The maintenance of cell fates is an essential mechanism in stem cells and also in differentiated cells. In the differentiated cells, it is not easy to distinguish the defect in the cell fate maintenance from that in the specification. However, because of invariant cell lineage and many cell fate markers, it is advantageous to study cell fate maintenance in C. elegans. We have previously shown that histone acetylation and histone variant HTZ-1/H2A.z are required for the maintenance of cell fate in multiple cell lineages through the transcriptional repression of DNA-binding transcriptional factors. For example, in somatic gonadal cells except for DTCs, the AcH4-binding protein, BET-1, that regulates the subnuclear localization of HTZ-1 represses
ceh-22 whose ectopic expression induces extra-DTC formation. However, it is not clear yet how this mechanism regulates the transcriptional repression. We found that the chromatin-remodeling complex, CeBAF, is required for the maintenance of cell fates. Interestingly, two regulatory components of CeBAF have distinct effect. Disruption of
swsn-6 caused defect in the maintenance of cell fates. In contrast, disruption of
ham-3 did not cause defect in the maintenance of cell fates, but enhanced it in the
bet-1 background. We also found that TFIIH complex that regulates transcriptional elongation controls the maintenance of cell fates. Disruption of components of the TFIIH complex showed a synergistic effect with the
bet-1 mutation, but not with the
swsn-6 mutation. We also found that
ham-3 and
zk1128.4 that encode components of the TFIIH are redundant. Therefore, BET-1, HAM-3 and the components of the TFIIH complex have a redundant function in the maintenance of cell fates. One of the explanations is that histone acetylation, histone variant, and chromatin remodeling complex CeBAF may regulate the transcriptional elongation through the TFIIH complex.