Worm Breeder's Gazette 15(1): 49 (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.
Dept. Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461
egl-5, a homolog of the Drosophila Abdominal B gene, is
one of the four C. elegans Hox genes clustered in the left
arm of chromosome III. Based on the egl-5 mutant phenotype
(Chisholm, 1991) and on results obtained with an egl-5::lac-Z
reporter (Wang et al., 1993), an egl-5 domain of expression
was identified in the tail of the worm. We are now using an
affinity purified anti-EGL-5 antibody and an egl-5::gfp
reporter to identify the cells expressing this gene during C.
elegans larval development. The expression data up to early
L3 was mainly obtained with the antibody. After L3, in males,
a large number of nuclei stains intensely and it has not been
possible to make identification of all cells. All antibody
staining observed was nuclear; with the egl-5::gfp reporter,
although the fluorescence was concentrated in the nuclei,
some cytoplasmic fluorescence was also observed.
Lateral hypodermis: expression was first detected in
V6.ppp (L2) and is mantained in its descendants V6.pppp and
V6.pppa in early L3, and the ray cell precursors R4, R5, and
R6 in mid-L3. In a few animals EGL-5 expression in R3 was
also observed. Later, the expression is maintained in R5- and
R6-derived cells (precursors of rays 5 and 6, respectively),
but not in descendants of R4 or R3 (precursors of ray 4 and
3, respectively). In hermaphrodites no lateral hypodermal
cells express EGL-5. The EGL-5 expression pattern in ray cell
precursors seems to be complementary to that previously
described by Salser & Kenyon (1996) to the Hox gene mab-5 ,
which is maintained in rays 2 and 4 but turned off in rays 3,
5, and 6.
Rectal epithelium: EGL-5 is expressed from L1in the B,
Y, U, F and K cells in both males and hermaphrodites. In
hermaphrodites the expression persists in these cells through
to adulthood. In males expression remains in at least some,
if not all, of the male-specific proctodeal descendants of B,
Y, U, and F. K.a is stained both in males and hermaphrodites.
Preanal ganglion: EGL-5 expression was detected in at
least some P12 descendants, such as P12.p and P12.pa. Some U
descendants in the preanal ganglion in males may also be
stained. Identification of the staining preanal ganglion
cells in later stages was not possible. The egl-5::gfp
reporter is expressed in adult males in a pair of neurons
that extend processes anteriorly in the ventral nerve cord
and into the nerve ring.
Mechanosensory neurons: The touch receptor neurons PLML
and PLMR stain with the anti-EGL-5 antibody both in males and
hermaphrodites throughout development.
Other neurons: other neuronal nuclei in the cloacal
ganglia in males, and in the dorsorectal ganglion and lumbar
ganglia of males and hermaphrodites also express EGL-5
throughout development. However, their identification is not
yet possible. Some candidates would be the PVC neurons in the
lumbar ganglia, K.p in the dorso-rectal ganglion, and neurons
descending from male B, Y, and F blast cells.
Male gonad: starting in late L1-early L2 a group of 6
cells (probably somatic) in the anterior of the male gonad
stains with the anti-EGL-5 antibody. The number of stained
cells seems to remain constant until late L3 and their
position is always in the migrating end of the gonad. In late
L3 and L4 the staining is observed in dividing cells that
form the seminal vesicle and in sperm nuclei.
Muscle cells: posterior dorsal and ventral body wall
muscle cell nuclei express EGL-5 in both sexes, confirming
results obtained with an egl-5::lac-Z reporter (Ahringer,
1996). This staining pattern is especially prominent from L2
on. Later, starting in late L3, egl-5 is expressed in the
male sex-specific muscles.
Ahringer, J. (1996). Genes Dev. 10, 1120
Chisholm, A. (1991). Development 111, 921
Salser, S.J. & Kenyon, C. (1996) Development 122, 1651.
Wang, B.B. et al. (1993) Cell 74, 29.