The dominant and poor penetrant phenotypes of the maize mutation Unstable factor for orange1 are caused by DNA methylation changes at a linked transposon
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PROVIDER: PRJNA483200 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional analysis of the Ufo1-1 mutant allele and wild type plants were used to identify the candidate gene using a k-mer based approach. The transcriptome data also revealed the altered expression of carbohydrate metabolic genes, which translates into elevated levels of soluble sugars in leaves and light-induced lesions found in mature Ufo1-1 leaves.
2019-01-16 | GSE117782 | GEO
Project description:The rupture of unstable atherosclerotic plaques, leading to debilitating or fatal thrombotic events, is a major health burden worldwide. Limited understanding as to the molecular drivers of plaque instability and rupture hinders efforts in diagnosis and treatment prior to thrombotic events. Utilising an advanced pre-clinical mouse model (Tandem stenosis (TS) model), which presents human-like unstable atherosclerotic disease, we apply high-end omic methods to characterize the molecular signatures associated with plaque instability in atherosclerotic arteries. Through quantitative proteomic profiling, we depict unique proteome signatures of unstable plaques compared to stable plaques and healthy arteries. Coupled with single-cell RNA-sequencing of leukocytes, we describe the heterodimer complex S100a8/S100a9 as unique to unstable plaque, with neutrophils implicated as the transcriptional drivers of S100a8/a9 expression. We confirm S100a9 expression in human carotid atherosclerotic plaques and we further utilise the TS pre-clinical model to pharmacologically inhibit S100a8/S100a9, resulting in plaque stabilisation. Thus, we establish the TS model as a sophisticated translational tool for the profiling of unstable atherosclerotic plaques and demonstrate that unstable and stable atherosclerosis are highly different disease entities.
2023-05-10 | PXD030857 | Pride
Project description:Transcriptional profiling of stable and unstable atherosclerotic plaque segments from human carotid endatrerectomies Objective Comparison of gene expression in stable versus unstable atherosclerotic plaque may be confounded by interpatient variability. The aim of this study was to identify differences in gene expression between stable and unstable segments of plaque obtained from the same patient. Human carotid endarterectomy specimens were segmented and macroscopically classified using a morphological classification system. Two analytical methods, an intraplaque and an interplaque analysis, revealed 170 and 1916 differentially expressed genes, respectively using Affymetrix gene chip analysis. A total of 115 genes were identified from both analyses. The differential expression of 27 genes was also confirmed using quantitative-polymerase chain reaction on a larger panel of samples. Eighteen of these genes have not been associated previously with plaque instability, including the metalloproteinase, ADAMDEC1 (37-fold), retinoic acid receptor responder-1 (5-fold), and cysteine protease legumain (3-fold). Matrix metalloproteinase-9 (MMP-9), cathepsin B, and a novel gene, legumain, a potential activator of MMPs and cathepsins, were also confirmed at the protein level. The differential expression of 18 genes not previously associated with plaque rupture has been confirmed in stable and unstable regions of the same atherosclerotic plaque. These genes may represent novel targets for the treatment of unstable plaque or useful diagnostic markers of plaque instability. Differential gene expression in stable and unstable plaque was assessed by whole transcriptome analysis. Intraplaque analysis by QT-PCR confirmed the differential expression of 18 genes not associated previously with plaque rupture. These genes may represent novel targets for the treatment of unstable plaque or useful diagnostic markers of plaque instability
2006-01-30 | E-TABM-190 | biostudies-arrayexpress
Project description:Macrophage recruitment into tumors is correlated with poor outcomes in cancer, which correlate with STAT6-dependent M2 macrophage polarization and wound healing-type responses. Using penetrant, genetic models of neuroblastoma, we found macrophage recruitment was protective against tumor formation while disabling STAT6-mediated M2 polarization had no effect on tumorigenesis, progression or expression of key immunosuppressive pathways. Thus while macrophages are drivers of cancer in this model, non-classical M2 STAT6-independent pathways are plausible targets for cancer therapy.
2018-05-01 | GSE98763 | GEO
Project description:We sequenced both the stable (WT) and unstable (rrp6delta) transcriptomes of three S.cerevisiae strains: S288c, Σ1278b, JAY291 and the S.paradoxus strain N17 for de novo annotation of cryptic unstable transcripts (CUTs). Doing so we have greatly expanded on previous CUTs which were limited to the S.cerevisiae strain S288c and have provided the first assessment of CUT expression conservation in yeast
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Project description:In all primary cells analyzed to date, aneuploidy is associated with poor proliferation. Yet, how abnormal karyotypes affect cancer – a disease characterized by both aneuploidy and heightened proliferative capacity – is largely unknown. Here, I demonstrate that the transcriptional alterations caused by aneuploidy in primary cells are also present in chromosomally-unstable cancer cell lines, but are not common to all aneuploid cancers. Moreover, chromosomally-unstable cancer lines display increased glycolytic and TCA-cycle flux, as is also observed in primary aneuploid cells. The biological response to aneuploidy is associated with cellular stress and slow proliferation, and a 70-gene signature derived from primary aneuploid cells is a strong predictor of increased survival in several cancers. Inversely, a transcriptional signature derived from clonal aneuploidy in tumors correlates with high mitotic activity and poor prognosis. I speculate that there are two types of aneuploidy in cancer: clonal aneuploidy, which is selected during tumor evolution and is associated with robust growth, and sub-clonal aneuploidy, which is caused by chromosomal instability (CIN) and more closely resembles the stressed state of primary aneuploid cells. Nonetheless, CIN is not benign: a subset of genes upregulated in high-CIN cancers predict aggressive disease in human patients in a proliferation-independent manner. The mRNAs from 3 different mouse embryo fibroblast (MEF) lines that are chromosomally stable were compared with mRNAs from 3 different MEF lines that were chromosomally unstable due to mutations in either BUBR1 or CDC20
2013-10-01 | E-GEOD-49894 | biostudies-arrayexpress
Project description:An irradiated but chromosomally stable CHO clone RT210B was used a reference to find differences in gene expression compared to radiation-induced chromosomally unstable isogenic clones. Equal quantities of two unstable different unstable clones were mixed prior to RNA extraction. Each mixture was tested twice versus the stable reference clone. Two different two clone mixtures were tested against the same chromosomally stable clone Keywords: repeat sample
2004-08-01 | GSE1626 | GEO
Project description:Survey of cryptic unstable transcripts in yeast
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Project description:20 patients with unstable angina were divided into patient group by using coronary angiography. The sex- and age-matched healthy individuals were enrolled as control group. Venous bloods were collected for extracting RNA. We used the Human Genome U133 plus 2.0 genechip produced by Affymetrix to detail the global gene expression in blood sample from normal human and unstable angina patient. 1 control and 2 test samples.
2011-12-31 | E-GEOD-34781 | biostudies-arrayexpress
Project description:Atherosclerosis is a serious and very common condition where plaque builds up inside arteries and that can lead to heart attack or stroke. The development and rupture of the plaque is a complex process, involving the interplay of many cell types and the extracellular environment. We performed RNAseq on stable and unstable regions dissected from fresh human carotid plaques obtained at carotid endarterectomy in symptomatic patients. The dissection of the plaques into stable and unstable regions was based on macroscopic appearance, with unstable regions characterised as the visible zone of plaque rupture.
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