Epigenetic activation of FLOWERING LOCUS C by Arabidopsis trithorax genes
|演題||Epigenetic activation of FLOWERING LOCUS C by Arabidopsis trithorax genes|
|講演者||Yosuke Tamada（National Institute for Basic Biology）|
Winter annual habit of Arabidopsis thaliana requires active alleles of FLOWERING LOCUS C (FLC), which encodes a potent flowering repressor, and FRIGIDA (FRI), an activator of FLC. FLC activation by FRI is accompanied by histone methylations, such as trimethylation of histone H3 at Lys 4 (H3K4me3). Such H3K4 methylation at the FLC locus requires two known classes of H3K4 methyltransferases, Drosophila Trithorax-class ARABIDOPSIS TRITHORAX1 (ATX1) and yeast Set1-class ATX-RELATED7 (ATXR7). The atx1 atxr7 double mutation completely suppresses the delayed flowering of a FRI-containing line. The rapid flowering of atx1 atxr7 is associated with reduced FLC expression and is accompanied by decreased H3K4 methylation at FLC. We further revealed that ATXR3, which encodes a member of a bikont-specific class of histone methyltransferase, also contributes to H3K4 methylation and the FLC activation. These data indicate that three different classes of H3K4 methyltransferases play a key role in FLC activation and thus establishing the winter-annual habit. We also analyzed the genetic relationships between the ATX genes and other FLC activators to understand the complicated transcriptional activation mechanisms of FLC.
Currently we are investigating the genome-wide relationship between transcription and histone methylations in the moss Physcomitrella patens. Trimethylation of histone H3 at Lys 27 (H3K27me3) functions in transcriptional repression, and is catalyzed by the only gene, P. patens CURLY LEAF (PpCLF), in Physcomitrella. A lesion in PpCLF causes complete loss of H3K27me3. However, unlike many other multicellular organisms that have been studied, the ppclf mutant is viable and exhibits several pleiotropic phenotypes. Now we are analyzing the genome-wide profiles of transcription, H3K27me3 and H3K4me3 in wild type and the ppclf mutant, to investigate the contributions of H3K27me3 to transcription and the active histone modification, H3K4me3. We have revealed a certain part of their relationship that has not been reported before.
倉田 哲也 (firstname.lastname@example.org)