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Histone marks such as H3K27ac, chromatin accessibility or transcription initiation facilitate the identification of active enhancers. Various high-throughput reporter assay with particular advantages and limitations allow genome-wide testing of enhancer activity, and, despite recent progress, most TREs remain largely uncharted. Despite their relevance, only a few cis-regulatory modules (CRMs) that constitute the essential transcriptional nodes of developmental gene regulatory networks are functionally understood. In contrast, the oftentimes complex expression of developmental regulatory genes (that is, transcription and signaling factors) is primarily controlled by distal regulatory elements. The expression of inducible genes in unicellular organisms is oftentimes driven by regulatory sequences proximal to the core promoter. Nevertheless, distinct sequences and chromatin features associate with the prevalence of enhancer and promoter activities among TREs. However, this exclusive functional distinction has been blurred by recent evidence that reveals local transcription initiation at enhancers and promoters that modulate the transcription of some other promoters. Traditionally, enhancers have been considered the modulators of distal transcription at core promoters (promoters thereafter), which integrate inputs from enhancers and ‘proximal promoters’ to initiate local transcription. Whereas promoters are TREs easily found by association with the transcription start sites (TSSs) of genes, the identification and functional characterization of TREs distal to TSSs (enhancers and silencers) remains challenging. ![]() Stage plot pro text on bottom drivers#Transcriptional regulatory elements (TREs) are the primary drivers of differential gene expression during metazoan development. This suggests that the sequence of regulatory mechanisms leading to transcriptional activation have distinct relevance at different levels of the developmental gene regulatory hierarchy deployed during embryogenesis. Furthermore, ATAC- and PRO-seq predictive value is stage dependent for the promoter-overlapping subset. ![]() For promoter-overlapping cis-regulatory elements in particular, the distribution of Pol II is the best predictor of enhancer activity in blastula embryos. ![]() Overall, chromatin accessibility and transcription have substantial power for predicting enhancer activity. Using the three functional genomic data types, machine learning models are trained and tested to classify and quantitatively predict the enhancer activity of several hundred genomic regions previously validated with reporter constructs in vivo. ATAC-seq, PRO-seq, and Pol II ChIP-seq from early and late blastula embryos are manually contrasted with experimental cis-regulatory analyses available in sea urchin embryos, with particular attention to common developmental regulatory elements known to have enhancer and silencer functions differentially deployed among embryonic territories. We evaluate the use of chromatin accessibility, transcription and RNA Polymerase II for their ability to predict enhancer activity of genomic regions in sea urchin embryos. The identification and functional characterization of distal regulatory elements remains challenging, even in tractable model organisms like sea urchins. The transcription of developmental regulatory genes is often controlled by multiple cis-regulatory elements. ![]() 11/6/2022 0 Comments How to treat poison ivy![]() Jordt says it's been difficult to attract study funding and to obtain tissue samples from poison ivy patients. Kim believes that T cells do cause the inflamed rash of poison ivy but that these other pathways provoke the itch: “In other words, what causes the itch is very different from what causes the rash.”īoth recently discovered mechanisms present new targets for treatment, but first scientists need to extend the work in humans. HOW TO TREAT POISON IVY SKINIn the past, dermatologists believed that urushiol rashes and itch were triggered by the immune system's T cells, which rally antibodies to attack the skin irritant. ![]() The mast-cell and IL-33 pathways are both “very new mechanisms,” Kim says. Also working with mice, Kim, along with scientists at Johns Hopkins University, has shown that immune system components called mast cells trigger itch neurons in the skin. Louis, has identified a second, nonhistamine pathway involved in poison ivy rashes. Because IL-33 is involved in asthma and eczema, at least two companies already are working on drugs to block it, but its role in poison ivy was a surprise.ĭermatologist Brian Kim, co-director of the Center for the Study of Itch & Sensory Disorders at Washington University in St. If either IL-33 or its receptor is blocked, the mice stop scratching-a finding that suggests a new route for treatment. Released by skin cells, it acts directly on sensory neurons in the skin. Working with urushiol-exposed mice, Jordt and his colleagues found that an immune chemical called interleukin 33 (IL-33) plays a key role in causing the infernal itch. (Cortisone pills do help if given early and in sufficient doses.) Why not? Animal studies indicate that the response to urushiol has nothing to do with histamines-bodily chemicals involved in many allergic reactions-so antihistamines are useless. HOW TO TREAT POISON IVY TORRENTIf you Google poison ivy, you will get a torrent of treatment advice such as to take antihistamines and apply cortisone cream. Among recent discoveries: surprising pathways that cause the itchy rash, new targets for treatment and-be still, my heart-a vaccine in development that aims to prevent the urushiol reaction. Jordt is one of a handful of scientists who take this nemesis seriously, and I am happy to report that they have made progress. And pharma companies see more profit in developing drugs for chronic skin condittions such as eczema than for an ephemeral rash. Contact dermatitis from poison ivy is usually treated by local doctors, not in big research centers, he says. “This condition is really underappreciated,” observes biochemist Sven-Eric Jordt, whose lab at Duke investigates pain and itch mechanisms. Given the toll in suffering and dollars, you would think serious attention would be paid to this worsening public health issue. HOW TO TREAT POISON IVY DRIVERA six-year study conducted at Duke University in the early 2000s found that elevated levels of carbon dioxide, a driver of climate change, induce the plant to produce a more allergenic form of urushiol, the oily resin responsible for the rash. To make matters worse, the climate crisis is turning poison ivy more toxic and expanding its range. Forest Service workers and lead one third of them in California, Oregon and Washington to miss work during fire seasons. According to some older studies, poison ivy and its cousins poison oak and poison sumac cause 10 percent of lost-time injuries among U.S. ![]() I wore gloves to weed and sow, but still I'd wind up with the devilishly itchy rash a few times a year, lasting three weeks at a stretch.Įvery year 10 million to 50 million Americans share my woes. ![]() I learned to avoid its red shoots of spring, waxy green triad of leaves in summer, crimson foliage of autumn, and hairy vines still lurking in winter. It was my own little Eden, complete, as it turned out, with a botanical snake in the garden: poison ivy. Eleven summers ago I moved into a small house surrounded by woods but with enough sunshine to indulge my gardening habit. ![]() |
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