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Fan Zhang

Publications and source records attributed to Fan Zhang.

2 recordsLinked to original sources
bioRxiv2020

DBSCAN-SWA: an integrated tool for rapid prophage detection and annotation

SummaryAs an intracellular form of a bacteriophage in the bacterial host genome, a prophage is usually integrated into bacterial DNA with high specificity and contributes to horizontal gene transfer (HGT). Phage therapy has been widely applied, for example, using phages to kill bacteria to treat pathogenic and resistant bacterial infections. Therefore, it is necessary to develop effective tools for the fast and accurate identification of prophages. Here, we introduce DBSCAN-SWA, a command line software tool developed to predict prophage regions of bacterial genomes. DBSCAN-SWA runs faster than any previous tool. Importantly, it has great detection power based on analysis using 184 manually curated prophages, with a recall of 85% compared with Phage_Finder (63%), VirSorter (74%) and PHASTER (82%) for raw DNA sequences. DBSCAN-SWA also provides user-friendly visualizations including a circular prophage viewer and interactive DataTables. Availability and implementationDBSCAN-SWA is implemented in Python3 and is freely available under an open source GPLv2 license from https://github.com/HIT-ImmunologyLab/DBSCAN-SWA/.

bioinformatics↗
bioRxiv2020

KLF4 Recruits SWI/SNF to Increase Chromatin Accessibility and Reprogram the Endothelial Enhancer Landscape under Laminar Shear Stress

Physiologic laminar shear stress (LSS) induces an endothelial gene expression profile that is vasculo-protective. In this report, we delineate how LSS mediates changes in the epigenetic landscape to promote this beneficial response. We show that under LSS, KLF4 interacts with the SWI/SNF nucleosome remodeling complex to increase accessibility at enhancer sites that promote expression of homeostatic endothelial genes. By combining molecular and computational approaches we discovered enhancers that loop to promoters of known and novel KLF4- and LSS-responsive genes that stabilize endothelial cells and suppress inflammation, such as BMPR2 and DUSP5. By linking enhancers to genes that they regulate under physiologic LSS, our work establishes a foundation for interpreting how non-coding DNA variants in these regions might disrupt protective gene expression to influence vascular disease.

molecular biology↗