Heterochromatin is the predominant architectural feature of genomes that ensures genomic stability across eukaryotes. It mostly functions in restricting expression of repeats, mobile elements such as transposons and other regions. The establishment, maintenance and spreading of heterochromatin requires several factors including chromatin modifiers. However, how exactly heterochromatin formation is avoided in protein-coding domains is poorly understood. Here we show that a plant specific paralogue of RNA polymerase (pol) II, named pol IV, is involved in avoidance of facultative heterochromatic marks in protein coding genes, in addition to silencing the repeats and transposons forming constitutive heterochromatin. In its absence, H3K27 trimethylation mark intrudes the protein coding genes, more profoundly in genes embedded with repeats. In a subset of genes that lack the compensatory silencing, spurious transcriptional activity results in small(s)RNA production leading to post-transcriptional gene silencing. We show that such effects are significantly pronounced in rice, a plant with larger genome with distributed heterochromatin when compared to Arabidopsis. Our results indicate the surprising division of labour among plant-specific polymerases, not just in establishing effective silencing via small RNAs and epigenetics, but also in influencing chromatin boundaries.
Across eukaryotes, gene regulation is manifested via chromatin states roughly distinguished as heterochromatin and euchromatin. The establishment, maintenance, and modulation of the chromatin states is mediated using several factors including chromatin modifiers. However, factors that avoid the intrusion of silencing signals into protein-coding genes are poorly understood. Here we show that a plant specific paralog of RNA polymerase (Pol) II, named Pol IV, is involved in avoidance of facultative heterochromatic marks in protein-coding genes, in addition to its well-established functions in silencing repeats and transposons. In its absence, H3K27 trimethylation (me3) mark intruded the protein-coding genes, more profoundly in genes embedded with repeats. In a subset of genes, spurious transcriptional activity resulted in small(s) RNA production, leading to post-transcriptional gene silencing. We show that such effects are significantly pronounced in rice, a plant with a larger genome with distributed heterochromatin compared withArabidopsis. Our results indicate the division of labor among plant-specific polymerases, not just in establishing effective silencing via sRNAs and DNA methylation but also in influencing chromatin boundaries.
Wounding is a general stress in plants that results from various pest and pathogenic infections in addition to environment induced mechanical damages. Plants have sophisticated molecular mechanisms to recognize and respond to pests and pathogens. Although several molecules such as phytohormones, peptides and receptors have been attributed to wound responses in dicots, such mechanisms for monocots probably having distinct wound responses are less understood. Here, we show the involvement of two distinct categories of temporally separated, endogenously derived peptides, namely, plant elicitor peptides (PEPs) and phytosulfokine (PSK), that mediate wound responses in rice. These peptides trigger a dynamic signal relay in which a novel receptor kinase named OsPSKR played a major role. OsPSKR perceived PSK ligand, acting in association with a co-receptor OsSERK1, to activate downstream responses in a kinase activity-dependent manner. Perturbation of OsPSKR expression in rice led to compromised development and constitutive autoimmune phenotypes. These results suggested that OsPSKR maintains the trade-off between growth and exaggerated defense responses, both during homeostasis and wounding. Collectively, these findings indicate the presence of a stepwise peptide-mediated signal relay that regulates the transition from defense to growth upon wounding in monocots.One line summaryEndogenous peptide signalling initiated wound responses through a receptor-like kinase OsPSKR to maintain the balance between growth and defense responses.
Paralogous variants of canonical histones guide accessibility to DNA and function as additional layers of genome regulation. Across eukaryotes, the occurrence, mechanism of action and functional significance of several variants of core histones are well known except that of histone H4. Here we show that a novel variant of H4 (H4.V), expressing tissue-specifically among members of Oryza genera, mediates specific epigenetic changes contributing majorly to salt tolerance. H4.V was incorporated to specific chromosomal locations where it blocked deposition of active histone marks. Under salt stress, large scale re-distribution of H4.V enabled incorporation of stress dependent histone H4 Lysine5 Acetylation (H4K5Ac) marks. Mis-expression of H4.V led to defects at morphological level especially in reproductive tissues, and in mounting stress responses. H4.V mediated these alterations by condensing chromatin at specific genomic regions as seen with cryo-EM structure of reconstituted H4.V containing nucleosomes. These results not only uncovered the presence of a H4 variant in plants, but also a novel chromatin regulation of stress responses that might have contributed to success of semi-aquatic Oryza members under variable water-limiting conditions.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.