In the genetic tests performed thus far, all seven mutants behave virtually identically. All are (at least semi-) dominant and closely linked to
dpy-13 locus on the linkage group IV. There is no evidence as yet for any maternal effects in the expression of amanitin resistance or sensitivity, Heterozygous (ama(R)/+) males were mated with
dpy-8 odites to test X linkage or dominance. The mated hermaphrodites were cloned in microtiter wells in amanitin, The sensitive, self progeny (DpyUnc) did not grow beyond the L1 stage, but ama(R) F1 hermaphrodites with normal movement and body shape developed to maturity along with the DpyUnc males. The results were the same for each of the seven mutants. The production of resistant (ama(R)/+) hermaphrodite progeny shows that ama(R) is dominant. The production of resistant males shows that it is autosomal. Crosses with strains carrying two linked chromosomal markers showed that the ama(R) allele,
m118 is not linked to standard reference markers on LG I, II or III and V, but it is closely linked to
dpy-13(IV). (The chromosomal markers were the following:
dpy-3( DR39)
unc-6(
e78)(x); 21)
unc-3(
e151)(x); )
unc-75(
e950)(I); )
unc-54(
e1301)(I);
unc-4(II);
unc-4(II);
daf-2(
e1370)
unc-32(III);
daf-7 I);
unc-24(IV);
unc-24(IV);
unc-22(IV); ;
dpy11 unc-51(V).) The preliminary two- factor crosses produced only one
dpy-13 ama(R)/dpy-13 + recombinant among 100 homozygous Dumpy segregants. This suggests that ama
(m118) locus may be within one map unit of
dpy-13. Subsequent crosses revealed that all the seven ama(R) alleles are closely linked to dpy- 13. Three-factor crosses with the
m118 in trans to recessive markers, +ama(R)+
unc-22, produced three of the four possible classes of recombinants: Unc-Resistant, tive, and Dpy- Sensitive DpyUnc progeny were invariably Sensitive (40/40 tested). In the total of six recombinants, two were obtained in the interval between
dpy-13 and ama(R), and four recombinants were obtained in the interval between ama(R) and
unc-22. Obviously, these data are preliminary, however, since all the ama(R) mutants are dominant and all appear to be closely linked to
dpy-13(IV) we suspect that they all may be allelic.