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      Chromatin marks and ambient temperature-dependent flowering strike up a novel liaison

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      Genome Biology
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          Abstract

          A distinct chromatin mark, H3K36me3, has been found to engage in temperature-dependent alternative splicing and ambient temperature-dependent flowering-time control in Arabidopsis.

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          Regulation of alternative splicing through coupling with transcription and chromatin structure.

          Alternative precursor messenger RNA (pre-mRNA) splicing plays a pivotal role in the flow of genetic information from DNA to proteins by expanding the coding capacity of genomes. Regulation of alternative splicing is as important as regulation of transcription to determine cell- and tissue-specific features, normal cell functioning, and responses of eukaryotic cells to external cues. Its importance is confirmed by the evolutionary conservation and diversification of alternative splicing and the fact that its deregulation causes hereditary disease and cancer. This review discusses the multiple layers of cotranscriptional regulation of alternative splicing in which chromatin structure, DNA methylation, histone marks, and nucleosome positioning play a fundamental role in providing a dynamic scaffold for interactions between the splicing and transcription machineries. We focus on evidence for how the kinetics of RNA polymerase II (RNAPII) elongation and the recruitment of splicing factors and adaptor proteins to chromatin components act in coordination to regulate alternative splicing.
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            Histone H3 lysine 36 methylation affects temperature-induced alternative splicing and flowering in plants

            Background Global warming severely affects flowering time and reproductive success of plants. Alternative splicing of pre-messenger RNA (mRNA) is an important mechanism underlying ambient temperature-controlled responses in plants, yet its regulation is poorly understood. An increase in temperature promotes changes in plant morphology as well as the transition from the vegetative to the reproductive phase in Arabidopsis thaliana via changes in splicing of key regulatory genes. Here we investigate whether a particular histone modification affects ambient temperature-induced alternative splicing and flowering time. Results We use a genome-wide approach and perform RNA-sequencing (RNA-seq) analyses and histone H3 lysine 36 tri-methylation (H3K36me3) chromatin immunoprecipitation sequencing (ChIP-seq) in plants exposed to different ambient temperatures. Analysis and comparison of these datasets reveal that temperature-induced differentially spliced genes are enriched in H3K36me3. Moreover, we find that reduction of H3K36me3 deposition causes alteration in temperature-induced alternative splicing. We also show that plants with mutations in H3K36me3 writers, eraser, or readers have altered high ambient temperature-induced flowering. Conclusions Our results show a key role for the histone mark H3K36me3 in splicing regulation and plant plasticity to fluctuating ambient temperature. Our findings open new perspectives for the breeding of crops that can better cope with environmental changes due to climate change. Electronic supplementary material The online version of this article (doi:10.1186/s13059-017-1235-x) contains supplementary material, which is available to authorized users.
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              Jumonji demethylases moderate precocious flowering at elevated temperature via regulation of FLC in Arabidopsis.

              As sessile organisms, plants have evolved multiple mechanisms to respond to environmental changes to improve survival. Arabidopsis plants show accelerated flowering at increased temperatures. Here we show that Jumonji-C domain-containing protein JMJ30 directly binds to the flowering-repressor FLOWERING LOCUS C (FLC) locus and removes the repressive histone modification H3 lysine 27 trimethylation (H3K27me3). At elevated temperatures, the JMJ30 RNA and protein are stabilized, and FLC expression is maintained at high levels to prevent extreme precocious flowering. The double mutant of JMJ30 and its homologue JMJ32, grown at elevated temperatures, exhibits an early-flowering phenotype similar to the flc mutant, which is associated with increased H3K27me3 levels at the FLC locus and decreased FLC expression. Furthermore, ectopic expression of JMJ30 causes an FLC-dependent late-flowering phenotype. Taken together, JMJ30/JMJ32-mediated histone demethylation at the FLC locus constitutes a balancing mechanism in flowering control at warm temperatures to prevent premature early flowering.
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                Author and article information

                Contributors
                dorothee.staiger@uni-bielefeld.de
                Journal
                Genome Biol
                Genome Biol
                Genome Biology
                BioMed Central (London )
                1474-7596
                1474-760X
                19 June 2017
                19 June 2017
                2017
                : 18
                : 119
                Affiliations
                ISNI 0000 0001 0944 9128, GRID grid.7491.b, , Molecular Cell Physiology, Faculty of Biology, Bielefeld University, ; Bielefeld, Germany
                Article
                1259
                10.1186/s13059-017-1259-2
                5474849
                3ddfbf6d-2c14-4cf8-9915-df21961882a7
                © The Author(s). 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft;
                Award ID: STA653
                Award ID: SPP1530
                Award Recipient :
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                © The Author(s) 2017

                Genetics
                Genetics

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