RT Journal Article
SR Electronic
T1 RETINOBLASTOMA RELATED (RBR) interaction with key factors of the RNA-directed DNA methylation (RdDM) pathway
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2022.01.06.474281
DO 10.1101/2022.01.06.474281
A1 Jesús, León-Ruiz
A1 Annie, Espinal-Centeno
A1 Ikram, Blilou
A1 Ben, Scheres
A1 Mario, Arteaga-Vázquez
A1 Alfredo, Cruz-Ramírez
YR 2022
UL http://biorxiv.org/content/early/2022/01/06/2022.01.06.474281.abstract
AB Transposable elements and other repetitive elements are silenced by the RNA-directed DNA methylation pathway (RdDM). In RdDM, POLIV-derived transcripts are converted into double stranded RNA (dsRNA) by the activity of RDR2 and subsequently processed into 24 nucleotide short interfering RNAs (24 -nt siRNAs) by DCL3. 24-nt siRNAs are recruited by AGO4 and serve as guides to direct AGO4 - siRNA complexes to chromatin bound POLV-derived transcripts generated from the template/target DNA. The interaction between POLV, AGO4, DMS3, DRD1, RDM1 and DRM2 promotes DRM2-mediated de novo DNA methylation.The Arabidopsis Retinoblastoma protein homolog is a master regulator of cell cycle, stem cell maintenance and development. In silico exploration of RBR protein partners revealed that several members of the RdDM pathway contain a motif that confers high affinity binding to RBR, including the largest subunits of POLIV and POLV (NRPD1 and NRPE1), the shared second largest subunit of POLIV and POLV (NRPD/E2), RDR1, RDR2, DCL3, DRM2 and SUVR2. We demonstrate that RBR binds to DRM2, DRD1 and SUVR2. We also report that seedlings from loss -of-function mutants in RdDM and in RBR show similar phenotypes in the root apical meristem. Furthermore, we show that RdDM and SUVR2 targets are up-regulated in the 35S::AmiGO-RBR background.Our results suggest a novel mechanism for RBR function in transcriptional gene silencing based on the interaction with key players of the RdDM pathway and opens several new hypotheses, including the convergence of RBR-DRM2 on the transcriptional control of TEs and several cell/tissue and stage -specific target genes.Competing Interest StatementThe authors have declared no competing interest.