Abstract

Single-stranded DNA-binding proteins (SSBs) are assumed to involve in DNA replication, DNA repairmen, and gene transcription. Here, we provide the direct evidence on the functionality of an Arabidopsis SSB, WHIRLY1, by using loss- or gain-of-function lines. We show that WHIRLY1 binding to the promoter of WRKY53 represses the enrichment of H3K4me3, but enhances the enrichment of H3K9ac at the region contained WHIRLY1-binding sequences and TATA box or the translation start region of WRKY53, coincided with a recruitment of RNAPII. In vitro ChIP assays confirm that WHIRLY1 inhibits H3K4me3 enrichment at the preinitiation complex formation stage, while promotes H3K9ac enrichment and RNAPII recruitment at the elongation stage, consequently affecting the transcription of WRKY53. These results further explore the molecular actions underlying SSB-mediated gene transcription through epigenetic regulation in plant senescence.

Highlights

  • Plant senescence is the last stage of plant development

  • We have found that enrichment of H3K4me3 and H3K9ac at promoter region contained WHIRLY1 binding domain and TATA box and translation start region of WRKY53, and recruitment of RNAPII, as well as transcription of WRKY53 are coordinated by WHRLY1 protein in a developmental manner

  • It demonstrates that the occupancy of WHIRLY1 represses the enrichment of H3K4me3 before senescence initiation and enhances the enrichment of H3K9ac and the recruitment of RNAPII at senescence initiation stage, and high ratio of H3K9ac/H3K4me2-3 determines the transcription level of WRKY53 and leaf senescence initiation

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Summary

Introduction

Plant senescence is the last stage of plant development. WRKY is a major transcription factor (TF) family of plants, in which many of them are the central players in gene regulation during leaf senescence. WRKY6 was found to activate several senescence-associated genes during leaf senescence (Robatzek and Somssich, 2002). Mutation and overexpression of WRKY6 retarded and accelerated both developmentally and darkinduced senescence (Robatzek and Somssich, 2002; Zhang et al, 2018). Overexpression or knockout of WRKY22 showed accelerated and delayed senescence phenotype in dark condition (Zhou et al, 2011). Loss of WRKY53 delayed the leaf senescence (Miao et al, 2004), while wrky mutant showed aggravated senescent phenotype during development and dark treatment (Ulker et al, 2007). WRKY54 can co-operate with WRKY70 to repress leaf senescence

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