Worm Breeder's Gazette 10(1): 102
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.
We have previously described the properties of ct46(I), a temperature-sensitive (ts) dominant maternal-effect lethal mutation ( Worm Meeting Abstracts, 1987). Gene dosage experiments indicate that the ct46 mutation results in a gain-of-function 'poison' gene product that competes with the wild-type product. We presented evidence that ct46 may interact with maternal-effect mutations of zyg-9(II). Mutations at both loci result in similar early defects characterized by a longitudinal first cleavage with formation of an anterior cytoplast. In addition, ct46/+;zyg-9 double mutants show a 500 fold enhancement of maternal-effect lethality under conditions that are semi-permissive for the individual mutations. We also described the isolation of mutations that showed dominant, trans acting suppression of ct46, as well as recessive nonconditional maternal-effect lethality. These suppressor alleles are likely to represent loss-of-function mutations based upon their frequency. After EMS mutagenesis, we found 4 alleles among 2000 animals in one screen, and at least 4 (and possibly as many as 11) additional alleles among 3500 animals in a second screen. The suppressors appear to have been induced by EMS, since we found no suppressors among 6800 non-mutagenized worms. The suppressors map <0.01 cM from ct46 (in the lin-10 - lin-28 interval), but the results of gene dosage experiments are difficult (although not impossible) to reconcile with their being in the same locus. At the May 1987 Worm Meeting, Ken Kemphues told us about the recessive maternal-effect lethal mutation, mei-1 (b284), which has properties strikingly similar to our suppressors of ct46 (see Springer and Kemphues, this issue). Both map to the same region and show the same early cleavage defects. We have now shown that our suppressors are alleles of mei-1. mei-1 (b284) both fails to complement the recessive maternal-effect lethality of our suppressors and also acts as a dominant, trans-acting suppressor of ct46. Since b284 was isolated independently of ct46, it is highly unlikely that the suppression results from a specific alteration of the mei-1 product to allow it to compensate for the ct46 lesion. As argued above, the dominant suppression probably results from loss of function at the mei- 1 locus. It is interesting to note that decreasing the wild-type activity of mei-1 by one-half in ct46+/+mei-1 animals relative to ct46+/++ increases the viability of eggs from 1% to 95% at 25 C. This may indicate that the stoichiometry between the mei-1 and ct46 gene products must be precisely controlled. Unexpectedly, deficiencies of this region (nDF23 and nDf24), which should be equivalent to mei-1 null mutations, do not suppress ct46. This may indicate that the suppression requires the presence of a non- functional mei-1 product, or that there are additional genes removed by these deficiencies which interact with the ct46 and mei-1. One such gene may have been defined by ct61(I), another member of our collection of ts, dominant maternal-effect lethal mutations. Embryos from ct61/+ mothers show defects distinct from those caused by ct46, zyg-9, or mei-1 mutations. The early cleavage furrows are indistinct and the spindles appear to be reduced in size. A very surprising result is that the defects resulting from ct61 are also suppressed by mei-1 alleles. At 25 C, only 0.3% of the eggs from ct61/+ mothers hatch, but 95% of the eggs from +ct61/mei-1+ mothers do so. ct61 is linked to ct46, but maps approximately 2 cM to the right, in the unc-29 - lin-11 interval. ct46 and ct61 were re-mapped to exclude the possibility that the stocks were mixed up. In addition, we were able to isolate ++ recombinants from ct46+/+ct61 animals at the expected frequency. Like ct46, ct61 is not suppressed by the deficiencies nDf23 and nDf24. These deficiencies remove the ct46 and ct61 loci in addition to mei-1, which may account for why they do not suppress similarly to the mei-1 mutations. Thus, ct46, ct61 and mei-1 appear to represent three maternally active genes whose products may interact during the first cleavage division. We are currently testing ct61 for enhancement of zyg-9 mutations, and we will examine the phenotypes of double mutants of ct61, ct46, mei-1 and zyg-9 to determine epistatic interactions.