Worm Breeder's Gazette 11(2): 80
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.
We have completed our study on the effects of 14 heterozygous LGV(
left) deficiencies on recombination in adjacent regions. The
deficiency chromosomes were marked with unc-46(e177) (1-3). Ten
deficiencies ('Major Inhibitors') severely inhibited recombination
between themselves and unc-46 (Fig. 1). In contrast, the remaining 4
deficiencies were 'Minor Inhibitors' (marked with '*' in Fig. 1).
[See Figure 1]
The effects of major inhibitors on recombination in different
intervals was measured. Fig. 2 gives the recombination rates in
terms of percent of the control rates. The results showed: (1)
Inhibition extended into the dpy-11 but not
into the ama-2 region. (2) Where measured, inhibition occurred to the
right of the deficiency but not to its left (sDf42, sDf27; also sDf50,
data not shown).
[See Figure 2]
Based on our results, we have erected a model for the manner in
which pairing for recombination occurs on LGV. To do so we postulate
the existence of a special site, deleted by minor but not by major
inhibitors, that is responsible for the difference between these two
classes. The site's existence is based on the following: Six
deficiencies are 'internal' deficiencies, i.e. they do not delete the
left-most marker, let-450. These six are all major inhibitors. We
hypothesize that the remaining 4 major inhibitors are also internal
deficiencies and do not extend as far to the left as do the 4 minor
inhibitors, each of which deletes let-450. Our model proposes that
pairing for recombination involves at least two chromosomal sites:
'initiation' and 'alignment' sites. These sites act secondarily to a
'homolog recognition site'. The latter is believed to be in LGV(right)
, as evidenced from the way recombination and segregation occurs in
eT1(III;V) heterozygotes [(4) and discussed by McKim et all. (5)].
Intimate pairing for recombination starts at and spreads from each
initiation site, if homologous sites are within a minimum distance
from each other. We propose that the special site postulated above (
at or near the left terminus) is such a site for LGV(left). Another
site must exist in LGV(right) to account for the recombination
occurring there in eT1 heterozygotes. The pairing process spreads
from each initiation site by 'buttoning-up' the homologs at sequential
alignment sites, which are ones that occur repeatedly between
initiation sites and have a common sequence. In the absence of
homologous left-end initiation sites (i.e. in heterozygous minor
inhibitors) pairing initiates only in LGV(right), proceeds toward the
left, aligns the homologs in a correct manner and no major inhibition
of recombination occurs. But in the presence of a heterozygous major
inhibitor, pairing proceeds from both ends of LGV. To the left of the
deficiency, homologous regions remain in register and recombine
normally. To its right, the sequential buttoning of alignment sites
causes a misalignment, heterologous regions become aligned, thus
inhibiting recombination. Based on our current data there would be a
minimum of three alignment sites in LGV(left).
A report on this study is currently in press in Genetics.
