Worm Breeder's Gazette 12(4): 57 (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.

Pairing of Homologous Chromosomes Inhibits Intrachromosomal Recombination

Anne M. Villeneuve

Figure 1

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

ctDp31 is a large tandem chromosomal duplication of approximately 40% of the X chromosome (Tanner and Wood, 1991 Meeting Abstracts). Hermaphrodites homozygous for ctDp31 are small, Dpy, slow-growing and often Egl, and males hemizygous for ctDp31 are small, Dpy, slow-growing, and have abnormal gonads and genitalia, rendering them sterile. These phenotypes revert spontaneously to wild-type at a frequency of 104 - 10-5, concomitant with loss of the duplicated DNA (Tanner et al., WBG 10:3). Such revertants could be due either to unequal crossing over between homologous chromosomes, or to intrachromosomal recombination.

Using the reversion of ctD31 as an assay, I have demonstrated that the absenee of a homologous chromosome that can act as a pairing partner dramatically increases the frequency of intrachromosomal recombination [See Figure 1]. This was shown in two ways, by measuring the reversion rate of ctDp31 in the germlines of her-1 ; ctDp3110 XO hermaphrodites and in the germlines of him-10 ; ctDp31 XX hermaphrodites. ( him-10 is a mitotic mutant that undergoes premeiotic loss of X chromosomes, producing some XO germ cell nuclei in an XX germline [A.V., WBG, this issue].) Lack of a homolog during meiosis resulted in a 250 - >1000 fold increase in the frequency of intrachromosomal recombination. This indicates that the pairing of homologous chromosomes during meiosis strongly inhibits intrachromosomal recombination events.

The meiotic behavior of this large tandem Dp reinforces the view that chromosome pairing initiates at a chromosome end and proceeds unidirectionally. This type of mechanism would preclude misalignment of the duplicated region despite the huge extent of homology. Further evidence that the two ctDp31 homologs are fully paired is provided by the fact that ctDp31 XX hermaphrodites produce >10-fold fewer spontaneous XO males than do wild-type hermaphrodites, implying a decrease in the incidence of non-recombinant X chromosomes.

The ctDp31 reversion assay can be used to identify mutations that reduce recombination between homologs but still permit intrachromosomal recombination. This was first shown in the Wood lab, where it was found that him-8 ( e1489 )caused a >100 fold increase in ctDp31 reversion (Burgess et al., 1987 Meeting Abstracts). I have shown that two new alleles of him-8 (obtained in my general screen for mutants with increased non-disjunction) also cause increased ctDp31 reversion. Observation of increased levels of intrachromosomal recombination in this assay suggest that the him-8 mutations are defective in some aspect of homolog pairing, consistent with the altered distribution of interchromosomal recombination events observed in him-8 mutants by Broverman and Meneely (1991 Meeting Abstracts). Not all defects in the homolog pairing process are expected to share this property however. For example, most models for homolog recognition, a crucial phase in the pairing process, involve a mechanism to search for DNA sequence homology; such a homology search would be required for both inter- and intrachromosomal recombination events. [See Figure]

Literature Cited:

Tanner and Wood, 1991 Meeting Abstracts.

Burgess et al., 1987 Meeting Abstracts.

Broverman and Meneely, 1991 Meeting Abstracts.

Tanner et al., WBG 10:3.

Figure 1