Arabidopsis RRP6L1 and RRP6L2 Function in FLOWERING LOCUS C Silencing via Regulation of Antisense RNA Synthesis

The exosome complex functions in RNA metabolism and transcriptional gene silencing. Here, we repart that mutations of a Arabidopsis genes encoding nuclear exosome components AtRRP6L1 and AtRRP6L2, cause de-repression of he main lowering repressor FLOWERING LOCUS C (FLC) and thus delay flowering in early-flowering Arabidopsis ecotypes. AtRRP6L mutations affect the expression of known FLC regulatory antisense (AS) RNAs AS I and II, and cause an increase in Histone ethylation (H3K4me3) at FLC AtRRP6L1 and AtRRP6L2 function redundantly in regulation of FLC and also act of the exosome core complex. Moreover, we discovered a navel, long non-coding, non-polyadenylated ASL, for Antisense Long) originating from he FLC locus in wild type plants The AtRRP6L proteins ASL synthesis, as these mutants h little or no ASL transcript. Unlike ASI/II ASL an function associate during ato h H3K27n1e3 regions of FLC, suggesting that it could function in the maintenance of H3K27 trimethylation during vegetative growth. AtRRP6L mutations also affect H3K27me3 levels and nucleosome density at the FLC locus. Furthermore, AtRRP6L1 physically associates with the ASL transcript and directly interacts with the FLC locus. We propose at AtRRP6L proteins participate in the maintenance of H3K27me3 at FLC via regulating ASL. Furthermore, AtRRP6Ls might participate in multiple FLC silencing pathways by regulating diverse antisense RNAs derived from the FLC locus.