The gene
pes-1 is transiently expressed in the early C.elegans embryo. The
pes-1/LacZ expression pattern can be divided into three lineage components. The earliest component is in a subset of cells within the AB lineage which are both ABa and ABp derived. The second component is within the D lineage from the 4D though to the 16D cell stage. The final component of the expression pattern is 2 cells, Z1 and Z4. My research is to understand what controls
pes-1/LacZ expression in these particular cells as this will provide insight into the mechanisms that lead to cell fate specification. This work focuses on the role of intercellular interactions in regulating
pes-1/LacZ expression. Previous work has shown that
pes-1/LacZ expression in the AB lineage is dependent on
glp-1 which encodes a putative membrane receptor protein and has been identified to function in two interactions that occur at the 4 cell and 12 cell stage. Mutations in
glp-1 remove the AB component of
pes-1/LacZ expression pattern. This work analyses the effects of three temperature sensitive alleles for
glp-1;
e2141,
e2142 and
e2144. Temperature shift experiments with
e2142 suggest that
glp-1 activity is required at three separate intervals. On the basis of these results I propose a 3 signal model for
glp-1 mediated induction of
pes-1/LacZ expression in the AB lineage. An initial signal occurs at around 12 cell stage that induces
pes-1/LacZ expression. This is followed by an inhibitory signal at around the 15 cell stage that represses expression in AB. A third signal at around the 24 to 28 cell stage induces expression.
apx-1 encodes a putative signalling ligand for
glp-1 and maternal
apx-1 has been shown to be required during the 4 cell stage interaction. Analyses of the effects of
apx-1 on the AB component of the
pes-1/LacZ expression pattern have shown that maternal and zygotic
apx-1 activity might be required during the 15 and 24 to 28 cell stage interactions respectively. Further analyses reveal that zygotic
apx-1 is required for
pes-1/LacZ expression in the D lineage. A mutation in
apx-1 leads to absence of expression at the 8D and 16D cell stage. Future work will characterise the effect of a temperature sensitive allele of
apx-1 to identify when its activity is required for expression within the D lineage. The
lag-1 gene is also involved in the
glp-1 signal transduction pathway and appears to act downstream of
glp-1. I am characterising the effect of
lag-1 on
pes-1/LacZ expression and results will be discussed.