2 MATERNAL GENES, APX-1 AND PIE-1, ARE REQUIRED TO DISTINGUISH THE FATES OF EQUIVALENT BLASTOMERES IN THE EARLY CAENORHABDITIS-ELEGANS EMBRYO

In a 4-cell Caenorhabditis elegans embryo, two sister blastomeres call ed ABa and ABp are born with equivalent developmental potential, but e ventually produce distinct patterns of cell fate. The different fates of ABa and ABp are specified at least in part by inductive interaction s with neighboring blastomeres. Previous studies indicate that, at the 4-cell stage, a signal from the posterior-most blastomere, P-2, is re quired for ABp to produce at least one of its unique cell types. This P-2/ABp interaction depends on glp-1, a putative receptor for intercel lular interactions. To investigate this early induction further, we is olated mutants in which ABp developed abnormally. We describe the effe cts of recessive mutations in apx-1, a maternal gene that appears to b e required for P-2 to signal ABp. In embryos from mothers homozygous f or mutations in apx-1 (apx-1 embryos), ABp fails to produce its charac teristic cell types. Instead, ABp from apx-1 embryos develops more lik e its sister ABa: it produces ABa-like pharyngeal cells and it recapit ulates ABa-like cell lineages. Because mutations in apx-1 affect the d evelopment of only the ABp blastomere, we suggest that the wild-type g ene encodes a component of the P-2/ABp signalling pathway. To explain the observation that ABp in apx-1 embryos adopts an ABa-like fate, we propose a model in which the P-2 signal is required to break the initi al equivalence of ABa and ABp. We performed two independent tests of t his model. First, we examined ABp development in pie-1 mutant embryos, in which P-2 adopts the identity of another blastomere. We find that, in pie-1 embryos, ABp fails to produce its characteristic cell types and instead adopts a fate similar to that of ABa. We conclude that the changed identity of P-2 in pie-1 embryos prevents the P-2/ABp interac tion. As a second test, we examined ABp development in wild-type embry os after physically removing P-2. These operated embryos produce extra pharyngeal cells, consistent with our proposal that a signal from P-2 breaks the initially equivalent developmental state of ABa and ABp. W e discuss the possibility that apx-1 acts as a ligand in this glp-1-de pendent signalling pathway.