68 research outputs found

    Abundance of Young Brown Shrimp in Natural and Semi-Impounded Marsh Nursery Areas: Relation to Temperature and Salinity

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    Samples of brown shrimp (Penaeus aztecus, 10 to 130 mm in total length) were collected with otter trawls weekly from 14 March to 20 August 1971 in brackish marsh areas at Marsh Island, Louisiana. Catches were largest from 1 May to 4 June in the natural marsh and from 1 May to 4 July in the semi-impounded marsh (influenced by weirs). Total catch was four times greater in the natural than in the semi-impounded marsh. However, brown shrimp apparently stayed longer in the semi-impounded areas, and emigrated at a larger size. Water temperatures above 20°C were apparently more conducive to the growth of young brown shrimp than was a particular salinity range. The range of recorded salinities was 0.57-12.85 ‰; catch per sample was highest in salinities from 2.0 to 2.99 ‰

    Joint single-cell DNA accessibility and protein epitope profiling reveals environmental regulation of epigenomic heterogeneity.

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    Here we introduce Protein-indexed Assay of Transposase Accessible Chromatin with sequencing (Pi-ATAC) that combines single-cell chromatin and proteomic profiling. In conjunction with DNA transposition, the levels of multiple cell surface or intracellular protein epitopes are recorded by index flow cytometry and positions in arrayed microwells, and then subject to molecular barcoding for subsequent pooled analysis. Pi-ATAC simultaneously identifies the epigenomic and proteomic heterogeneity in individual cells. Pi-ATAC reveals a casual link between transcription factor abundance and DNA motif access, and deconvolute cell types and states in the tumor microenvironment in vivo. We identify a dominant role for hypoxia, marked by HIF1α protein, in the tumor microvenvironment for shaping the regulome in a subset of epithelial tumor cells

    Abundance of Young Brown Shrimp in Natural and Semi-Impounded Marsh Nursery Areas: Relation to Temperature and Salinity

    No full text
    Samples of brown shrimp (Penaeus aztecus, 10 to 130 mm in total length) were collected with otter trawls weekly from 14 March to 20 August 1971 in brackish marsh areas at Marsh Island, Louisiana. Catches were largest from 1 May to 4 June in the natural marsh and from 1 May to 4 July in the semi-impounded marsh (influenced by weirs). Total catch was four times greater in the natural than in the semi-impounded marsh. However, brown shrimp apparently stayed longer in the semi-impounded areas, and emigrated at a larger size. Water temperatures above 20°C were apparently more conducive to the growth of young brown shrimp than was a particular salinity range. The range of recorded salinities was 0.57-12.85 ‰; catch per sample was highest in salinities from 2.0 to 2.99 ‰

    Suppression of PGC-1α Is Critical for Reprogramming Oxidative Metabolism in Renal Cell Carcinoma

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    Long believed to be a byproduct of malignant transformation, reprogramming of cellular metabolism is now recognized as a driving force in tumorigenesis. In clear cell renal cell carcinoma (ccRCC), frequent activation of HIF signaling induces a metabolic switch that promotes tumorigenesis. Here, we demonstrate that PGC-1α, a central regulator of energy metabolism, is suppressed in VHL-deficient ccRCC by a HIF/Dec1-dependent mechanism. In VHL wild-type cells, PGC-1α suppression leads to decreased expression of the mitochondrial transcription factor Tfam and impaired mitochondrial respiration. Conversely, PGC-1α expression in VHL-deficient cells restores mitochondrial function and induces oxidative stress. ccRCC cells expressing PGC-1α exhibit impaired tumor growth and enhanced sensitivity to cytotoxic therapies. In patients, low levels of PGC-1α expression are associated with poor outcome. These studies demonstrate that suppression of PGC-1α recapitulates key metabolic phenotypes of ccRCC and highlight the potential of targeting PGC-1α expression as a therapeutic modality for the treatment of ccRCC

    Analysis of p53 Transactivation Domain Mutants Reveals Acad11 as a Metabolic Target Important for p53 Pro-Survival Function

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    The p53 tumor suppressor plays a key role in maintaining cellular integrity. In response to diverse stress signals, p53 can trigger apoptosis to eliminate damaged cells or cell-cycle arrest to enable cells to cope with stress and survive. However, the transcriptional networks underlying p53 pro-survival function are incompletely understood. Here, we show that in oncogenic-Ras-expressing cells, p53 promotes oxidative phosphorylation (OXPHOS) and cell survival upon glucose starvation. Analysis of p53 transcriptional activation domain mutants reveals that these responses depend on p53 transactivation function. Using gene expression profiling and ChIP-seq analysis, we identify several p53-inducible fatty acid metabolism-related genes. One such gene, Acad11, encoding a protein involved in fatty acid oxidation, is required for efficient OXPHOS and cell survival upon glucose starvation. This study provides new mechanistic insight into the pro-survival function of p53 and suggests that targeting this pathway may provide a strategy for therapeutic intervention based on metabolic perturbation

    The HIF target MAFF promotes tumor invasion and metastasis through IL11 and STAT3 signaling

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    Hypoxia plays a critical role in tumor progression including invasion and metastasis. To determine critical genes regulated by hypoxia that promote invasion and metastasis, we screen fifty hypoxia inducible genes for their effects on invasion. In this study, we identify v-maf musculoaponeurotic fibrosarcoma oncogene homolog F (MAFF) as a potent regulator of tumor invasion without affecting cell viability. MAFF expression is elevated in metastatic breast cancer patients and is specifically correlated with hypoxic tumors. Combined ChIP- and RNA-sequencing identifies IL11 as a direct transcriptional target of the heterodimer between MAFF and BACH1, which leads to activation of STAT3 signaling. Inhibition of IL11 results in similar levels of metastatic suppression as inhibition of MAFF. This study demonstrates the oncogenic role of MAFF as an activator of the IL11/STAT3 pathways in breast cancer
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