Histone variant HTB4 delays leaf senescence by epigenetic control of Ib bHLH transcription factor-mediated iron homeostasis
Histone variant HTB4 delays leaf senescence by epigenetic control of Ib bHLH transcription factor-mediated iron homeostasis
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DOI：
10.1111/nph.19008
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发表时间：
2023-06-02
期刊：
影响因子：
9.4
通讯作者：
Li，Zhonghai
中科院分区：
文献类型：
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作者：
Yang，Qi;Wang，Ting;Li，Zhonghai
叶片衰老是一个受多种内在因素和多种环境胁迫（包括营养缺乏）调控的有序过程。组蛋白变异参与调节植物生长发育。然而，它们在叶片衰老中的功能和潜在的调控机制仍不清楚。在这里，我们发现H2B组蛋白变体HTB4作为叶片衰老的负调控因子。HTB4的功能缺失导致了早期的叶片衰老表型，这些表型被功能互补所挽救。RNA - seq分析显示，参与铁（铁）稳态的几个Ib亚群碱性螺旋-环-螺旋（bHLH）转录因子（TFs），包括bhlh038、bHLH039、bHLH100和bhlh101，在htb4突变体中被抑制，从而影响了铁摄取机制的两个重要组成部分——ric还原氧化酶2（FRO2）和diron调节转运蛋白（IRT1）的表达。染色质免疫沉淀-定量聚合酶链反应分析显示，HTB4可以结合Ib bHLH tf的启动子区域，并通过促进其转录起始位点附近活性标记H3K4me3的富集来增强其表达。此外，Ib bHLH TFs或irt1的过表达抑制了htb4突变体的过早衰老表型。我们的工作建立了一个信号通路，HTB4 - bHLH， tf - FRO2/IRT1 - Fe稳态，调控叶片衰老的发生和进展。
Leaf senescence is an orderly process regulated by multiple internal factors and diverse environmental stresses including nutrient deficiency. Histone variants are involved in regulating plant growth and development. However, their functions and underlying regulatory mechanisms in leaf senescence remain largely unclear.Here, we found that H2B histone variant HTB4 functions as a negative regulator of leaf senescence. Loss of function of HTB4 led to early leaf senescence phenotypes that were rescued by functional complementation. RNA‐seq analysis revealed that several Ib subgroup basic helix–loop–helix (bHLH) transcription factors (TFs) involved in iron (Fe) homeostasis, includingbHLH038,bHLH039,bHLH100, andbHLH101, were suppressed in thehtb4mutant, thereby compromising the expressions ofFERRIC REDUCTION OXIDASE 2(FRO2) andIRON‐REGULATED TRANSPORTER(IRT1), two important components of the Fe uptake machinery.Chromatin immunoprecipitation‐quantitative polymerase chain reaction analysis revealed that HTB4 could bind to the promoter regions of Ib bHLH TFs and enhance their expression by promoting the enrichment of the active mark H3K4me3 near their transcriptional start sites. Moreover, overexpression of Ib bHLH TFs orIRT1suppressed the premature senescence phenotype of thehtb4mutant.Our work established a signaling pathway, HTB4‐bHLH TFs‐FRO2/IRT1‐Fe homeostasis, which regulates the onset and progression of leaf senescence.