Worm Breeder's Gazette 12(5): 27 (February 1, 1993)

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 New Componenet of the EMS-ABa Blastomere Interaction

Caroline Goutte, James R. Priess

Fred Hutchinson Cancer Research Center, Seattle, Washington

Inductive cell interactions determine the developmental fate of certain blastomeres of the C elegans embryo. For example, the interaction of the ABa and EMS blastomeres, or their descendants, is required for the production of pharyngeal cells by descendants of the ABa blastomere (1). We are interested in identifying the molecules that mediate this early inductive cell interaction in nematode embryos. One player has already been identified as the product of the glp-1 gene, which also is required to mediate an inductive event during the development of the germ line (2, 3). Animals that are homozygous for a glp-1 mutation (that does not affect the germ line) cannot make viable progeny. The embryos of such animals arrest during embryogenesis with only a partial pharynx - they produce the posterior half of the pharynx which is generated by descendants of the EMS blastomere, but lack the anterior half, normally produced by ABa descendants. Molecular analysis of glp-1 has revealed that it is a member of the Notch family of transmembrane proteins (4).

We have found a candidate for a second gene product required to mediate the EMS-ABa interaction. This gene, aph-1 (for anterior pharynx defective), is defined by two alleles ( zu123 and z147 )that result in a matemal-effect embryonic lethality indistinguishable from that of glp-1 . Embryos from aph-1 homozygous mothers arrest in development and lack an anterior pharynx. The hypodermal defect (extra lateral hypodermal cells) observed in glp-1 embryos also is observed in aph-1 embryos. The zu147 auele of aph-1 has a weaker

effect than zu123 ,and allows for more complete morphogenesis and a very low sunrival rate.

The striking similarity between the embryonic phenotypes of aph-1 and glp-1 mutant embryos suggests that these genes are involved in the same event in embryonic development. However, two lines of evidence lead us to believe that the aph-1 and glp-1 gene products have very distinct functions. First, in contrast to glp-1 , aph-1 does not appear to be involved in cell interactions which occur post-embryonically during germ line development. The phenotype of aph-1 ( zu147 )/ nDf25 is indistinguishable from that of aph-1 ( zu147 )/ aph-1 ( zu123 ),and aph-1 ( zu123 )/ nDf25 ,and shows only the maternal effect lethality described above. We have failed to observe any effect on the germ line, and have found normal brood sizes for aph-1 ( zu123 )or aph-1 ( zu147 )homozygous animals. Second, aph-1 does not appear to have a zygotic role in late embryogenesis, as glp-1 does. Lambie and Kimble have shown that in a lin-12 background, glp-1 has an essential zygotic role: lin-12 , glp-1 double mutants die soon after hatching (4). We have constructed the aph-1 ( zu123 ); lin-12 ( ng41 ),doublemutant, and find viable adults. Thus, aph-1 and glp-1 may be involved in mediating the same inducdve cell interaction event during early emb~yogenesis, but their specific functions appear to be distinct.

We are currently trying to better define the role of aph-1 in development, and are attempting to clone the aph-1 gene. By genetic mapping, it is located on the right arm of chromosome I, between unc-29 and lin-11 .We have localized the aph-1 locus within about seven cosmids by RFLP analysis, and are now attempting cosmid-rescue.

Literature Cited:

(1) Priess, J.R. and Thomson, J.N. (1987). Cell 48, 241-250.

(2) Austin, J., and Kimble, J. (1987). Cell 51, 589-599.

(3) Priess, J.R., Schnabel, H., and Schnabel, R. (1987). Cell 51, 601-


(4) Yochem, J. and Greenwald, I. (1989). Cell 58. 553-563.

(5) Lambie, E.J. and Kimble, J. (1991). Development 112, 231-240.