RT Journal Article
SR Electronic
T1 Arabidopsis TRB proteins function in H3K4me3 demethylation by recruiting JMJ14
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2023.01.10.523456
DO 10.1101/2023.01.10.523456
A1 Ming Wang
A1 Zhenhui Zhong
A1 Javier Gallego-Bartolomé
A1 Suhua Feng
A1 Yuan-Hsin Shih
A1 Mukun Liu
A1 Jessica Zhou
A1 John Curtis Richey
A1 Charmaine Ng
A1 Yasaman Jami-Alahmadi
A1 James Wohlschlegel
A1 Keqiang Wu
A1 Steven E. Jacobsen
YR 2023
UL http://biorxiv.org/content/early/2023/01/10/2023.01.10.523456.abstract
AB Arabidopsis telomeric repeat binding factors (TRBs) can bind telomeric DNA sequences to protect telomeres from degradation. TRBs can also recruit Polycomb Repressive Complex 2 (PRC2) to deposit tri-methylation of H3 lysine 27 (H3K27me3) over certain target loci. Here, we demonstrate that TRBs also associate and colocalize with JUMONJI14 (JMJ14) and trigger H3K4me3 demethylation at some loci. The trb1/2/3 triple mutant and the jmj14-1 mutant show an increased level of H3K4me3 over TRB and JMJ14 binding sites, resulting in up-regulation of their target genes. Furthermore, tethering TRBs to the promoter region of genes with an artificial zinc finger (TRB-ZF) successfully triggers target gene silencing, as well as H3K27me3 deposition, and H3K4me3 removal. Interestingly, JMJ14 is predominantly recruited to ZF off-target sites with low levels of H3K4me3, which is accompanied with TRB-ZFs triggered H3K4me3 removal at these loci. These results suggest that TRB proteins coordinate PRC2 and JMJ14 activities to repress target genes via H3K27me3 deposition and H3K4me3 removal.Competing Interest StatementThe authors have declared no competing interest.