Ida-2
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB62448 | ENA |
REPOSITORIES: ENA
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Project description:Background Gastric Helicobacter pylori colonization leads to iron deficiency anemia (IDA), especially in children and adolescents. However the pathogenesis is poorly understood. Objective We sought to identify specific H. pylori genes involved in IDA development, by comparing bacterial genome-wide expression profiling in patients affected or not. Methods H. pylori were isolated from four children with IDA and four from matched controls without IDA. Based on these isolates, cDNA microarrays under iron-replete or depleted conditions were systematically performed to compare gene expression profiles at the whole genome level. Real-time reverse-transcription (RT-) PCR and protein assays were performed for further assessing the profile differentiation of the identified H. pylori IDA-associated genes. Results We identified 29 and 11 genes with significantly higher or lower expression in the IDA isolates compared to non-IDA isolates, respectively. Especially notable were higher expression of sabA gene encoding sialic acid-binding adhesin in the IDA isolates, which was confirmed by real-time RT-PCR study. Moreover, iron-depletion in vitro led to up-regulation of fecA1 and frpB1 genes and down-regulation of pfr, as predicted. Known iron-regulated genes such as fur, pfr, fecA, and feoB did not significantly differ between both groups. The IDA isolates had significantly higher expression of vacuolating cytotoxin gene vacA than non-IDA isolates, consistent with the results of VacA protein assays. There were no significant differences in bacterial growth value between IDA and non-IDA isolates. Conclusions It is likely that H. pylori carrying high expression of sabA causes IDA, especially in children and adolescents who have increased daily iron demand. In addition, it is possible that several host-interactive genes, including vacA, may play a synergistic role for sabA in IDA development.
2017-07-25 | GSE101807 | GEO
Project description:The integration of T-DNA to plant genomes is widely used for basic research and agriculture. High heterogeneity in the number of integration events per genome, their configuration and impact on genome integrity highlight both, the critical need and great challenge to detect the genomic locations of T-DNA insertions and their associated chromosomal rearrangements. Here we present ‘4SEE’, a circular chromosome conformation capture (4C) based method for robust, rapid and cost-efficient detection of the entire scope T-DNA locations. Moreover, by measuring the chromosomal architecture at plant genome flanking the T-DNA insertions, 4SEE outlines their associated complex chromosomal aberrations. Applying 4SEE to a collection of confirmed T-DNA lines revealed previously unmapped T-DNA insertions and chromosomal rearrangements such as inversions and translocations. Uncovering such events in feasible, robust and cost-effective manners by 4SEE in any plant of interest have implications for accurate annotation and phenotypic characterization of T-DNA insertion mutants and transgene expression in basic science applications as well as for plant biotechnology.
2020-04-05 | GSE147542 | GEO
Project description:Chromosomal rearrangements are prevalent events in the human population, occurring both constitutionally in the general population and somatically in the majority of cancers. Detection of balanced rearrangements, such as reciprocal translocations and inversions, is troublesome with many rearrangements remaining undetected. This is particularly detrimental in oncology where rearrangements play diagnostic and prognostic roles and can influence choice and efficacy of treatment protocols. New methods to detect and characterize balanced rearrangements are therefore required for both research and clinical applications. Here we describe the use of the chromosome conformation capture derived method Hi-C as a tool for detection of both balanced and unbalanced chromosomal rearrangements in cell lines and human tumor samples, with the ability to detect gene fusions and define chromosomal breakpoints to base pair resolution. In addition, we show that copy number information can also be obtained from the same data, allowing rearrangements, gains, amplifications and deletions of genomic regions to be detected in a single experiment.
2017-05-23 | GSE81879 | GEO
Project description:Most sarcomas have complex karyotype and are characterized by multiple chromosomal rearrangements. Moreover, sarcomas very frequently maintain their telomeres by recombination in the process called Alternative Lengthening of Telomeres (ALT) which enables their continuous growth and immortalization. Previously our group showed that orphan receptors bind specifically to the ALT telomeres and that their presence is important for the ALT mechanism. In these studies we focus on the function of orphan receptors at the telomeres and their contribution to telomeric recombination. We demonstrate that orphan receptors induce proximity of their binding sites in telomeric and genomic context and reveal novel aspects of ALT which are telomere-genome rearrangements which can underlie complexity of sarcomas. Our data perturb the dogma of telomere function in protecting the genome integrity. Here we show that in some cases telomeres may in fact drive genomic instability and chromosomal rearrangements by recombination with genomic sites. Characterization of TRF2 and orphan receptor NR2F/C2 binding sites in ALT (-) and ALT (+) cells.
2015-02-23 | E-GEOD-46237 | biostudies-arrayexpress
Project description:Detecting complex chromosomal rearrangements from long DNA reads.
| PRJDB9494 | ENA
Project description:Forced expression of ASCL1, Nurr1, Lmx1a, miRNA-124 and p53shRNA (ANLmp) in fibroblasts reprograms fibroblasts to induced dopaminergic neurons (iDA). While human lung fibroblasts can be converted rapidly and efficiently, iDA of dermal fibroblast is very unefficient and incompleted. To address this issue, we performed time series RNAseq on both lung and dermal fibroblasts during the first four days of ANLmp induced neuron convertion. Bioinformatics analysis revealed the stable fibroblast gene regulatory network (GRN) was a potential repressive factor for iDA in human dermal fibroblasts.
2019-06-17 | GSE125692 | GEO
Project description:Forced expression of ASCL1, Nurr1, Lmx1a, miRNA-124 and p53shRNA (ANLmp) in fibroblasts reprograms fibroblasts to induced dopaminergic neurons (iDA). While human lung fibroblasts can be converted rapidly and efficiently, iDA of dermal fibroblast is very unefficient and incompleted. To address this issue, we performed time series RNAseq on both lung and dermal fibroblasts during the first several days of ANLmp induced neuron convertion. Bioinformatics analysis revealed the stable fibroblast gene regulatory network (GRN) was a potential repressive factor for iDA in human dermal fibroblasts.
2019-06-17 | GSE129358 | GEO
Project description:Since iron deficiency anemia (IDA) is one of the most common diseases in worldwide, it is an essential issue to prevent and to treat the IDA in public healthcare system. However, the precise adaptive responses and their mechanisms of the hematopoietic system induced by iron deficient state are not fully understood. In this study, low iron diet conditions which induce sever iron deficiency anemia in mice were established. Transcriptome analyses in erythroblasts under normal or iron deficient states were performed to describe the pathological details of IDA. Under iron deficient state, extensive gene expression changes and mitophagy disorder were induced during the terminal maturation of erythroblasts. These findings provide a new insight into pathophysiology and molecular biology of IDA and the function of iron as a coordinator of gene expression networks in erythrocyte maturation.
2016-12-14 | GSE77694 | GEO