We are using the C. elegans postembryonic mesodermal lineage, the M lineage, as a model to study mesodermal patterning and cell fate specification. The M lineage arises from a single pluripotent cell, the M mesoblast, during embryogenesis. In hermaphrodites, the M cell first undergoes a dorsal-ventral division and then a left-right division to produce four cells located in four quadrants of the L1 larva. These four cells subsequently undergo two to three more rounds of cell divisions along the anterior-posterior axis to produce 18 cells: 14 body wall muscles (BWMs), 2 coelomocytes (CCs), and 2 sex myoblasts (SMs). In particular, M.dlp and M.drp each give rise to an anterior CC and a posterior BWM. In an RNAi screen for transcription factors important for proper M lineage development, we identified the Six2 homeodomain factor
ceh-34 for its requirement in the proper specification of M-derived CC fates.
ceh-34(RNAi) results in a fate transformation of the anterior CC to its posterior sister cell, the BWM. We have generated translational
ceh-34::gfp fusions and found that in the M lineage,
ceh-34 is specifically expressed in the CC precursor cells. To understand the mechanisms underlying the asymmetric expression pattern of
ceh-34, we determined the roles of the Wnt/beta-catenin asymmetry pathway in the M lineage because this pathway has been shown to regulate other asymmetric cell fates along the anterior-posterior axis. We have found that during both of the anterior-posterior cell divisions in the early M lineage, the TCF homolog POP-1 is enriched in the anterior daughters while the beta-catenin homolog SYS-1 is enriched in the posterior daughters. Furthermore,
sys-1(
q544) loss-of-function mutants have extra M lineage-derived CCs, while
pop-1(RNAi) leads to a loss of M-derived CCs. We showed that
ceh-34(RNAi) is epistatic to
sys-1(
q544) mutations and that
ceh-34::gfp is ectopically expressed in the M lineage in
sys-1(RNAi) animals but reduced in
pop-1(RNAi) animals. These observations suggest that
ceh-34 functions downstream of
pop-1 and
sys-1 in the M lineage. We are currently testing if POP-1 and SYS-1 directly regulate the asymmetric expression of
ceh-34 in M lineage development.