Mutations in the par genes lead to a maternal effect lethal phenotype characterized by alterations in cleavage pattern and timing, aberrant partitioning of P granules, and extensive alterations in cell fates. We have proposed that the par genes encode components of a maternal system for asymmetric intracellular localization in early embryos and that proper functioning of this system is required for specification of early embryonic cell fates. Here we provide evidence that the par gene functions are necessary to establish proper lineage- specific transcription patterns in early cleavage stage embryos. Recently, the CeMyoD gene was shown to be an early marker of lineage specific transcription, with its earliest expression limited to the 2- 4 cells of the MS lineages at the 24-28 cell stages of embryogenesis. ( Krause et al., Cell 63,907). Andy Fire and Mike Krause anticipated our interest in this marker and generously gave us prepublication access to their data and a transgenic strain carrying a CeMyoD- -gal transcription reporter construct. We have constructed strains that segregate par homozygous worms carrying the reporter gene and are presently assaying -gal activity in the mutant embryos. Conclusions thus far: 1 ) All pars thus far examined (
par-2,3,5) show ectopic expression of the CeMyoD reporter at the 32-cell stage (equivalent chronologically to wild type 24-28 cell stage). 2) No expression is seen prior to the 32-cell stage. 3) At least part of the early ectopic expression in
par-3 and
par-5 is transient; while many 32-and 64-cell-stage embryos are -gal positive in all nuclei, all embryos past the 64-cell stage have significant numbers of -gal negative nuclei. 4) ectopic 13-gal expression in
par-2 embryos is limited to the posterior half of most embryos.