Worm Breeder's Gazette 13(3): 23 (June 1, 1994)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Interactions Between mei-1 and the unc-116 Kinesin

Paul E. Mains

Dept. of Medical Biochemistry, University of Calgary, Calgary, Alberta, Canada

The mei-1 gene encodes a spindle component required for meiosis in the female germline. Previous results showed that MEI-1 is found only in the meiotic spindle and mei-1 (lf) alleles disrupt only meiosis. In contrast, a mei-1 (gf)mutation results in a product that ectopically assembles into the mitotic spindles, disrupting the early embryonic mitotic divisions. The disorganized spindles characteristic of mei-1 alleles are reminiscent of those caused by mutations in kinesin-like motor proteins in other organisms (e.g. ncd and nod in Drosophila; kar3 , cin8 and kip1 in Saccharomyces). Therefore, we were interested to see the report by Hall et al. (1993 Worm Meeting Abstracts) that a mutation in a C elegans kinesin, unc-116 ( rh24 ),results in first cleavage defects similar to those seen for mei-1 (gf).These include a spindle that is reduced in size, often with a dorsal-ventral orientation, in the posterior of the embryo. We had previously shown that mutations in mel-26 and zyg-9 also cause this phenotype and act as enhancers of mei-1 (gf).

We found that the maternal-effect lethality of unc-116 is weakly semidominant, resulting in 12% embryonic lethality at 20°. To determine if there is a genetic interaction between unc-116 /+and mutations of mei-1 (gf), mel-26 and zyg-9 ,we constructed double mutants and scored hatching at 20°, a semipermissive temperature for all of the mutations. All combinations showed synergistic effects, resulting in from 8 - 38 fold less hatching than predicted from the corresponding single mutants. This mutual enhancement may be indicative of an interaction, at some unspecified level, between mei-1 , mel-26 and zyg-9 and unc-116 .

The unc-116 ( rh24 )allele used in these experiments may not be a null. The deficiency nDf20 uncovers unc-116 but does not cause semidominant maternal-effect lethality and shows little or no interaction (1.4 fold or less enhancement) with mei-1 (gf), mel-26 or zyg-9 .

True kinesins are the canonical members of the kinesin superfamily of microtubule-based motor proteins, but unc-116 is the first one with clear affects on spindle function. Other true kinesins have been primarily implicated in axon function (hence the Unc phenotype of unc-116 ).Genes with mutations affecting spindles are classified as kinesin-related proteins, belonging to different subfamilies of the kinesin superfamily. Therefore it might not be surprising that rh24 is a gain-of-function mutation, which perhaps changes its specificity to allow it to ectopically assemble into the mitotic spindle.