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The LUMINIDEPENDENS protein is a general repressor of transcription in Arabidopsis [LD ChIP-Seq]

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NIAID Data Ecosystem2026-05-10 收录
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https://www.ncbi.nlm.nih.gov/sra/SRP571585
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资源简介:
Genomic integrity is constantly challenged by transcription/replication conflicts, a major source of replication stress and instability across all life forms. While extensive studies have uncovered transcription/replication conflicts resolution mechanisms in animals, yeast, and prokaryotes, their counterparts in plants remain largely unexplored. Through a forward genetic screen, we identified the LUMINIDEPENDENS (LD) protein, previously known for regulating the flowering repressor FLC, as a key player in mitigating replication stress in plants. Strikingly, transcriptomic analyses reveal that loss of LD results in the upregulation of over 13,000 genes, establishing LD as a global transcriptional repressor. Consistent with this role, LD binds a substantial portion of the Arabidopsis genome and interacts with the MED18 subunit of the Mediator complex to modulate RNA polymerase II phosphorylation. These findings uncover a fundamental function of LD in fine-tuning transcription genome-wide, with an additional role in suppressing transcription/replication conflicts by locally dampening transcription and promoting replication fork progression. Our work highlights a previously unrecognized genome-protective strategy in plants, opening new avenues for understanding transcription/replication conflict management in eukaryotic systems. Overall design: ChIP-seq samples from Arabidopsis thaliana whole plantlets of the Id mutant genotype expressing the pLD-LD-GFP fusion protein, with two biological replicates and their corresponding input controls. These samples aim to investigate the LD-GFP DNA binding under the Id mutant background. The design also incorporates RNA polymerase II phosphorylation states (S2P and SSP) and histone H3K9ac modification profiles in both wild-type (Col-0) and Id mutant genotypes, with input controls and replicates for each condition.
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2025-11-18
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