MicroRNA signature of murine CD4+ T cell subpopulations under different skewing conditions
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ABSTRACT:
PROVIDER: PRJNA432537 | ENA |
REPOSITORIES: ENA
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Project description:Background: Skewing root patterns provide key insights into root growth strategies and mechanism that produce root architectures Roots exhibit skewing and waving when grown on a tilted, impenetrable surface, and while the genetics guiding these morphologies have been examined, the underlying molecular mechanisms of skewing and waving remain unclear. In this study, transcriptome data were derived from two Arabidopsis ecotypes, WS and Col-0, under three tilted growth conditions in order to identify candidate genes involved in skewing. WS is a skewing ecotype. Col-0 is a non-skewing ecotype. Results: This work identifies a number of genes that are likely involved in skewing, using growth conditions that differentially affect skewing and waving. Comparing the gene expression profiles of WS and Col-0 in different tilted growth conditions identified 11 candidate genes as potentially involved in the control of skewing. These 11 genes are involved in several different cellular processes, including sugar transport, salt signaling, cell wall organization, and hormone signaling. Conclusions: Many of the 11 identified genes are involved in signaling and perception, rather than the physical restructuring of roots, leading to the conclusion that root skewing is enabled through diverse environmental signaling pathways. These findings revealed further insights into the molecular mechanisms behind root skewing. This work investigated the transcriptional differences between skewing and non-skewing roots. Comparisons within WS revealed gees that that responded to the angle of growth (Agp) during the process of skewing. These genes were cross referenced with transcripts differing between the WS and Col-0 genotypes to refine the list of genes that are most probably be involved in root skewing. More of the highly probable skew gene candidates (HPSGC) are associated with environmental sensing (e.g. salt, sugar, hormones, darkness) than with physical growth differences (e.g. cell wall remodeling, cell division, cell elongation). Thus, the root behavior of skewing appears to be primarily driven by pathways that respond to disparate signals from the root local environment. Future studies could investigate the HPSGC to find the specific pathways and molecular mechanisms contributing to root skewing.
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Project description:Although several recent publications have suggested that microRNAs contribute to the pathogenesis of diabetic nephropathy, the role of miRNAs in vivo still remains poorly understood. Using an integrated in vitro and in vivo comparative miRNA expression array, we identified miR-29c as a signature miRNA in the diabetic environment. We validated our profiling array data by examining miR-29c expression in the kidney glomeruli obtained from db/db mice in vivo and in kidney microvascular endothelial cells and podocytes treated with high glucose in vitro. Functionally, we found that miR-29c induces cell apoptosis and increases extracellular matrix protein accumulation. Indeed, forced expression of miR-29c strongly induced podocyte apoptosis. Conversely, knockdown of miR-29c prevented high glucose-induced cell apoptosis. We also identified Sprouty homolog 1 (Spry1) as a direct target of miR-29c with a nearly perfect complementarity between miR-29c and the 3'-untranslated region (UTR) of mouse Spry1. Expression of miR-29c decreased the luciferase activity of Spry1 when co-transfected with the mouse Spry1 3'-UTR reporter construct. Overexpression of miR-29c decreased the levels of Spry1 protein and promoted activation of Rho kinase. Importantly, knockdown of miR-29c by a specific antisense oligonucleotide significantly reduced albuminuria and kidney mesangial matrix accumulation in the db/db mice model in vivo. These findings identify miR-29c as a novel target in diabetic nephropathy and provide new insights into the role of miR-29c in a previously unrecognized signaling cascade involving Spry1 and Rho kinase activation.
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