Pre-harvest aflatoxin contamination (PAC) in groundnut is a serious quality concern globally, and drought stress before harvest further exacerbate its intensity, leading to the deterioration of produce quality. Understanding the host–pathogen interaction and identifying the candidate genes responsible for resistance to PAC will provide insights into the defense mechanism of the groundnut. In this context, about 971.63 million reads have been generated from 16 RNA samples under controlled and Aspergillus flavus infected conditions, from one susceptible and seven resistant genotypes. The RNA-seq analysis identified 45,336 genome-wide transcripts under control and infected conditions. This study identified 57 transcription factor (TF) families with major contributions from 6570 genes coding for bHLH (719), MYB-related (479), NAC (437), FAR1 family protein (320), and a few other families. In the host (groundnut), defense-related genes such as senescence-associated proteins, resveratrol synthase, seed linoleate, pathogenesis-related proteins, peroxidases, glutathione-S-transferases, chalcone synthase, ABA-responsive gene, and chitinases were found to be differentially expressed among resistant genotypes as compared to susceptible genotypes. This study also indicated the vital role of ABA-responsive ABR17, which co-regulates the genes of ABA responsive elements during drought stress, while providing resistance against A. flavus infection. It belongs to the PR-10 class and is also present in several plant–pathogen interactions.
The present study reports profiling of the elevated CO2 concentration responsive global transcriptome in chickpea along with a combinatorial approach for exploring interlinks of physiological and transcriptional changes, important for the climate change scenario. Various physiological parameters were recorded from chickpea cultivars (JG 11 and KAK 2) raised in OTC (Open-Top-Chamber) under ambient (380 ppm) and two stressed/elevated CO2 concentrations (550 ppm and 700 ppm) under different stages of plant growth. The elevated CO2 concentrations altered shoot and root length, nodulation (number of nodules), total chlorophyll content and NBI (Nitrogen Balance Index) significantly. RNA-Seq from 12 tissues representing vegetative and reproductive growth stages of both cultivars under ambient and elevated CO2 concentrations identified 18,644 differentially expressed genes (DEGs) including 9,687 transcription factors (TF). The differential regulations in genes, gene networks, and quantitative real time PCR (qRT-PCR) derived expression dynamics of stress responsive TFs were observed in both cultivars studied. A total of 138 pathways, mainly involved in sugar/starch metabolism, chlorophyll and secondary metabolites biosynthesis, deciphered the crosstalk operating behind the responses of chickpea to elevated CO2 concentration.
Background: Gene environment interactions leading to epigenetic alterations play pivotal role in the pathogenesis of Coronary Artery Disease (CAD). Altered DNA methylation is one such epigenetic factor that could lead to altered disease etiology. In this study, we comprehensively identified methylation sites in several genes that have been previously associated with young CAD patients.
Methods:The study population consisted of 42 healthy controls and 33 young CAD patients (age group < 50 years). We performed targeted bisulfite sequencing of promoter as well as genic regions of several genes in various pathways like cholesterol synthesis and metabolism, endothelial dysfunction, apoptosis, which are implicated in the development of CAD.
Results:We observed that the genes like GALNT2, HMGCR were hypermethylated in the promoter whereas LDLR gene promoter was hypomethylated indicating that intracellular LDL uptake was higher in CAD patients. Although APOA1 did not show significant change in methylation but APOC3 and APOA5 showed variation in methylation in promoter and exonic regions. Glucokinase (GCK) and endothelial nitric oxide synthase 3 (NOS3) were hyper methylated in the promoter. Genes involved in apoptosis (BAX/BCL2/AKT2) and inflammation (PHACTR1/LCK) also showed differential methylation between controls and CAD patients.
Conclusions:This study is unique because it highlights important gene methylation alterations which might predict the risk of young CAD in Indian population. Large scale studies in different populations would be important for validating our findings and understanding the epigenetic events associated with CAD.
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