Worm Breeder's Gazette 11(2): 83
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.
Mapping of the spontaneous duplications against him-1 mutations has been complex. him-1 was originally mapped to the interval between unc- 38 and dpy-5 (Hodgkin et al. 1979: Genetics 91: 61). Our duplication mapping with most duplications is in agreement with this result (see map in accompanying article). In contrast, two of the unc-68(+); spontaneous duplications, hDp21 and hDp79, plus hDp21, which is probably spontaneous but this is not known for sure, were him-1(-). These three duplications failed to complement the lethal phenotype of him-1(h134) and in addition, hDp21 failed to complement the Him phenotype of the viable allele e879. To explain these results and be consistent with the original him-1 position, we propose that in the formation of hDp21, hDp23 and hDp79, a new him-1 mutation was induced on the duplication chromosome. The duplication that complements him-1(h134) with the right-most breakpoint is hDp76. In addition to hDp21, hDp23 and hDp79, hDp29 and hDp59 are also him-1(-) despite having a breakpoint to the left of hDp76. A total of eight spontaneous duplications with a breakpoint to the left of hDp76 have been isolated and four of these are associated with a him-1 mutation. All of the progenitor duplications were tested and found to be him-1(+). There is either a very high mutation rate at the him-1 locus when a duplication spontaneously shortens, or the him-1 gene is inactivated by another mechanism, such as position effects, relating to the structure of the duplications. These observations and those described in the accompanying article indicate there are some complex changes during spontaneous duplication breakage. Three shortening events were associated with attachment to another intact chromosome. All of these chromosomes are viable and stable as homozygotes. hDp78 is linked to unc-54 at the right end of chromosome I. hDp79, a spontaneous derivative of hDp6, is linked to an autosome we have not identified. hDp83 (not shown in figure), a spontaneous derivative of hDp26, is tightly linked to dpy-9(IV). Although attachment of duplications to an autosome is accompanied by deletion of material from the parental chromosome, these events are rare. An unbiased set of fourteen spontaneous duplications were analyzed and all of them were free. Is breakage and healing of duplications restricted to meiosis, or can it also occur during mitotic proliferation of the germ line? If a duplication were to lose material during the mitotic divisions in the germ line, then one would expect to recover more than one exceptional duplication from a single worm. In all cases where it has been possible to observe a cluster, only a single exceptional duplication was produced by any one worm. This observation comes from the observation of 13 breakage events. We are continuing the search for pre-meiotic breakage and healing events. This evidence suggests, but does not prove, breakage and healing events are restricted to meiosis or events soon after. [Figure not provided in original]