Institut de biologie moléculaire des plantes du CNRS, Strasbourg, France.
Nat Plants. 2024 Nov;10(11):1698-1709. doi: 10.1038/s41477-024-01814-9. Epub 2024 Oct 4.
Plants have evolved sophisticated DNA repair mechanisms to cope with the deleterious effects of ultraviolet (UV)-induced DNA damage. Indeed, DNA repair pathways cooperate with epigenetic-related processes to efficiently maintain genome integrity. However, it remains to be deciphered how photodamages are recognized within different chromatin landscapes, especially in compacted genomic regions such as constitutive heterochromatin. Here we combined cytogenetics and epigenomics to identify that UV-C irradiation induces modulation of the main epigenetic mark found in constitutive heterochromatin, H3K9me2. We demonstrated that the histone demethylase, Jumonji27 (JMJ27), contributes to the UV-induced reduction of H3K9me2 content at chromocentres. In addition, we identified that JMJ27 forms a complex with the photodamage recognition factor, DNA Damage Binding protein 2 (DDB2), and that the fine-tuning of H3K9me2 contents orchestrates DDB2 dynamics on chromatin in response to UV-C exposure. Hence, this study uncovers the unexpected existence of an interplay between photodamage repair and H3K9me2 homeostasis.
植物已经进化出复杂的 DNA 修复机制来应对紫外线(UV)诱导的 DNA 损伤的有害影响。事实上,DNA 修复途径与表观遗传相关过程合作,有效地维持基因组的完整性。然而,如何在不同的染色质景观中识别光损伤,特别是在致密的基因组区域如组成型异染色质中,仍有待破译。在这里,我们结合细胞遗传学和表观基因组学来鉴定 UV-C 照射诱导组成型异染色质中主要表观遗传标记 H3K9me2 的调节。我们证明了组蛋白去甲基酶 Jumonji27(JMJ27)有助于 UV 诱导的染色质中心 H3K9me2 含量的减少。此外,我们发现 JMJ27 与光损伤识别因子 DNA 损伤结合蛋白 2(DDB2)形成复合物,并且 H3K9me2 含量的精细调节协调了 DDB2 在 UV-C 暴露时在染色质上的动力学。因此,本研究揭示了光损伤修复和 H3K9me2 动态平衡之间存在意想不到的相互作用。