Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1055115 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27351655_1.fastq.gz | Fastqsanger.gz | |||
| SRR27351655_2.fastq.gz | Fastqsanger.gz | |||
| SRR27351656_1.fastq.gz | Fastqsanger.gz | |||
| SRR27351656_2.fastq.gz | Fastqsanger.gz | |||
| SRR27351657_1.fastq.gz | Fastqsanger.gz |
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Project description:Snakes possess a unique sensory system for detecting infrared radiation, enabling them to generate a ‘thermal image’ of predators or prey. Infrared signals are initially received by the pit organ, a highly specialized facial structure that is innervated by nerve fibers of the somatosensory system. How this organ detects and transduces infrared signals into nerve impulses is not known. Here we use an unbiased transcriptional profiling approach to identify TRPA1 as the infrared receptor on sensory neurons that innervate the pit organ. TRPA1 from pit bearing snakes (rattlesnakes and pythons) are the most heat sensitive vertebrate ion channels thus far identified, consistent with their role as primary transducers of infrared stimuli in these animals. Thus, snakes detect infrared signals through a mechanism involving radiant heating of the pit organ, rather than photochemical transduction. These findings illustrate the broad evolutionary tuning of TRP channels as thermosensors in the vertebrate nervous system. Gene expression measurements implicate TRPA1 as the heat-sensitive channel in diverse pit snakes
2010-03-16 | E-GEOD-19911 | biostudies-arrayexpress
Project description:Snakes possess a unique sensory system for detecting infrared radiation, enabling them to generate a ‘thermal image’ of predators or prey. Infrared signals are initially received by the pit organ, a highly specialized facial structure that is innervated by nerve fibers of the somatosensory system. How this organ detects and transduces infrared signals into nerve impulses is not known. Here we use an unbiased transcriptional profiling approach to identify TRPA1 as the infrared receptor on sensory neurons that innervate the pit organ. TRPA1 from pit bearing snakes (rattlesnakes and pythons) are the most heat sensitive vertebrate ion channels thus far identified, consistent with their role as primary transducers of infrared stimuli in these animals. Thus, snakes detect infrared signals through a mechanism involving radiant heating of the pit organ, rather than photochemical transduction. These findings illustrate the broad evolutionary tuning of TRP channels as thermosensors in the vertebrate nervous system.
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Project description:Ion channels and transporters have increasingly recognized roles in cancer progression through the regulation of cell proliferation, migration, and death. Glioblastoma stem-like cells (GSCs) are a source of tumor formation and recurrence in glioblastoma multiforme, a highly aggressive brain cancer, suggesting that ion channel expression may be perturbed in this population. However, little is known about the expression and functional relevance of ion channels that may contribute to GSC malignancy. Using RNA sequencing, we assessed the enrichment of ion channels in GSC isolates and non-tumor neural cell types. We identified a unique set of GSC-enriched ion channels using differential expression analysis that stratify by molecular subtype and are associated with distinct gene mutation signatures. In support of potential clinical relevance, expression of selected GSC-enriched ion channels evaluated in human glioblastoma databases of The Cancer Genome Atlas and Ivy Glioblastoma Atlas Project correlated with patient survival times. Finally, genetic knockdown or pharmacological inhibition of individual or classes of GSC-enriched ion channels constrained growth of GSCs compared to normal neural stem cells. This first-in-kind global examination characterizes ion channels enriched in GSCs and explores their potential clinical relevance to glioblastoma molecular subtypes, gene mutations, survival outcomes, regional tumor expression, and experimental responses to loss-of-function. Together, the data support the potential biological and therapeutic impact of ion channels on GSC malignancy and provide strong rationale for further examination of their mechanistic and therapeutic importance.
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Project description:Cleft palate interferes with eating, drinking, breathing, and speech, causing significant human suffering. Fetal exposure to many medications that target ion channels increases the incidence of cleft palate. Cleft palate could be prevented by understanding how ion channels contribute to palatal development. Ion channels regulate the electrical properties of cells. We discovered that the mouse embryonic palate mesenchymal cells are electrically active, like neurons. In neurons, electrical activity regulates transcription cell-autonomously and regulates the secretion of chemical cues. We discovered that electrical activity regulates secretion of bone morphogenetic protein (BMP4) from mouse palate mesenchymal cells. The next important step is to determine how electrical activity affects transcription to control palate development. Loss of a potassium channel called Kcnj2 (Kcnj2KO/KO) alters electrical activity in palate mesenchyme cells and causes cleft palate in mice. We compared single cell RNA sequencing datasets from Kcnj2KO/KO and wildtype E13.5 mouse anterior palate shelves to define how electrical activity affects gene expression cell autonomously and in surrounding cells. Our data reveal that Kcnj2KO/KO alters a network of calcium-induced transcription factors and downstream effectors. These data also reveal that loss of Kcnj2 affects gene expression outside of the cells that express Kcnj2 consistent with disruption of BMP signaling.
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Project description:Pitx2 is the homeobox gene located in proximity to the human 4q25 familial atrial fibrillation locus. Pitx2 haploinsufficient mice are prone to pacing induced atrial fibrillation indicating that reduced Pitx2 promotes an arrhythmogenic substrate within the atrium. Here, we inactivated Pitx2 in postnatal heart and discovered that unstressed adult Pitx2 mutant mice had sinus node dysfunction with impaired atrial conduction, an arrhythmia closely associated with atrial fibrillation. A genome-wide search for Pitx2 transcriptional targets using ChIP-sequencing and RNA expression profiling shows that Pitx2 represses target genes encoding cell junction proteins, ion channels, and critical transcriptional regulators many of which have been implicated in human atrial fibrillation by genome wide association studies. Our findings unveil a Pitx2 postnatal arrhythmogenic function, novel Pitx2 target genes relevant to atrial fibrillation, and reveal that Pitx2 stabilizes the intercalated disc in postnatal atrium. Genomic occupancy profiling of transcriptional factor Pitx2 in postnatal heart.
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