Meiotic mutations in the genes
him-3(
e1256)IV,
him-6(
e1423)IV and
him-8(
e1489)(IV) were originally isolated by Hodgkin et al. (1979) because they caused a high level of X-chromosome nondisjunction. Him- 6 and Him-3 hermaphrodites were found to have elevated levels of autosomal nondisjunction. Him-8 hermaphrodites produced many male progeny due to random disjunction of their X-chromosomes. Unlike the first two mutants,
him-8 did not appear to affect autosomal disjunction. I have tested the effects of
him-3 and
him-6 on recombination frequency in different regions of chromosomes I, III, V and X and tested the effects of all three mutants on the segregation patterns of free duplications. Previous to this study,
him-3 and
him-6 were known to map on the right end of chromosome IV between
dpy-13 and
unc-31 (Figure). In order to position them more accurately, him males were crossed to a series of deficiencies from the right end of chromosome IV.
him-3 was complemented by all the deficiencies tested.
him-6 failed to complement sDf2 and sDf60 but complemented mDf7. This placed
him-6 close to
unc-22 (Figure). The frequency of males from
him-6/sDf60 ( 18/83 = 0.22) and
him-6/sDf2 (49/264 = 0.19) hermaphrodites was slightly higher than in
him-6/him-6 hermaphrodites (average of 13.7% in recombination experiments). In addition, the number of progeny produced by
him-6/sDfs hermaphrodites (279/7 = 40) was less than from
him-6/him-6 hermaphrodites (average of 110 in recombination experiments). Because the phenotype of
e1423 was more severe when heterozygous to a deficiency, the
e1423 mutation may be a hypomorph. Recombination: Compared to the controls,
him-3 mutants had a reduced recombination frequency on chromosome I. The reductions were more severe in the
bli-3 (25% of control) than in the
dpy-5 (68% of control). The severity of the reduction in the
bli-3 of
him-3 hermaphrodites was confirmed when different markers (
let-362 dpy-5) on the left end of chromosome I were used. Similar results were found on chromosomes III where
him-3 mutants reduced recombination in the dpy- 17
unc-64 interval (65% of control) and to a lesser degree in the unc- 45 (80% of control). On chromosome V, recombination in the
unc-60 was reduced to 50% of the control frequency. On the X-chromosome,
him-3 had little effect on recombination frequencies. The recombination frequency in the
unc-1 dpy-7 interval was 82% of controls and in the
dpy-7 unc-3 interval the recombination frequency 97% of controls. Considering the high level of X-chromosome nondisjunction in Him-3 hermaphrodites, approximately 15% of the progeny from
him-3 hermaphrodites were males, the small reduction on X chromosome recombination was surprising. In addition, the lack of an effect of
him-3 on X-chromosome recombination differed from the observations made on the autosomes.
him-6 also caused reductions in recombination frequency. In the bli- 3
unc-11 region, recombination frequency was reduced in
him-6 (75% of control) but not to the degree of reduction in
him-3 mutants. There appeared to be no effect of
him-6 in the
dpy-5 unc-54 region. In contrast, recombination was reduced over the entire lengths of chromosome III and chromosome V. Recombination was also generally reduced on the X-chromosome. Unlike the situation with
him-3, the X- chromosome nondisjunction phenotype of
him-6 correlated with the reduction in recombination frequency. Autosomal nondisjunction. The level of chromosome I nondisjunction in
him-3 and
him-6 hermaphrodites was assayed by crossing hT2/+ males to
dpy-5;
unc-64;
unc-36; odites. If a disomy I gamete was produced by the Him strain, then there was a 25% chance it would be fertilized by a I(R)III(R)hT2; IIIN sperm to produce a
dpy-5 worm (the I(R)III(R)hT2; III(N) chromosome of hT2(I;III) does not carry
dpy-5(+). In the control, hT2/+ males were crossed to
dpy-5; odites. No Dpy or Unc progeny were observed in 1882 progeny. Thus, the normal chromosome I nondisjunction frequency was less than 0.002. From the
him-3 cross 14
dpy-5 hermaphrodites and 4 Dpy-5 males were recovered in 114 wild-type hermaphrodites and 106 wild-type males. The excess of Dpy-5 hermaphrodites may have resulted from viability differences between hermaphrodites and males or from a segregation pattern such that disomic I gametes were often disomic X as well. The frequency of chromosome I nondisjunction in the Him-3 oocytes was ( 18/238) 0.076. In the
him-6 cross, seven Dpy-5 hermaphrodites and five Dpy-5 males were recovered in 471 wild-type hermaphrodites and 451 wild-type males. In this case there was no excess of Dpy-5 hermaphrodites. The frequency of chromosome I nondisjunction in the Him-6 oocytes was (12/934) 0.013. Effects on duplication segregation: We tested the effects of
him-3, egregation of chromosomal duplications. In scoring the self-fertilization progeny of hDpx; odites, the him mutants did not increase the frequency of chromosome loss (mitotic and meiotic). The effects of the him mutants on the segregation of duplications from the X chromosome was tested by crossing
dpy-5; him-y males to
dpy-5; odites. In normal males, hDp12 segregated from the X-chromosome by a non-homologous process (see Herman et al. 1979).
him-3 disrupted the nonhomologous segregation of hDp12 resulting in equal numbers of male and hermaphrodite wild-types and Dpy progeny. In contrast,
him-6 and
him-8 did not effect non- homologous segregation of hDp12 males. hDp31 carries part of the left end of the X-chromosome joined to chromosome I sequences and homologously pairs and recombines with the X chromosome. hDp31 continued to segregate from the X-chromosome in both
him-3 and
him-8 males, although the efficiency of segregation was reduced compared to controls. The segregation of hDp31 in these strains might be by the nonhomologous process. [See Figure 1]