Pempheris klunzingeri
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ABSTRACT:
PROVIDER: PRJNA1090818 | ENA |
REPOSITORIES: ENA
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Project description:Pempheris klunzingeri (Rough Bullseye) genome, fPemKlu1, haplotype 2
| PRJNA1090819 | ENA
Project description:We investigated effects of the t haplotype in house mice, an autosomal male meiotic driver, on genome-wide gene expression patterns in males and females. We analysed gonads, liver and brain in adult sibling pairs differing in genotype, allowing us to identify t-associated differences in gene regulation. In testis, only 40% of differentially expressed genes mapped to the approximately 708 annotated genes comprising the t haplotype. Thus much of the activity of the t haplotype occurs in trans, and as up-regulation. Sperm maturation functions were enriched among both cis and trans acting t haplotype genes. Within the t haplotype, more down-regulation and differential exon usage was observed. In ovaries, liver, and brain, the majority of expression differences mapped to the t haplotype, and were largely independent of the differences seen in the testis. Overall, we found widespread transcriptional effects of this male meiotic driver in the house mouse genome.
2019-10-28 | GSE138839 | GEO
Project description:Aim of this project is to characterize colony morphology in the M28 strain, identifying the peculiar genomic traits determining the rough phenotype
2016-04-30 | E-SYBR-10 | biostudies-arrayexpress
Project description:The 9p21.3 cardiovascular disease locus is the most influential common genetic risk factor for coronary artery disease, accounting for ~10-15% of disease among non-African populations. The ~60kb risk haplotype is human-specific and lacks coding genes, hindering efforts to decipher its function. Genetic studies implicate the 9p21.3 locus and other risk genes to effects in the vascular wall. Here, we use genome editing to delete the entire risk on non-risk haplotype from the genomes of human iPSCs and perform genomewide transcriptional profiling along the timecourse of their differentiation into vascular smooth muscle cells (VSMCs). These studies identify a network of ~3000 genes governed by the risk haplotype in VSMCs that predict deficits in cell division, adhesion and contraction, which we confirmufunctionally. Remarkably, deleting the risk haplotype reverts VSMCs to resemble the non-risk VSMCs, suggesting that the risk region drives a cell state transition. transcriptionally and functionally. . Deleting the risk haplotype reverts these cells to reverted to the non-risk of iPSCs we show that the non-risk haplotype has little effect on locus we produce iPSCs from risk and non-risk individuals, delete each haplotype using genome editing and generate vascular smooth muscle cells (VSMCs). We show that risk VSMCs exhibit aberrant adhesion and contraction, concomitant with dramatically altered global transcriptional changes that are enriched in previously identified cardiovascular disease genes and pathways. Unexpectedly, deleting the risk haplotype rescues VSMC transcriptional identity and function, while expressing the 9p21.3-associated long non-coding RNA ANRIL induces risk phenotypes in non-risk VSMCs. This studies shows that the risk haplotype dominantly predisposes VSMCs to adopt perturbed phenotypes associated with cardiovascular disease and establishes haplotype-edited iPSCs as powerful tools for functionally annotating human-specific variation in non-coding genomic regions.
2018-12-05 | GSE120099 | GEO
Project description:Purpose: to determine the differentially expressed genes in the phase-variable rough and smooth colony isolates of C. difficile Methods: C. difficile R20291 was grown on BHIS agar to obtain distinct colonies. Individual rough and smooth colonies were chosen for propagation on BHIS-agar for 24 hours as described in Garrett, et al., PLoS Biology, 2019. Growth was collected from n = 2 biological replicates. RNA was purified using TriSure and chloroform, beadbeating, and isopropanol/ethanol precipitation. Quality was verified with Bioanalyzer Assay. Samples were submitted to Genewiz for depletion of rRNA using the TruSeq RiboZero Gold Kit, library preparation, and single-end sequencing on the Illumina HiSeq 2500 platform. RNA sequencing analysis was done using CLC Genomic Workbench v20. Reads were mapped to C. difficile R20291 genome using the software's default menalties for mismatch, deletion, and insertion differences from the reference genome. Transcript reads were normalized as RPKM. Results: 88 genes were differentially expressed between bacteria from rough versus smooth colonies, with equal to or greater than a 2-fold change and p < 0.05 with FDR correction.
2020-09-27 | GSE158225 | GEO