Worm Breeder's Gazette 10(3): 141
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.
In order to determine factors governing meiotic pairing for recombination in C. elegans, we decided to take advantage of our LGV( left) deficiencies. In the course of their mapping, we had noticed that certain deficiencies inhibited recombination well beyond their respective breakpoints (Rosenbluth, Rogalski, Johnsen, Addison and Baillie, 1988, Genet. Res., in press). We are now systematically analyzing the degree and extent of recombination suppression caused by deleting specific regions in LGV(left). The origins of most deficiencies used are described in the work cited above or by Johnsen and Baillie 1988 (Mut. Res. 201:137-147). The deficiency sDf39(s521) was originally identified as a gamma induced allele of let-336.Our results to date are of two types. Column 2 of the Table shows the recombination between the deficiency (column 1) and cis-linked unc-46 in heterozygous hermaphrodites. The data given are in percent of the expected value. The remaining columns show recombination within specific intervals on LGV, when markers are trans to the deficiency. Again, the data are in percent of the control values. All the deficiencies listed, except possibly sDf33, suppressed recombination to their right. The most striking results are those of sDf32 and sDf39 which strongly inhibit recombination for at least 16 to 18 map units. Since the deficiencies are not all overlapping, suppression of recombination cannot be due to deletion of a single common site. The anomalous results of sDf33 are puzzling. We do not know how far the chromosome extends to the left of let-450 and it is possible that sDf33 differs from all the others in that it is the only one that deletes the end of LGV. As more lethal mutations are analyzed (see Johnsen and Baillie newsletter note), a gene may be identified that distinguishes the left hand breakpoints of sDf33 and sDf39. The distance suppressed differs for the three deficiencies sDf34, sDf39 and sDf50. This might be a consequence of the location and/or size of each deficiency. Alternatively, a boundary near unc-42, beyond which no more suppression can occur, might lead to results of this type. As we compare the effects on recombination in other regions and those of other deficiencies, a pattern should emerge that will indicate the nature of factors causing the inhibition. [See Figures 1 & 2]