Cells born in all regions of the C. elegans embryo appear to recognize their polarity with respect to that of the embryo. We have shown previously that the HMG domain protein POP-1 is asymmetrically localized in the nuclei of all sisters born of anterior-posterior (A-P) divisions and that
pop-1 activity is required for A-P fate differences between sisters. Although a Wnt signal from P2 has been shown to polarize EMS and regulates POP-1 asymmetry between the daughters of EMS, MS and E, there appears to be a distinct global mechanism for the regulation of POP-1 asymmetry. First, zygotic POP-1 is expressed at 24-cell stage and is asymmetrically localized in
pop-1(
zu189) embryos that lack maternal POP-1. Second, mutants for some components of the P2-EMS signal have a POP-1 asymmetry defect primarily in the MS and E sisters, while mutants for other components have a more universal defect. Using a GFP::POP-1 reporter, we show that although the GFP::POP-1 asymmetry is disrupted between MS and E in
mom-2(
or39) mutant embryos, it is re-established as MS and E divide and remains so in their descendents. On the other hand, GFP::POP-1 remains symmetric in all A-P descendents in the EMS lineage in embryos depleted of
lit-1,
mom-4, or
wrm-1. Embryonic A-P polarity is established upon fertilization. Many genes, including pars, have been shown to function in establishment and/or maintenance of various aspects of A-P polarity. We investigate the requirement of these genes for POP-1 A-P asymmetry using a reporter GFP::POP-1. Surprisingly, despite the early role of PAR-2 in establishing embryonic polarity, GFP::POP-1 asymmetry is properly maintained in
par-2(
lw32) mutant embryos. On the contrary, POP-1 asymmetry is defective in
par-3(
it71),
par-6(
zu222), or
pkc-3(RNAi) embryos. Approximately 50% of A-P sisters have similar levels of GFP::POP-1 while the other 50% have asymmetric GFP::POP-1 with a random orientation. The randomly oriented POP-1 asymmetry is dependent on WRM-1 activity. The pattern of GFP::POP-1 in
par-2(
lw32);
par-3(
it71) mutant embryos resembles that in
par-3(
it71) embryos, suggesting that PAR-3, and not PAR-2, activity is required for the asymmetry as well as the orientation of asymmetry of nuclear POP-1. GFP::POP-1 asymmetry appears to be normal in
par-1(
zu310), consistent with PAR-1 functioning downstream of PAR-2 and PAR-3 in the maintenance of A-P polarity. Using candidate gene and RNAi library screen approaches, we hope to identify factors involved in establishment and transmission of the A-P positional cue that directs reiterative nuclear asymmetry of POP-1.