Search bioRxivSearch

Biology subjects

Kelley, D.

Publications and source records attributed to Kelley, D..

2 recordsLinked to original sources

Quantitative proteomic analysis of auxin signaling during seedling development

Auxin induces rapid gene expression changes throughout plant development. How these transcriptional responses relate to changes in protein abundance is not well characterized. We have identified auxin regulated proteins in whole seedlings, roots and hypocotyls and at three different time points (30 min, 120 min and 3 hours) using an iTRAQ (isobaric tags for relative and absolute quantification) based quantitative proteomics approach. These profiling experiments detected 4,701 proteins from seedling tissue, 6,740 proteins from root tissue and 3,925 proteins from hypocotyl tissue. Comparisons between the differentially expressed proteins data sets showed little overlap, suggesting that auxin proteomes exhibit both temporal and spatial specificity. Numerous proteins showed significant changes in abundance following auxin treatment independent of changes in cognate transcript abundance. This includes several well characterized proteins with various roles in auxin pathways, suggesting that complex gene regulation mechanisms follow auxin signaling events. Specifically, regulation of translation may play a role as inferred from MapMan categorization analyses and protein interaction networks comprised of auxin regulated proteins. Additionally, functional categorization of auxin regulated proteins indicates rapid and complex metabolic changes occur in both roots and hypocotyls in response to auxin which are not apparent from transcriptome analyses. Altogether these data describe novel auxin-regulated proteomes and are an excellent resource for identifying new downstream signaling components related to auxin-mediated plant growth and development.

plant biology

Epigenetic Regulation of Gene Expression in Cancer: Techniques, Resources, and Analysis

Cancer is a complex disease, driven by aberrant activity in numerous signaling pathways in even individual malignant cells. Epigenetic changes are critical mediators of these functional changes that drive and maintain the malignant phenotype. Changes in DNA methylation, histone acetylation and methylation, non-coding RNAs, post-translational modifications are all epigenetic drivers in cancer, independent of changes in the DNA sequence. These epigenetic alterations, once thought to be crucial only for the malignant phenotype maintenance, are now recognized as critical also for disrupting essential pathways that protect the cells from uncontrolled growth, longer survival and establishment in distant sites from the original tissue. In this review, we focus on DNA methylation and chromatin structure in cancer. While associated with cancer, the precise functional role of these alterations is an area of active research using emerging high-throughput approaches and bioinformatics analysis tools. Therefore, this review describes these high-throughput measurement technologies, public domain databases for high-throughput epigenetic data in tumors and model systems, and bioinformatics algorithms for their analysis. Advances in bioinformatics data integration techniques that combine these epigenetic data with genomics data are essential to infer the function of specific epigenetic alterations in cancer, and are therefore also a focus of this review. Future studies using these emerging technologies will elucidate how alterations in the cancer epigenome cooperate with genetic aberrations to cause tumorigenesis initiation and progression. This deeper understanding is essential to future studies that will precisely infer patients prognosis and select patients who will be responsive to emerging epigenetic therapies.

cancer biology