Worm Breeder's Gazette 7(2): 15

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.

Autosomal Genes Affected by X-Chromosome Dose

P. Meneely, B. Wood

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.