Ultraviolet (UV) component of solar radiation impairs genome stability by inducing the formation of pyrimidine-pyrimidone (6-4) photoproducts [(6-4)PPs] in plant genomes. (6-4)PPs disrupt growth and development by interfering with transcription and DNA replication. To resist UV stress, plants employ both photoreactivation and nucleotide excision repair that excises oligonucleotide containing (6-4)PPs through two subpathways: global and transcription-coupled excision repair (TCR).
View Article and Find Full Text PDFIndian J Gastroenterol
October 2022
Background: Nonalcoholic steatohepatitis (NASH), a severe form of nonalcoholic fatty liver disease, can lead to advanced liver damage and has become an increasingly prominent health problem worldwide. Predictive models for early identification of high-risk individuals could help identify preventive and interventional measures. Traditional epidemiological models with limited predictive power are based on statistical analysis.
View Article and Find Full Text PDFPlants depend on light for energy production. However, the UV component in sunlight also inflicts DNA damage, mostly in the form of cyclobutane pyrimidine dimers (CPD) and (6-4) pyrimidine-pyrimidone photoproducts, which are mutagenic and lethal to the plant cells. These lesions are repaired by blue-light-dependent photolyases and the nucleotide excision repair enzymatic systems.
View Article and Find Full Text PDFThe circadian clock in plants temporally coordinates biological processes throughout the day, synchronizing gene expression with diurnal environmental changes. Circadian oscillator proteins are known to regulate the expression of clock-controlled plant genes by controlling their transcription. Here, using a high-throughput RNA-Seq approach, we examined genome-wide circadian and diurnal control of the transcriptome, finding that the oscillation patterns of different transcripts of multitranscript genes can exhibit substantial differences and demonstrating that the circadian clock affects posttranscriptional regulation.
View Article and Find Full Text PDFNucleotide excision repair is a versatile mechanism to repair a variety of bulky DNA adducts. We developed excision repair sequencing (XR-seq) to study nucleotide excision repair of DNA adducts in humans, mice, Arabidopsis thaliana, yeast and Escherichia coli. In this protocol, the excised oligomers, generated in the nucleotide excision repair reaction, are isolated by cell lysis and fractionation, followed by immunoprecipitation with damage- or repair factor-specific antibodies from the non-chromatin fraction.
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