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.