Worm Breeder's Gazette 12(1): 45 (September 1, 1991)

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 Translocation Balancer for Chromosomes I and III

Nahlah Ayed, Hakyung Kang, Ann Rose

Department of Medical Genetics, University of British Columbia, Vancouver, B.C. V6 T1Z3

In an effort to extend the regions of chromosomes I and III that are balanced, we have tested hT2 (I;III)for its ability to recover and maintain lethal mutations. hT2 ,which is homozygous viable, was induced by treating bli-4 ( e937 )males with 1500 R gamma radiation and recovered by screening for pseudo-linkage between unc-13 (I)and dpy-18 (III).The extent of cross-over suppression and implications for meiotic pairing behavior have been described (McKim, Peters, and Rose, in preparation). In order to screen for lethals, the strain hT2 [+ bli-4 + unc-29 ;+]/ dpy-5 + unc-13 +; dpy-18 was constructed and treated with 12 mM EMS. 275 putative lethals were recovered from 1500 treated chromosomes (Steen, McKay and Rose, unpublished). Approximately 100 of these strains have been crossed to N2 males. Two types of out-cross heterozygote were expected, one that carried the translocation which was detected by the segregation of Bli Uncs; and one that carried the normal chromosomes. The latter was expected to segregate either Dpy Uncs (if the lethal mapped to chromosome III) or Dpys (if the lethal mapped to chromosome I). By scoring the self progeny of the heterozygote, we mapped 29 lethals to chromosome I (ranging from 0 to 20 map units from the markers) and 17 to chromosome III (ranging from 0 to 15 map units from dpy-18 ).In this preliminary data set, a large number (18) had reduced numbers of both Dpys and Dpy Uncs as if lethals had been induced on both chromosomes. Since the scoring data is not large, it is likely that some of these resulted from statistical variation. The lethals will be rescued with regionally specific balancers (duplications, for example) to confirm their linkage and to refine their map position. A number of false positives (strains with no lethal) came through this pilot screen, which we hope to eliminate in future screens.

The recovery frequency for hT2 is approximately 12%, about twice the recovery frequency for eT1 (Rosenbluth, Cuddeford and Baillie, 1983). Since hT2 covers two gene clusters and eT1 was estimated to cover the equivalent of one gene cluster, this recovery frequency seems about what one would expect. Such a high recovery frequency results in a lot of lethals to be maintained and characterized. The advantage, however, is that less screening need be done to approach saturation of chromosomes I and III.