We use the C. elegans postembryonic mesodermal lineage, the M lineage, as a model system to study mesodermal patterning and cell fate specification. The M lineage arises from a single pluripotent cell, the M mesoblast, during embryogenesis. During postembryonic development of a hermaphrodite animal, the M cell undergoes a series of cell divisions to first produce 18 cells: 14 striated bodywall muscles (BWMs), 2 non-muscle coelomocytes (CCs), and 2 sex myoblasts (SMs), which further divide to produce the egg-laying vulval and uterine muscles (VMs and UMs). We and others have previously identified a number of transcription factors important for the proper patterning and fate specification in this lineage. In order to identify additional transcription factors that play a role in the M lineage, we used RNAi feeding and screened through over 500 putative chromatin-associated factors for their role in the M lineage using cell-type specific GFP reporters. One of the factors identified from the screen is the histone chaperone RBA-1. Both rba-1(RNAi) and rba-1(0) null mutants exhibit an extra VM phenotype. These extra VMs appear to arise from the fate transformation of M-derived CCs and BWMs to the VM precursors, the SMs. We have found that this M lineage defect is specific to rba-1 loss-of-function, because a null mutation in the rba-1 paralog lin-53 did not cause any M lineage defects, and forced expression of lin-53 failed to rescue the M lineage phenotype of rba-1(0) mutants. We are currently determining whether RBA-1 exerts its function by working with specific transcription factors important in CC and BWM fate specification in the M lineage.