Worm Breeder's Gazette 10(2): 150

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.

A Ring Chromosome in C. elegans?

Craig P. Hunter and W.B. Wood

Figure 1

The free duplication of the right arm of LGIII, eDp6, was isolated 
by J.  Hodgkin in association with the deficiency eDf2 (Genetics 96.  
649-664, 1980).  We have used eDp6 extensively in the mosaic analysis 
of tra-1 and have made several observations that are consistent with 
this duplication being a ring chromosome.  The strongest evidence 
comes from the generation and analysis of deletions in the duplication.
vab-7(e1564)dpy-18(e364)unc-64(e246);eDp6 hermaphrodites were 
irradiated with 1500 rads of gamma rays.  Of 5500 F1 duptication-
bearing progeny, 13 were identified that contained altered 
duplications (see figure).  Altered duplications that failed to 
complement two of the three markers and duplications that railed to 
complement a single marker were generated at similar frequencies, 
suggesting that partial deletions of the duplication were the primary 
mutational event.  Evidence that eDp6 is circular comes from the 
deletion events of classes D and E in the figure.  These classes, 
which arose at about the same frequency as the others, could have 
arisen from a single event in a circular chromosome but would require 
two independent events in a linear chromosome.  Additional 
circumstantial evidence for circularity is that simple recombinants 
between the duplication and LGIII are not recovered, suggesting that 
recombination either does not occur or is lethal.  However, we have 
recovered a complex recombinant, suggesting that recombination can 
occur.  The phenotype of the complex recombinant was identical to that 
of strain CB1517, which is homozygous for eDf2 and carries an 
undetermined number of copies of eDp6 (Hodgkin, op.  cit.).  
Complementation analysis of the complex recombinant showed that the 
resulting LGIII is deficient for vab-7, 
unc-32, suggesting that the 
recombination resulted in a deficiency of this region, similar to eDf2.
That complex recombinants can be recovered and simple recombinants 
are not suggests that the latter events are lethal.  Although simple 
recombinants between eDp6 and the chromosome have not been recovered, 
recombinants between ctDp2 (a class A isolate; see figure), and LGIlI 
are frequent.  eDp6 is meiotically unstable; it is recovered in only 
50% of the self progeny of duplication hermaphrodites.  Mitotically 
the duplication is stable (loss/cell division is about 1/1000-5000).  
ctDp2, which covers vab-7, unc-64 
is recovered in only 15% of self progeny and is lost mitotically at a 
rate of about 1/250 cell divisions.  The class B isolate, which 
complements all three markers, is recovered in only 25% of self 
progeny and is lost mitotically at an estimated 1/100 cell divisions (
not carefully determined).  These results suggest that either a 
segregator function on the duplication has been deleted or that the 
change in structure or size of these derivatives has a profound effect 
on segregation (e.g., perhaps ring duplications are mitotically more 
stable than linear duplications).  The circumstances in which eDp6 was 
isolated (Hodgkin op.  cit.) suggest that this duplication and the 
accompanying deficiency were generated by a single intrachromosomal 
recombination event.  This could have generated a circular free 
duplication and a deletion chromosome capped by a telomere.

Figure 1