16 research outputs found

    Growth Response from Herbicide, Prescribed Fire and Fertilizer Treatments in Midrotational Loblolly Pine: First-Year Results

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    This study was initiated to determine growth response resulting from the application of prescribed fire and herbicide, with and without fertilizatio.n. In. southeast Texas, herbicide, prescribed fire and fertilizer treatments were applied in m1d:rotat1onal loblolly pine plantations 1.5 years after thinning. Five replications were established at. each of two study sites located on similar soils, aspects and slopes. Half of each replication. was randomly selected and fertilized. Eight treatment plots were established 1n e~ch replication with one of each of the four treatments of control, herbicide, fire, and herb1c1de/flre randomly applied to fertilized plots and one of each of the four treatments randomly applied to non-fertilized plots. Pre-treatment measurements were taken in a 0.04 ha measurement plot nested within each treatment plot. A late season herbicide treatment of. lmazapyr and Arsenal was applied in October 1999. Burning was conducted in early spring of 2000 followed by fertilizer applications of diammonium phosphate and urea. ~osHreatment measurements were taken in December 2000. Growth response and s1gnif1cant treatment differences are presented in this paper

    An empirical Bayes model for gene expression and methylation profiles in antiestrogen resistant breast cancer

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    <p>Abstract</p> <p>Background</p> <p>The nuclear transcription factor estrogen receptor alpha (ER-alpha) is the target of several antiestrogen therapeutic agents for breast cancer. However, many ER-alpha positive patients do not respond to these treatments from the beginning, or stop responding after being treated for a period of time. Because of the association of gene transcription alteration and drug resistance and the emerging evidence on the role of DNA methylation on transcription regulation, understanding of these relationships can facilitate development of approaches to re-sensitize breast cancer cells to treatment by restoring DNA methylation patterns.</p> <p>Methods</p> <p>We constructed a hierarchical empirical Bayes model to investigate the simultaneous change of gene expression and promoter DNA methylation profiles among wild type (WT) and OHT/ICI resistant MCF7 breast cancer cell lines.</p> <p>Results</p> <p>We found that compared with the WT cell lines, almost all of the genes in OHT or ICI resistant cell lines either do not show methylation change or hypomethylated. Moreover, the correlations between gene expression and methylation are quite heterogeneous across genes, suggesting the involvement of other factors in regulating transcription. Analysis of our results in combination with H3K4me2 data on OHT resistant cell lines suggests a clear interplay between DNA methylation and H3K4me2 in the regulation of gene expression. For hypomethylated genes with alteration of gene expression, most (~80%) are up-regulated, consistent with current view on the relationship between promoter methylation and gene expression.</p> <p>Conclusions</p> <p>We developed an empirical Bayes model to study the association between DNA methylation in the promoter region and gene expression. Our approach generates both global (across all genes) and local (individual gene) views of the interplay. It provides important insight on future effort to develop therapeutic agent to re-sensitize breast cancer cells to treatment.</p

    Brf1 loss and not overexpression disrupts tissues homeostasis in the intestine, liver and pancreas

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    RNA polymerase III (Pol-III) transcribes tRNAs and other small RNAs essential for protein synthesis and cell growth. Pol-III is deregulated during carcinogenesis; however, its role in vivo has not been studied. To address this issue, we manipulated levels of Brf1, a Pol-III transcription factor that is essential for recruitment of Pol-III holoenzyme at tRNA genes in vivo. Knockout of Brf1 led to embryonic lethality at blastocyst stage. In contrast, heterozygous Brf1 mice were viable, fertile and of a normal size. Conditional deletion of Brf1 in gastrointestinal epithelial tissues, intestine, liver and pancreas, was incompatible with organ homeostasis. Deletion of Brf1 in adult intestine and liver induced apoptosis. However, Brf1 heterozygosity neither had gross effects in these epithelia nor did it modify tumorigenesis in the intestine or pancreas. Overexpression of BRF1 rescued the phenotypes of Brf1 deletion in intestine and liver but was unable to initiate tumorigenesis. Thus, Brf1 and Pol-III activity are absolutely essential for normal homeostasis during development and in adult epithelia. However, Brf1 overexpression or heterozygosity are unable to modify tumorigenesis, suggesting a permissive, but not driving role for Brf1 in the development of epithelial cancers of the pancreas and gut

    biocore/emp: Release for manuscript publication (doi:10.1038/nature24621)

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    Release of the EMP GitHub repository for archiving in Zenodo (DOI: 10.5281/zenodo.1009693) for publication of the manuscript on EMP 16S Release 1 in Nature. The title of that manuscript is "A communal catalogue reveals Earth's multiscale microbial diversity", and its DOI is 10.1038/nature24621
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