Worm Breeder's Gazette 11(2): 82
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.
The mutation mn164 recovered after X-ray treatment promotes X chromosomal nondisjunction when homozygous or heterozygous. The mutation was mapped to the left end of the X chromosome and it was proposed that a structural abnormality was affecting segregation of the X chromosome. Equational nondisjunction of the mn164 bearing chromosome, but not its homolog, was observed in heterozygotes (Herman et al. (1982) Genetics 102, 379-400). As most him mutations show reductional nondisjunction, it was of interest to look at the cytogenetics of a him mutation causing equational nondisjunction. The first meiotic division is reductional in C. elegans, and abnormal bivalents have been seen at diakinesis in some of the him mutants that cause reductional nondisjunction. Thus, in mn164, abnormalities were expected at the second meiotic division. However, abnormal chromosome segregation was seen at both meiotic divisions in embryos from mn164/dpy-3 hermaphrodites, and at diakinesis in these hermaphrodites a large trivalent and four normal-sized bivalents were seen. In mn164 homozygotes a univalent was present in addition to the one large and four normal-sized bivalents. The large bivalent is reminiscent of mnT12(IV,X), suggesting that mn164 is a translocation. In situ hybridization of the ribosomal DNA probe (pCe7) to the middle of the large chromosome identified LGI as one member of the translocation. Hybridization of pCe7 and a probe for the right end of the X (mlc-1,2) to embryonic metaphases showed hybridization at 40-50% from one end of the long chromosome (pCe7) and on the end (mlc-1,2). These observations suggested that mn164 is a translocation involving joining of the left end of X to the right end of LGI. Hybridization of pCe7 to the ribosomal DNA appears reduced and therefore the univalent seen in oocytes of mn164 homozygotes, an extra copy of LGI, may be necessary for viability. Since these cytogenetic observations were made on mn164 animals some time after the original description of the mutation, it was possible that the Cambridge stock had changed from the original. Therefore Claire Kari and Bob Herman thawed a stock of mn164, frozen on January 5, 1981 and pseudolinkage between unc-54(I) and dpy-3(X) was confirmed by mating mn164 males with unc-54(I);dpy-3(X) hermaphrodites.