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KDM5C safeguards the appropriate timing of early neurodevelopment [ATAC-seq]

ABSTRACT: We generated human induced pluripotent cells from intellectual disability patients carrying the c.2T>C mutation in KDM5C (Called “Mutant”). We generated a paired, isogenic human iPS cell line (called “Corrected”) using CRISPR/Cas9 and PiggyBac gene-editing technologies and conducted neuronal differentiation based on “Yichen Shi et al. Nat. Protoc. 7, 1836–1846 (2012)” to define differences in gene expression between the Mutant and Corrected and Mutant and Corrected treated with either a Wnt inhibitor (indicated as "+inh") or activator (indicated as "+W") during neuronal differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE210090 | GEO | 2023/09/25

REPOSITORIES: GEO

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KDM5C safeguards the appropriate timing of early neurodevelopment [RNA-seq]

Project description:We generated human induced pluripotent cells from intellectual disability patient carrying the c.2T>C mutation in KDM5C (Called “Mutant”). We generated a paired, isogenic human iPS cell line (called “Corrected”) using CRISPR/Cas9 and PiggyBac gene-editing technologies and conducted neuronal differentiation based on “Yichen Shi et al. Nat. Protoc. 7, 1836–1846 (2012)” to define differences in gene expression between the Mutant and Corrected and Mutant and Corrected treated with either a Wnt inhibitor (indicated as "+inh") or activator (indicated as "+W") during neuronal differentiation.

2023-09-25 | GSE211063 | GEO

KDM5C safeguards the appropriate timing of early neurodevelopment

Project description:We generated human induced pluripotent cells from intellectual disability patients carrying the c.2T>C mutation in KDM5C (Called “Mutant”). We generated a paired, isogenic human iPS cell line (called “Corrected”) using CRISPR/Cas9 and PiggyBac gene-editing technologies and conducted neuronal differentiation based on “Yichen Shi et al. Nat. Protoc. 7, 1836–1846 (2012)” to define differences in gene expression between the Mutant and Corrected during neurodevelopment.

2023-10-13 | E-MTAB-7551 | biostudies-arrayexpress

KDM5C safeguards the appropriate timing of early neurodevelopment [CUT&RUN]

Project description:We generated human induced pluripotent cells from intellectual disability patients carrying the c.2T>C mutation in KDM5C (Called “Mutant”). We generated a paired, isogenic human iPS cell line (called “Corrected”) using CRISPR/Cas9 and PiggyBac gene-editing technologies and conducted neuronal differentiation based on “Yichen Shi et al. Nat. Protoc. 7, 1836–1846 (2012)” to define differences in binding of the KDM5C gene in Mutant and Corrected cells.

2023-09-25 | GSE210857 | GEO

RNA-Seq analysis of leaves of maize drought tolerant mutant line Chang7-2t under water deficit

Project description:Identification of gene expression changes responding to water deficit in leaves of maize drought tolerant mutant line Chang7-2t.

2022-02-28 | E-MTAB-11331 | biostudies-arrayexpress

Isonicotinylation is Isonicotinylation is a histone mark induced by the anti-tuberculosis first-line drug isoniazida histone mark induced by the anti-tuberculosis first-line drug isoniazid

Project description:Isoniazid (INH) is the first-line anti-tuberculosis drug used for nearly seventy years. Metabolites of INH showed hepatotoxicity in human and tumorigenicity in rodents. However, mechanism underlying the side effects of INH is elusive. Histone acylation is known to be modulated by intracellular metabolites. Here, we report INH and its metabolites induces a novel post-translational modification (PTM) on histones, the lysine isonicotinylation (Kinic), also called 4-picolinylation, in cells and mice. INH functions as a donor to promote biosynthesis of isonicotinyl-CoA that is used for a co-factor of intracellular isonicotinylation reaction. Twenty-six isonicotinylation sites were identified on histones in HepG2 cells by mass spectrometry. Acetyltransferases CREB-binding protein (CBP) and P300 were found to catalyze histone Kinic, whilst histone deacetylase HDAC3 functions as a deisonicotinylase. MNase sensitivity assay and RNA-seq analysis showed that histone Kinic relaxes chromatin structure and promotes gene transcription. Importantly, INH-mediated histone Kinic upregulates PIK3R1 gene expression and activates PI3K/Akt/mTOR signaling pathway in liver cancer cells, linking INH to the tumorigenicity in liver. Further, Kinic was found increased in liver cancer patients with concomitant raised PIK3R1 protein level. In addition, histone Kinic also affects TNF and GABAergic synapse signaling pathways that are closely related to INH-caused side effects. Taken together, we demonstrated that lysine isonicotinylation represents the first histone acylation mark with the pyridine ring that may arise broad biological effects. Therefore, INH-induced isonicotinylation is likely a mechanism accounting for side effects in patients who taking long-term INH for anti-tuberculosis therapy and this modification may also increase cancer risk in human.

2021-08-20 | PXD025490 | Pride

Project description:shi

| PRJEB10335 | ENA

Examining the basis of isoniazid tolerance in nonreplicating Mycobacterium tuberculosis using transcriptional profiling

Project description:Background: Understanding how growth state influences Mycobacterium tuberculosis responses to antibiotic exposure provides a window into drug action during patient chemotherapy. In this article, we describe the transcriptional programs mediated by isoniazid (INH) during the transition from log-phase to nonreplicating bacilli, from INH-sensitive to INH-tolerant bacilli respectively, using the Wayne model. Results: INH treatment did not elicit a transcriptional response from nonreplicating bacteria under microarophilic conditions (NRP2), unlike the induction of a robust and well-characterized INH signature in log-phase bacilli. Conclusion: The differential regulation (between drug-free NRP2 and log-phase bacilli) of genes directly implicated in INH resistance could not account for the abrogation of INH killing in nongrowing bacilli. Thus, factors affecting the requirement for mycolic acids and the redox status of bacilli are likely responsible for the reduction in INH efficacy. We speculate on additional mechanisms revealed by transcriptome analysis that might account for INH tolerance. Data is also available from <ahref=http://bugs.sgul.ac.uk/E-BUGS-104 target=_blank>BuG@Sbase</a>

2011-01-17 | E-BUGS-104 | biostudies-arrayexpress

Glycine max cultivar:Shi-shi

Project description:Glycine max cultivar:Shi-shi Raw sequence reads

| PRJNA302826 | ENA

Expression data between FOXP3 wild type and 2T>C(mut)

Project description:Investigation of the role of FOXP3 in CD4+ T effector cells. FOXP3 is transiently upregulated in T effector cells under activation. This temporary expression in Teff cells is insufficient to suppress expression of reported targets of FOXP3 repressor activity. The role of FOXP3 in T effector cells remains unclear. We used microarray analysis to detail the differentially expressed genes between FOXP3 wild type and 2T>C(mut) clones and identified classes of up-regulated or down-regulated genes based upon FOXP3 expression. We used T effector cells from one IPEX disease carrier mother that consist of a mixed population ofFOXP3 wild type and 2T>C(mut) clones. We activated them using anti-CD3, anti-CD28. We compareFOXP3 wild type and 2T>Cl clones at different stages: resting phase and activated phase at 72hrs.

2013-03-08 | E-GEOD-41087 | biostudies-arrayexpress

Novel genes involved in the pathophysiology of gonadotropin-dependent adrenocortical tumorigenesis in mice.

Project description:The inh-alpha/Tag mouse is a murine adrenocortical tumor model that combines gonadotropin-dependent tumorigenesis with SV40Tag expression (which inhibits p53). These mice have been extensively used to study adrenocortical and gonadal tumorigenesis, as they initially present with gonadal tumors. To induce adrenocortical tumorigenesis, the inh-alpha/Tag mice need to be prebubertally gonadectomized. Generally, females develop adrenal tumors faster and larger in size than males, with a very high individual variations of tumor volume and histological appearance. In this study, we used the inh-alpha/Tag mouse model to analyze the molecular basis of the LH-dependent adrenal tumorigenesis. Experimental inh-alpha/Tag and control littermates (C57Bl/6N) mice of both sexes were used as the animal model. inh-alpha/Tag and WT mice were gonadectomized at 21-24 days of age. Mice were sacrificed at the age of 30 weeks (+/-1 week) and adrenals snap-frozen in liquid nitrogen for microarray analysis. Additionally, a group of 27 week-old inh-alpha/Tag mice (+/-1 week) were treated for 3 weeks with GnRH antagonist cetrorelix acetate (#C5249, Sigma-Aldrich) (3mg/kg/48h). Mice were sacrificed at the age of 30 weeks (+/-1 week) and adrenals snap-frozen in liquid nitrogen for microarray analysis.

2017-02-01 | E-MTAB-5310 | biostudies-arrayexpress

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