All are equal, but some are more equal than others: Epigenetic regulation of germline stem cell fate in <i>Drosophila</i> <i>melanogaster</i>

Abstract

Adult stem cells are capable of both symmetric and asymmetric cell divisions. Asymmetric cell division allows self-renewal and gives rise to intermediate cells that ultimately differentiate into specific cell types. Consequently, adult stem cells play a key role in development and tissue homeostasis during the life span of an organism. Typically, adult stem cell divisions are regulated through coordination between non-autonomous signaling from the niche and cell-autonomous influences from stem cell-intrinsic factors. Although localized distribution of proteins, RNA and organelles during cell division contributes significantly to the differences between fates of daughter cells, recent studies have also implicated epigenetic factors in this process. A number of epigenetic modifications remain associated with the chromosomes during mitosis and serve as a template to reestablish fates after mitosis. Whether the distribution of epigenetic modifications is random on each chromatid or there is a bias in their distribution is therefore under extensive investigation. The nonrandom distribution of epigenetic modifications on mitotic chromosomes provides an attractive possible explanation of how bias is generated during chromatid segregation. In Drosophila male germline stem cells, the histone modifications present in the stem cells are distinct from those in the differentiating daughter cells. These modifications help to retain pre-existing histones in the mother cell while imparting newly synthesized histones to the daughter cell. Importantly, the retention of pre-existing histones in the stem cells is a prerequisite to maintain their ability to self-renew. Here we summarize recent studies that focus on the role of different epigenetic modifications in the regulation of asymmetric adult germline stem cell divisions in Drosophila. We further describe how epigenetic modifications potentially lead to variations in the otherwise equivalent chromatids, and discuss the role of biased chromatid segregation in asymmetric cell divisions.