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    Review of 'Linker histone H1 regulates defense priming and immunity in plants'

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    Linker histone H1 regulates defense priming and immunity in plantsCrossref
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    Linker histone H1 regulates defense priming and immunity in plants

    Linker H1 histones play an important role in animal and human pathogenesis, but their function in plant immunity is poorly understood. Here, we analyzed mutants of the three canonical variants of Arabidopsis H1 histones, namely H1.1, H1.2 and H1.3. We observed that double h1 . 1h1 . 2 and triple h1 . 1h1 . 2h1 . 3 ( 3h1 ) mutants were resistant to Pseudomonas syringae and Botrytis cinerea infections. Transcriptome analysis of 3h1 mutant plants showed that histone H1s play a key role in regulating the expression of early and late defense genes upon pathogen challenge. Moreover, 3h1 mutant plants showed enhanced production of reactive oxygen species and activation of mitogen activated protein kinases upon pathogen-associated molecular pattern (PAMP) treatment. However, 3h1 mutant plants were insensitive to priming with flg22, a well-known bacterial PAMP (pathogen-associated molecular pattern) which induces enhanced resistance in WT plants. The defective defense response in 3h1 was correlated with the enhanced DNA methylation and reduced H3K56ac levels upon priming. Our data place H1 as a molecular gatekeeper in governing dynamic changes in the chromatin landscape of defense genes during plant pathogen interaction.
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      10.14293/S2199-1006.1.SOR-LIFE.A5GCQ7.v1.RZYWZD
      This work has been published open access under Creative Commons Attribution License CC BY 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Conditions, terms of use and publishing policy can be found at www.scienceopen.com.

      Quantitative & Systems biology,Plant science & Botany
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      The authors did excellent works to support the linker Histone H1 regulates defense primig and plant immunity. 

      1. In Figure1, does H1.2 mutant showed a growth defect compared with WT and other mutants?

      2. Did the authors tried shorttime treatment (e.g. 0.5h) for the stress response? Some of the defense response was triggered in a shorttime treatment.

      3. Figure1C, is the reduced pesion area in 3h1 mutants due to the HR?

      4. Did the author transfer any of the H genes back to the  3h1 mutants and detect the compleentation of the plant innate immune response?

      5. H1.1, H1.2 and H1.3, which of the H1 gene plays a key role in the process of plant innate immunity? 

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