Worm Breeder's Gazette 15(1): 50 (October 1, 1997)
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.
Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Ave. Bronx, NY 10461
During male ray development, seam cells send inhibitory
signals to their neighbors to inhibit ray production. For example,
seam cell T sends a signal to its anterior neighbor V6 to inhibit
production of rays 2 through 6. pal-1, which encodes a homolog of
Drosophila caudal, acts in V6 autonomously to override this inhibitory
signal [1]. To identify the signal from seam cell T, as well as other
components which can bypass this inhibitory signal to allow V6 to
produce rays 2 through 6, we performed a screen for suppressors of
pal-1(e2091). 19 alleles defining 15 genes were obtained from 4000
genomes screened. We are trying to clone four of them: sop-1(bx92,
bx93, bx104, bx107), sop-2(bx91), sop-3(bx96), and sop-4(bx106).
sop-1 is located on the X chromosome, about +1.18. In the
strongest allele, bx92, 97% of sides have normal V6 rays in pal-1
mutant background. Besides suppressing pal-1, sop-1 also can
partially suppress mab-5(e1239); the rays in mab-5; sop-1 mutant are
dependent on egl-5 activity. No other obvious phenotype has been
observed. Recently, we cloned sop-1. It encodes a 3520 amino acid
protein which contains transmembrane domain(s). It shows significant
similarity to one uncharacterized human gene. A sop-1-GFP reporter
gene has been constructed. Preliminary data shows it is expressed in
the head region and in several tail cells in both sexes. Surprisingly,
it seems to be in nucleus.
sop-2 is mapped on chromosome II, about -19.32. In sop-2, 7%
of male sides have rays 2 and 3 transformed to rays 4, 5, and 6. This
suggests possible misregulation of egl-5 in the V6 lineage (see
Ferreira, Zhang and Emmons, this issue). In some males there are
several rays as well as fan-like cuticlular structures in the central
body region. In 30% of hermaphrodites, alae are discontinuous.
Besides suppressing pal-1, sop-2 also can suppress lin-32 (e1926 and
u282). The sop-2 mutant has other phenotypes, including affects on
vulval development. To determine whether these pleiotropic effects are
due to ectopic expression of Hox genes, we are studying the Hox gene
expression pattern in sop-2 mutant (many thanks to QueeLim Chng and
Dr. Cynthia Kenyon for mab-5-lacZ, mab-5-GFP, lin-39-lacZ and
egl-5-lacZ reporter genes).
sop-3 is mapped on chromosome I: both tDf3 and tDf4 delete
sop-3. The effect of sop-3 mutation is very similar to sop-1, both
have maternal effect and partially suppress mab-5(e1239). In sop-3,
there is a low frequency of ray fusion, and ray 6 is sometimes
missing. The cosmids from this region have been requested to do
transformation rescue.
sop-4 is also located on chromosome I. It is close to
unc-11, and the deficiencies and duplications from this region are
being tested. In sop-4; pal-1 mutant, 71% of sides have normal V6
rays. sop-4 alone has no obvious phenotype.
pal-1 is required for mab-5 expression in V6 [2], so we are
using mab-5-lacZ and mab-5-GFP reporter genes to study whether mab-5 is
expressed in a pal-1 background in sop-1, sop-2, sop-3, and sop-4
mutant.
[1] Waring, D. A. & Kenyon, C Nature 350, 712-715; Cell 60, 123-131.
[2] Salser, S. J. & Kenyon, C Development 122, 1651-1661.