Project description:Global warming imposes a major threat to plant growth and crop production. In some plants including Arabidopsis thaliana, elevated temperatures induce a series of morphological and developmental adjustments, termed thermomorphogenesis to facilitate plant cooling under high-temperature conditions. Plant thermal response is suppressed by histone variant H2A.Z. At warm temperatures, H2A.Z is evicted from nucleosomes at thermo-responsive genes, resulting in their activation. However, the mechanisms that regulate H2A.Z eviction and subsequent transcription activation are largely unknown. Here, we show that the ino80 chromatin-remodeling complex (ino80-C) promotes thermomorphogenesis and activates the expression of thermo-responsive and auxin-related genes. ino80-C associates with PHYTOCHROME-INTERACTING FACTOR 4 (PIF4), a potent regulator in thermomorphogenesis, and mediates temperature-induced H2A.Z eviction at PIF4 targets. Moreover, ino80-C directly interacts with COMPASS-like and transcription elongation factors to promote active histone modification Histone H3 lysine 4 trimethylation (H3K4me3) and RNA Polymerase II (RNA Pol II) elongation, leading to the thermal induction of transcription. Notably, transcription elongation factors are required for the eviction of H2A.Z at PIF4 targets, suggesting the cooperation of ino80-C and transcription elongation in H2A.Z removal. Our results demonstrate that the (PIF4)-(ino80-C)-(COMPASS-like)-(transcription elongator) module controls plant thermal response, and establish a link between H2A.Z eviction and active transcription.
Project description:Global warming imposes a major threat to plant growth and crop production. In some plants including Arabidopsis thaliana, elevated temperatures induce a series of morphological and developmental adjustments, termed thermomorphogenesis to facilitate plant cooling under high-temperature conditions. Plant thermal response is suppressed by histone variant H2A.Z. At warm temperatures, H2A.Z is evicted from nucleosomes at thermo-responsive genes, resulting in their activation. However, the mechanisms that regulate H2A.Z eviction and subsequent transcription activation are largely unknown. Here, we show that the ino80 chromatin-remodeling complex (ino80-C) promotes thermomorphogenesis and activates the expression of thermo-responsive and auxin-related genes. ino80-C associates with PHYTOCHROME-INTERACTING FACTOR 4 (PIF4), a potent regulator in thermomorphogenesis, and mediates temperature-induced H2A.Z eviction at PIF4 targets. Moreover, ino80-C directly interacts with COMPASS-like and transcription elongation factors to promote active histone modification Histone H3 lysine 4 trimethylation (H3K4me3) and RNA Polymerase II (RNA Pol II) elongation, leading to the thermal induction of transcription. Notably, transcription elongation factors are required for the eviction of H2A.Z at PIF4 targets, suggesting the cooperation of ino80-C and transcription elongation in H2A.Z removal. Our results demonstrate that the (PIF4)-(ino80-C)-(COMPASS-like)-(transcription elongator) module controls plant thermal response, and establish a link between H2A.Z eviction and active transcription.
Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
Project description:The INO80 chromatin remodeling complex promotes thermomorphogenesis by connecting H2A.Z eviction and active transcription in Arabidopsis
Project description:The INO80 chromatin remodeling complex promotes thermomorphogenesis by connecting H2A.Z eviction and active transcription in Arabidopsis[RNA-seq]
Project description:The INO80 chromatin remodeling complex promotes thermomorphogenesis by connecting H2A.Z eviction and active transcription in Arabidopsis[ChIP-seq]
Project description:Many plants, including Arabidopsis thaliana, respond to elevated ambient temperatures by altering their growth through a process known as thermomorphogenesis. This response involves the depletion of the repressive histone variant H2A.Z from the gene bodies of PIF4-regulated auxin-related genes, enabling their transcriptional activation. Interestingly, this activation also requires the histone deacetylase HDA9, raising the question of how histone deacetylation, typically associated with transcriptional repression, can instead promote gene activation. Here, we identify FVE as a co-regulator that partners with HDA9 to activate PIF4 target genes at elevated temperatures. PIF4 directly interacts with and recruits the FVE-HDA9 complex to its target genes to remove acetylation from histone H4 and H2A.Z. We show that H2A.Z acetylation is required for recruiting the SWR1 complex, which deposits H2A.Z. Consequently, FVE-HDA9-mediated deacetylation reduces SWR1 complex binding and limits H2A.Z deposition. Moreover, we demonstrate that in addition to limiting H2A.Z deposition, H2A.Z depletion also results from H2A.Z eviction mediated by the INO80 complex. Together, these findings uncover a dual mechanism contributing to H2A.Z depletion: INO80-mediated active eviction and histone deacetylation-mediated inhibition of H2A.Z deposition, which underlies PIF4 target gene activation and explain the paradoxical role of histone deacetylation in transcriptional activation.