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Series GSE213962 Query DataSets for GSE213962
Status Public on Dec 04, 2023
Title Temporally-coordinated bivalent histone modifications of BCG1 enable fungal invasion and immune evasion
Organisms Triticum aestivum; Fusarium graminearum PH-1
Experiment type Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Summary Bivalent histone modifications, including functionally opposite H3K4me3 and H3K27me3 marks simultaneously on the same nucleosome, control various cellular processes by fine-tuning the gene expression in eukaryotes. However, the role of bivalent histone modifications in fungal virulence remains elusive. Here, we report that bivalent chromatin modification of BCG1 (bivalent chromatin-marked gene1) is critical for Fusarium graminearum (Fg) successfully invading the host plant. By mapping the genome-wide landscape of H3K4me3 and H3K27me3 dynamic modifications in Fg during invasion, we identified the infection-related bivalent chromatin-marked genes (BCGs). BCG1, which encodes a xylanase containing a novel G/Q-rich motif, possessed the highest bivalent modification. We showed that the G/Q-rich motif of BCG1 is required for its xylanase activity and is essential for the full virulence of Fg. Intriguingly, this G/Q-rich motif can be recognized by pattern-recognition receptors (PRRs) to trigger plant immunity. Therefore, Fg tightly regulates BCG1 expression during different infection stages. During initial infection stages, Fg employs H3K4me3 modification to induce BCG1 expression required for host cell wall degradation. Upon breaching the cell wall barrier, this active chromatin state was reset to bivalency by co-modifying with H3K27me3, which enables epigenetic silencing of BCG1 to escape from host immune surveillance. Collectively, our study highlights how fungal pathogens deploy bivalent epigenetic modification to achieve temporally-coordinated activation and suppression of a critical fungal gene, thereby facilitating successful infection and host immunity evasion.

This SuperSeries is composed of the SubSeries listed below.
 
Overall design It was proved by ChIP-seq data and sequential ChIPd ata that modulation of BCG1 expression dynamics by bivalent histone methylations enables fungal pathogen to evade host immunity.

Refer to individual Series
 
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Submission date Sep 22, 2022
Last update date Dec 05, 2023
Contact name zhao xiao zhen
E-mail(s) zhaoxiaozhen@ahau.edu.cn
Phone 17768116791
Organization name Anhui Agricultural University
Street address Anhui Agricultural University, 130 Changjiangxilu, Shushan District, Hefei, Anhui Province, China
City Hefei
ZIP/Postal code 230036
Country China
 
Platforms (2)
GPL23509 Illumina HiSeq 4000 (Triticum aestivum)
GPL32260 Illumina HiSeq 4000 (Fusarium graminearum PH-1)
Samples (37)
GSM6596986 RNA-Seq of Fusarium graminearum PH-1:PH-1 at 0hpi rep1
GSM6596987 RNA-Seq of Fusarium graminearum PH-1:PH-1 at 0hpi rep2
GSM6596988 RNA-Seq of Fusarium graminearum PH-1:PH-1 at 0hpi rep3
This SuperSeries is composed of the following SubSeries:
GSE213960 Bivalent histone modification of BCG1 enables fungal pathogen to evade host immunity (RNA-Seq)
GSE213961 Bivalent histone modification of BCG1 enables fungal pathogen to evade host immunity (ChIP-Seq)
Relations
BioProject PRJNA883376

Download family Format
SOFT formatted family file(s) SOFTHelp
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Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE213962_RAW.tar 409.5 Mb (http)(custom) TAR (of BW)
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