiments revealed tubulin isotype preferences of the MEI-1/MEI-2 severing complex. When MEI-1 and MEI-2 are limiting,
tbb-2(RNAi) resulted in meiotic defects while
tbb-1(RNAi) did not. Thus, MEI-1/MEI-2 prefers the TBB-2 isotype as a substrate. Similarly, TBA-2 is the preferred -tubulin substrate. Therefore, although TBB-1/TBB-2 and TBA-1/TBA-2 isotype pairs are functional redundant, our results reveal differences in their functions. 1. Srayko, M., Buster, D.W., Bazirgan O.A., McNally, F.J. and Mains, P.E. (2000). Genes Dev. 14, 1072-1084.