Worm Breeder's Gazette 9(3): 47

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.

y9: An XO-Specific Lethal Mutation that Suppresses the Known XX-Specific Lethal Mutations

L. Miller and B. Meyer

y9 suppresses the XX-specific lethality of mutations in dpy-26. 
solated as a spontaneous 
revertant of dpy-28(yl) III, a temperature-sensitive, maternal-effect 
mutation preferentially lethal to XX animals. A dpy-28(yl); 
90) strain produces 69% dead eggs, 4% Dpy adult 
hermaphrodites and 27% adult wild-type males at 20 C. By contrast, a 
dpy-28(yl); 90); y9 strain produces 57% dead eggs, 
25% non-Dpy Egl hermaphrodites, and 18% males. Approximately 20% of 
the non-Dpy hermaphrodites have a small blip in the pre-anal region of 
the tail. Similar suppression is also seen when y9 is placed in 
combination with dpy-26(n199), 18), and dpy-28(s939)
. All three strains produce non-Dpy Egl hermaphrodites (some sterile, 
some with pre-anal tail blips) and males. The percentage of XX animals 
rescued by the y9 mutation in these strains has not yet been 
determined; however, it is clear that these animals are dramatically 
healthier than without the y9 mutation. The ability of one mutation to 
suppress several XX-specific lethal mutations is extremely interesting 
and implies the involvement of these mutations in a common pathway for 
dosage compensation.
y9 is an X-linked. XO-specific lethal mutation. When y9 was 
separated from dpy-28(yl), the resulting him-5(e1490); y9 strain 
produced phenotypically wild-type hermaphrodites but no males. Both 
the inability to produce XO males and the suppression of the XX-
specific lethality of yl mapped to the X chromosome. Threefactor 
crosses place y9 between dpy-7 X and unc-9 X.
We have eliminated the possibility that y9 simply suppresses the 
ability of the him-S mutation to produce nullo-X oocytes. This was 
demonstrated by showing the patroclinous inheritance of the lin-14(
n179) X marker in the male progeny of the cross unc-32(e189); 
90); y9 hermaphrodites mated by him-5; 
79) males.
Appropriate genetic tests have demonstrated that y9 does not 
transform XO animals into hermaphrodites. Moreover, in progeny counts 
of the him-S; y9 strain, the following results were obtained: 51% of 
the eggs laid developed into adult hermaphrodites and 49% of the eggs 
were dead. In a him-5(e1490) strain 55% of the eggs laid developed 
into adult hermaphrodites, 27% developed into adult males, and 18% of 
the eggs were dead.
The lethality of y9 is XO-specific rather than male-specific because 
XX tra-1(e1488); 90); y9 pseudomales are healthy. (
No XO wild-type males are produced).
Mutations in dpy-26  the XO 
lethality of y9. The dpy-28(yl); 90); y9 strain 
produces approximately 27% males, which is very close to the number 
expected from an e1490 strain. Although some of the males in this 
strain are sick, 
are healthy and mate well. Similar results have been obtained with 
dpy-26(n199), 18), and dpy-28(s939). Thus, the 
mutual suppression exhibited between y9 and the XX-specific lethal 
mutations is neither allele-specific nor gene-specific.
Another extragenic suppressor of Y9 is located on the X chromosome. 
The XO-specific lethality of y9 can be used in a powerful reversion 
scheme. Thus far, several revertants of y9 have been isolated by EMS 
mutagenesis of him-S(e1490); y9. One extragenic mutation, y16, is 
located on the X chromosome between y9 and unc-3 and restores males to 
the him-5(e1490); y9 strain. The males look completely wild-type and 
mate very well. Hermaphrodites homozygous for the y9y16 double, 
however, are dead. The phenotype of yl6 by itself is not yet known.
Future experiments will reveal if either y9 or yl6 alter X-linked 
gene expression and/or interfere with proper sex determination.