C. elegans female meiosis requires two meiotic-specific genes,
mei-1 and
mei-2. Loss of
mei-1 or
mei-2 function blocks female meiotic spindle formation while the subsequent mitotic cleavages are normal. In a
mei-1 gain-of-function mutant, however, the mitotic cleavages are disrupted after normal meiotic divisions. Wild-type MEI-1 and MEI-2 localize to the meiotic, but not mitotic spindle.1,2 However, MEI-1(gf) and MEI-2 ectopically localize to mitotic spindles in
mei-1(gf) embryos.
mei-1 and
mei-2 encode homologs of
p60 and
p80 subunits of the sea urchin microtubule severing protein katanin, respectively, and MEI-1 and MEI-2 together disassemble interphase microtubules in a HeLa cell system.2 We propose that MEI-1 and MEI-2 form a complex in meiosis and regulate meiotic spindle formation by katanin-like activities. In a
mei-1(gf) suppressor screen, we recovered three extragenic suppressors. One of them,
sb26, was found to be a missense mutation in a b -tubulin gene,
tbb-2.
tbb-2(
sb26) also enhances a weak
mei-2(lf) allele. Together, these results suggest that
tbb-2 is required for the function of
mei-1 and
mei-2. Antibody staining shows that TBB-2 is widely expressed during worm development. Neither
tbb-2 nor
tbb-1 (another b -tubulin highly similar to
tbb-2) RNAi has severe effects during early development. However,
tbb-2 and
tbb-1 double RNAi results in 100% dead eggs indicating that they act redundantly during embryogenesis. We are doing experiments to examine the interactions of MEI-1/MEI-2 with
tbb-2 and
tbb-1. 1. Clark-Maguire, S. and Mains, P.E. (1994). J. Cell Biol. 126, 199-209. 2. Srayko, M., Buster, D.W., Bazirgan O.A., McNally, F.J., and Mains, P.E. (2000). Genes Dev. 14 (9).