Worm Breeder's Gazette 15(1): 68 (October 1, 1997)
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.
Department of Biology, Haverford College, Haverford, PA 19041
Mutations in the autosomal gene cause a very high frequency X-chromosome nondisjunction without apparently affecting meiotic segregation of the autosomes. As one approach to understanding X-chromosome meiosis, we cloned him-8 by transformation rescue several years ago (S. Broverman, Meneely, and others). The putative gene as identified by transformation consists of 3 exons and is predicted to encode a novel and somewhat unremarkable protein of 195 amino acids. This structure differs from the prediction by Genefinder for this region; the first two exons are the same, but Genefinder predicts a much larger gene that does not include the third exon and whose downstream exons have homology to phosphatases. No cDNAs of this part of the gene have been found. Using RT-PCR, we have confirmed that our predicted third exon is transcribed and is spliced to the predicted second exon; in addition, the transcript is trans-spliced to SL1. We are now attempting to clarify the relationship (if any) of exons of the him-8 gene with the exons of the larger phosphatase gene downstream. Two possibilities are being explored: alternative splicing of one gene to give the smaller three exon him-8 product and the larger twelve exon phosphatase; or two genes compressed into one by Genefinder. On a related project, a simple experiment was done to explore if spontaneous males arise from X-chromosome loss during hermaphrodite oogenesis or hermaphrodite spermatogenesis. Wild-type males were mated with hermaphrodites marked with a recessive X-linked marker and the progeny scored for the presence (or absence) of patroclinous males-- that is, wild-type males arising from a nullisomic ovum and the paternal X chromosome. No patroclinous males have been found yet, suggesting that most if not all spontaneous males arise from X chromosome loss during hermaphrodite spermatogenesis. This result, in combination with previous data from others, suggests a simple idea. There is probably only one exchange per chromosome during oogenesis, based on observed interference on the X chromosome and inferences from the genetic map (Barnes et al, 1995). Zetka and Rose (1990) showed that there is less recombination on the autosomes during spermatogenesis than during oogenesis, implying that there may be slightly less than one exchange per chromosome during spermatogenesis. In addition, Hodgkin et al. (1979) showed that, in one case examined, double crossovers on the autosomes do arise during spermatogenesis, which we have confirmed. The combination of less interference and less crossing-over on the autosomes is expected to lead to a non-exchange chromosome during spermatogenesis occasionally. Perhaps there is some (unknown) mechanism by which the X chromosome is preferentially the non-exchange chromosome, accounting for its rate of loss during hermaphrodite spermatogenesis.