Weed Control for Reduced Tillage Systems

PDF pages:

Mapping Inherited Fractures in the Critical Zone Using Seismic Anisotropy From Circular Surveys

International audienc

Genomic Breakpoint Characterization and Transcriptome Analysis of Metastatic, Recurrent Desmoplastic Small Round Cell Tumor

Desmoplastic small round cell tumor (DSRCT) is a rare pediatric cancer caused by the EWSR1-WT1 fusion oncogene. Despite initial response to chemotherapy, DSRCT has a recurrence rate of over 80% leading to poor patient prognosis with a 5-year survival rate of only 15–25%. Owing to the rarity of DSRCT, sample scarcity is a barrier in understanding DSRCT biology and developing effective therapies. Utilizing a novel pair of primary and recurrent DSRCTs, we present the first map of DSRCT genomic breakpoints and the first comparison of gene expression alterations between primary and recurrent DSRCT. Our genomic breakpoint map includes the lone previously published DSRCT genomic breakpoint, the breakpoint from our novel primary/recurrent DSRCT pair, as well as the breakpoints of five available DSRCT cell lines and five additional DSRCTs. All mapped breakpoints were unique and most breakpoints included a 1–3 base pair microhomology suggesting microhomology-mediated end-joining as the mechanism of translocation fusion and providing novel insights into the etiology of DSRCT. Through RNA-sequencing analysis, we identified altered genes and pathways between primary and recurrent DSRCTs. Upregulated pathways in the recurrent tumor included several DNA repair and mRNA splicing-related pathways, while downregulated pathways included immune system function and focal adhesion. We further found higher expression of the EWSR1-WT1 upregulated gene set in the recurrent tumor as compared to the primary tumor and lower expression of the EWSR1-WT1 downregulated gene set, suggesting the EWSR1-WT1 fusion continues to play a prominent role in recurrent tumors. The identified pathways including upregulation of DNA repair and downregulation of immune system function may help explain DSRCT’s high rate of recurrence and can be utilized to improve the understanding of DSRCT biology and identify novel therapies to both help prevent recurrence and treat recurrent tumors

Forest vulnerability to drought controlled by bedrock composition

International audienceForests are increasingly threatened by climate-change-fuelled cycles of drought, dieback and wildfires. However, for reasons that remain incompletely understood, some forest stands are more vulnerable than others, leaving a patchwork of varying dieback and wildfire risk after drought. Here, we show that spatial variability in forest drought response can be explained by differences in underlying bedrock. Our analysis links geochemical measurements of bedrock composition, geophysical measurements of subsurface weathering and remotely sensed changes in evapotranspiration during the 2011-2017 drought in California. We find that evapotranspiration plummeted in dense forest stands rooted in weathered, nutrient-rich bedrock. By contrast, relatively unweathered, nutrient-poor bedrock supported thin forest stands that emerged unscathed from the drought. By influencing both subsurface weathering and nutrient supply, bedrock composition regulates the balance of water storage and demand in mountain ecosystems. However, rather than enhancing forest resilience to drought by providing more water-storage capacity, bedrock with more weatherable and nutrient-rich minerals induced greater vulnerability by enabling a boom-bust cycle in which higher ecosystem productivity during wet years drives excess plant water demand during droughts