Worm Breeder's Gazette 12(4): 58 (October 1, 1992)

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.

A C. elegans Mitotic Mutant

Anne M. Villeneuve

Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305

In the course of analyzing a large collection of new and previously identified him mutants, I have found one mutant, him-10 ( e1511ts ),that is defective in mitotic rather than meiotic chromosome segregation. At 20°, him-10 ( e1511ts )hermaphrodites produce on average about 10% self-progeny males and a significant number of dead embryos. There is an unusually high variance between broods in the number of self-progeny males produced, with a range from 1% to 30%; the occurrence of apparent jackpot events is consistent with premeiotic loss of X chromosomes during the mitotic proliferation of the germline. him-10 ( e1511ts )hermaphrodites shifted to 25° during larval development produce mostly dead embryos, and the strain does not propagate.

Staining of germline nuclei of adult hermaphrodites that had been raised as larvae at 25° revealed gross abnormalities in mitotic chromosome segregation. First, while the syncytial pachytene nuclei of wild-type hermaphrodites are of uniform size and appearance, pachytene nuclei in the him-10 ( e1511ts )hermaphrodites varied markedly in size and staining intensity; small dots of staining, perhaps corresponding to isolated single chromosomes, were frequent in the him-10 ( e1511ts )gonads but were never observed in wild-type gonads. Second, oocyte nuclei in him-10 ( e1511ts )hermaphrodites contained widely varying numbers of chromosomes, some with far more chromosomes than normal, some with far fewer. Since oocytes are arrested in meiotic prophase prior to the meiosis I division, the observation of aberrant numbers of chromosomes in oocytes and pachytene nuclei is clear evidence of a premeiotic defect in mitotic chromosome segregation. (Mutants with chromosome segregation defects specific to meiosis have a normal number of chromosomes at these stages.)

I have not yet tested whether the him-10 ( e1511ts )mutation causes mitotic defects in somatic tissues as well as in the germline. If it does, this mutation might be useful as a tool to increase the mitotic instability of free Dps for mosaic analyses, or for the generation of chromosome loss mosaics. Moreover, this mutant provides an entry point for further analysis of the mitotic segregation of holokinetic chromosomes.