We are interested in understanding mesodermal patterning and fate specification by studying the C. elegans postembryonic mesodermal lineage, the M lineage. The M lineage is derived from a single precursor cell, the M mesoblast, and gives rise to six cell types: striated bodywall muscles (BWMs), nonmuscle coelomocytes (CCs), and four classes of non-striated sex muscles which are descendants of the sex myoblasts (SMs). We are studying the function of the
mls-2 (mesodermal lineage specification) gene in M lineage patterning and fate specification. The
mls-2(
cc615) mutation causes randomization of division planes in the M lineage, and subsequent fate transformation of CCs and BWMs to SMs. In addition,
cc615mutants have defects in SM migration and show some larval and adult lethality. We have cloned the wild type
mls-2 gene (C39E6.4).
mls-2 encodes a homeodomain protein that belongs to the HMX family of homeodomain proteins that are also present in sea urchin, Drosophila and vertebrates., We examined the expression pattern of
mls-2 using both functional
mls-2::gfp fusion construct and affinity purified anti-MLS-2 antibodies. We found that the MLS-2 protein is localized in nuclei of early M lineage cells and a subset of head neurons. Furthermore,
mls-2 expression in the M lineage and the head neurons appears to require distinct cis-acting elements. Overexpression of
mls-2 in the early M lineage where
mls-2 is normally expressed caused a variety of defects in the M lineage. Forced expression of
mls-2 in the later M lineage such as in SMs where
mls-2 is not normally expressed resulted in extra rounds of divisions of SMs. This suggests that
mls-2 may have multiple roles in the M lineage and that MLS-2 protein level is critical for the correct patterning of the M lineage. The M lineage defects of
mls-2(
cc615) are very similar to those of
mab-5,
hlh-1,
egl-27 and
egl-20 mutants. We are currently carrying out molecular and genetic epistasis experiments to investigate the relationship between
mls-2 and those factors.