Homozygotes for
dpy-21 that have 2 X-chromosomes are Dpy, whereas 1X homozygotes are nonDpy. We have been investigating the interaction between
dpy-21 and X-chromosome duplications, attempting to define the region on the X or the amount of X that affects the
dpy-21 phenotype. The two largest duplications tested, mnDp25 and mnDp10, are each recognized as an additional X-chromosome, at least partly: mnDp25/+;
dpy-21/dpy-21; XO animals may be Dpy or semiDpy. mnDp25 is about a quarter of the X map, and mnDp10 is about 30%. Three smaller duplications, recognized as an additional X- chromosome in duplication heterozygotes. However, a male homozygous for
dpy-21 and heterozygous for both mnDp33 and mnDP9 (which together represent about 30% of the X genetic map) is Dpy. This result indicates that there are several different regions on the X which together can affect
dpy-21. (See our note in the last newsletter for more details.) We have extended these results to various duplication homozygotes. Males homozygous for
dpy-21 and mnDp9 (the largest duplication not recognized as an additional X in duplication heterozygotes) are Dpy. Moreover, we were unable to make stocks homozygous for
dpy-21 and either mnDp25 or mnDp10, implying that these duplication homozygotes are lethal in
dpy-21 homozygotes. This observation is consistent with a second
dpy-21 phenotype Jonathan Hodgkin told us about: 3X:2A
dpy-21 homozygotes are also apparently inviable. Thus in both male and hermaphrodite
dpy-21 animals, one and two copies of a duplication may have different effects on
dpy-21.We looked for other Dpy mutants that are X-chromosome dependent by mutagenizing
him-5 and picking all the F2 Dpys we could find. Most of these either were 3X animals or segregated Dpy males, but three produced only nonDpy males. One of these mutants is probably a new allele of
dpy-21. Two others, both weak Dpys, fail to complement and map on linkage group IV. The stronger of the two has been tested with the transformer mutants
tra-1 and
her-1; like
dpy-21, its effect is independent of sexual phenotype. We have begun testing its interaction with the X chromosome duplications. It is more sensitive to these duplications than
dpy-21, since mnDp9 is recognized as an additional X in duplication heterozygotes. The results with other duplications correspond to the
dpy-21 results; mnDp33 and mnDp1 are not recognized as an additional X chromosome while mnDp10 is. (mnDp25 has not been tested yet.) We have not tested these mutants for lethality yet, nor have we attempted to make double mutants with
dpy-21. It is possible that these two mutants are weak alleles of
dpy-26 (see note by Jonathan); complementation tests are in progress. We have tried to make a crossover suppressor for the region around
dpy-21 by mating gamma-irradiated
rol-4 odites with
dpy-21 males. (
rol-4 is about 10 map units to the left of
dpy-21 and
unc-51 about 10 map units to the right of
dpy-21). From this cross we looked for F1 hermaphrodites that gave Unc but no Rol progeny. Two candidates have been retained after two backcrosses. Each is maintained in the form
rol-4 +
unc-51/+ ; cks are quite fertile and segregate Unc Rol, wild type, and Dpy, but no Rol. For both, the Unc tes are fertile. We are currently testing these chromosomes for their ability to balance other LGV markers. We have used one of them in a preliminary screen for
dpy-21 deficiencies. We have tried unsuccessfully to isolate stable duplications of other regions of the X, notably
unc-6. We would like to test other X duplications for their interaction with
dpy-21 and our new mutants if anyone has a stable duplication we don't know about.