Progenitor cells divide to produce a variety of differentiated cells that express specific sets of genes. Such characters of differentiated cells must be kept stable, possibly by maintaining chromatin structures to keep transcriptional state of each gene. We isolated
bet-1 mutants by abnormal T cell lineage phenotype.
bet-1 encodes an evolutionally conserved protein containing the bromodomain that is known to binds to acetylated histones.
bet-1 mutants showed defects in maintenance of gene expression pattern. Each descendants of the wild-type neural progenitor cell, V5.pa, start to express a cell type specific marker shortly after its birth (for example,
dat-1::gfp and
osm-6::gfp for PDE), then those expressions are maintained at later stages. In
bet-1 mutants, the descendants that normally do not express those markers frequently start expressing them ectopically at much later stages. In addition,
osm-6::gfp-positive neurons frequently lose its expression. These results indicate that BET-1 functions to keep gene expression pattern by chromatin factors including histones. In addition to the V5.pa lineage, ectopic expression of a DTC marker,
lag-2::gfp, or AVM/PVM marker,
mec-4::gfp, was also observed in the Z1/Z4 or Q lineages, respectively. Ectopic
lag-2::gfp or
mec-4::gfp expression also started at much later stages than start of the normal expression. These results suggest that BET-1 is involved in maintenance of gene expression pattern in multiple cell lineages. In
bet-1, all the cells that ectopically express the marker genes are produced from the same progenitor cells with the normally expressing cells. In addition, in the V5.pa lineage, ectopic
osm-6::gfp expression was observed more frequently in the sister or its progeny of PDE than in its cousins. These results suggest that distinct gene expression patterns were fixed progressively through a series of asymmetric cell division, so that differences between sister cells are more highly dependent on
bet-1 than those between cousins. Among distantly related cells, differences of gene expression are maintained in
bet-1-indpenedent manner.