SRA

Heterochromatin formation and maintenance, key for epigenetic inheritance of cells and organisms, have two major unsolved problems: One is the unclear source and action mode of repeat-derived RNAs in the process and the second is distinct machineries employed by different organisms, as the siRNA and piRNA pathways respectively used in fission yeast and Drosophila germline both require RNA amplification, but such mechanism does not seem to exist in somatic cells of flies and mammals. We attack these problems by defining the origins of repeat-derived RNAs and their specific chromatin registers in Drosophila S2 cells that lack active piRNA. We demonstrate that Dicer-2 is responsible for processing diverse repeat-derived RNAs, particularly those transcribed from active Gypsy elements, which act in cis and trans to maintain pericentromeric heterochromatin. These findings suggest that somatic cells trade genome vulnerability for stable genetic inheritance while germ cells use RNA amplification to abate such trade-off. Overall design: Examination of H3K9me3, H3K27me3 and H3K4me3 three different histone modifications in S2 cells in four different conditions.