Project description:Resistance to synthetic auxin herbicides was recently confirmed in a population of Amaranthus powellii. Following field studies, an RNA-seq experiment was devised to determine the mechanism of resistance to MCPA (a synthetic auxin herbicide) by comparing the level of gene expression of genes in the auxin pathway between the resistant and a susceptible population of Amaranthus powellii. The results identified several differentially expressed genes (DEGs) in the auxin pathway that were significantly downregulated in the resistant samples indicating that the resistance mechanism may be linked to a target site modification.
Project description:Assay for Transposase Accessible Chromatin by sequencing (ATAC-seq) provides an accurate way to depict the chromatin regulatory state and altered mechanisms guiding gene expression in disease. However bulk sequencing entangles information from different cell types and obscures cellular heterogeneity. Here, we develop and validate Cellformer, a novel deep learning method, that deconvolutes bulk ATAC-seq into cell type-specific expression across the whole genome. Cellformer enhances the bulk ATAC-seq resolution and allows an efficient cell type specific open chromatin profiling on large size cohorts at a low cost. Applied to 191 bulk samples from 3 brain regions, Cellformer identifies cell type-specific gene regulatory mechanisms and putative mediators involved in resilient to Alzheimer’s disease (RAD), an uncommon group of cognitively healthy individuals that harbor a high pathological load of Alzheimer’s disease (AD). Cell type-resolved chromatin profiling unveils cell type specific pathways and nominates potential epigenetic mediators underlying RAD that may illuminate therapeutic opportunities to limit the cognitive impact of this highly prevalent yet incurable disease. Cellformer has been made freely and publicly available to advance analysis of high-throughput bulk ATAC-seq in future investigations.
Project description:One of the most recognizable physiological phenomena is the adrenergic-induced fight-or-flight increase in heart rate and cardiac contraction. For the β-adenergic agonist-induced enhancement of calcium influx and transients, and contractility in the heart, we identify the dual requirement of a subpopulation of Rad-bound calcium channels under basal conditions and PKA phosphorylation of Rad. In mice expressing a non-phosphorylatable Rad mutant, basal cardiac contractility is reduced and adrenergic-augmentation of the calcium current and contractility are disabled. Expression of mutant calcium channel β-subunits that cannot bind the mutant Rad restored contractility, revealing a highly specific therapeutic approach to mimic the contractility imparted by adrenergic agonists. Our findings place Rad and its modulation of calcium channels at the nexus of adrenergic modulation of cardiac responses.
Project description:Transcriptional profiling of Arabidopsis rossette leaves comparing WT Col-0 with a transgenic line overexpressing Ah24 gene from Amaranthus hypochondriacus.
Project description:Transcriptional profiling of Arabidopsis rossette leaves comparing WT Col-0 with a transgenic line overexpressing AhDGR gene from Amaranthus hypochondriacus.
Project description:Transcriptional profiling of Arabidopsis rossette leaves comparing WT Col-0 with a transgenic lines overexpressing AhNF-YC gene from Amaranthus hypochondriacus in three different conditions.
Project description:Transcriptional profiling of Arabidopsis rossette leaves comparing WT Col-0 with a transgenic line overexpressing AhERF or AhDOF genes from Amaranthus hypochondriacus under different conditions.