Data for \u3c\u3c Shifting hotspots: Climate change projected to drive contractions and expansions of invasive plant abundance ranges\u3e\u3e

Invasive plant abundance data. Abundance data for 175 invasive plant species across the lower 48 United States. Each abundance record includes a UniqueID (numbers or characters that appeared to be a unique ID from the original dataset), the dataset from which the datapoint was derived from (see dataset_information.csv file for additional information on each dataset), decimal Longitude (Long), decimal Latitude (Lat), Species Code (SpCode, unique species identifier from USDA PLANTS database), cover (percentage cover), and CoverType (the type of abundance measurement in the cover column; either PercentCover, CoverClass, or AverageCoverClass).https://scholarworks.umass.edu/data/1168/thumbnail.jp

Shifting hotspots: Climate change projected to drive contractions and expansions of invasive plant abundance ranges

This file contains maps of current and future abundance suitable habitat for 144 invasive plant species in the United States. Each tiff file represents the current or future range prediction maps of habitat suitable for supporting abundant populations (greater than or equal to 5% cover) of 144 invasive plant taxa, projected across the lower 48 States of the United States. Each tiff file is named with the USDA species code (SpCode) (see \u271Species_information_Nov15.xlsx\u27 file for full species names), with species codes followed by .2c indicating maps related to future climatic conditions under a +2oC warming scenario. Areas predicted to be climatically suitable for supporting abundant populations is based on model agreement and range from 0 (no models identify that area as suitable) to 15 (all model outputs identify the area as suitable). Values of 300 represent areas that are masked due to climate dissimilarity. See main publication for model fitting details.https://scholarworks.umass.edu/data/1167/thumbnail.jp

The Cytokine TNF Promotes Transcription Factor SREBP Activity and Binding to Inflammatory Genes to Activate Macrophages and Limit Tissue Repair

Cytokine tumor necrosis factor (TNF)-mediated macrophage polarization is important for inflammatory disease pathogenesis, but the mechanisms regulating polarization are not clear. We performed transcriptomic and epigenomic analysis of the TNF response in primary human macrophages and revealed late-phase activation of SREBP2, the master regulator of cholesterol biosynthesis genes. TNF stimulation extended the genomic profile of SREBP2 occupancy to include binding to and activation of inflammatory and interferon response genes independently of its functions in sterol metabolism. Genetic ablation of SREBP function shifted the balance of macrophage polarization from an inflammatory to a reparative phenotype in peritonitis and skin wound healing models. Genetic ablation of SREBP activity in myeloid cells or topical pharmacological inhibition of SREBP improved skin wound healing under homeostatic and chronic inflammatory conditions. Our results identify a function and mechanism of action for SREBPs in augmenting TNF-induced macrophage activation and inflammation and open therapeutic avenues for promoting wound repair. ?? 2019 Elsevier Inc.TNF-mediated macrophage polarization is important for inflammatory disease pathogenesis, but the mechanisms regulating polarization are not clear. Kusnadi et al. find that TNF stimulation of macrophages results in late-phase activation of cholesterol regulator SREBP2. SREBP2 binds to inflammatory and interferon response target genes and promotes inflammation. Inhibition of SREBP activity promotes M2-like polarization and improves wound healing