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Expression analysis of neuronal differentiation of single mutants UBE3A/PHLDA2/SLC22A18 and double mutant PHLDA2/SLC22A18 cells

ABSTRACT: Expression analysis of neuronal differentiation of single mutants UBE3A/PHLDA2/SLC22A18 and double mutant PHLDA2/SLC22A18 cells

PROVIDER: PRJEB58997 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10783357.fastq.gz	Fastqsanger.gz
	ERR10783358.fastq.gz	Fastqsanger.gz
	ERR10783359.fastq.gz	Fastqsanger.gz
	ERR10783360.fastq.gz	Fastqsanger.gz
	ERR10783361.fastq.gz	Fastqsanger.gz

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Expression analysis of neuronal differentiation of single mutants UBE3A/PHLDA2/SLC22A18 and double mutant PHLDA2/SLC22A18 cells

Project description:Transcriptome analysis of UBE3A, PHLDA2, SLC22A18 and PHLDA2/SLC22A18 mutants during neuronal differentiation

2024-04-30 | E-MTAB-12504 | biostudies-arrayexpress

Expression analysis of neuronal differentiation of HOXA6/HOXB6/UBE3A mutants cells

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Expression analysis of neuronal differentiation of HOXA6/HOXB6/UBE3A mutants cells

Project description:Expression analysis of neuronal differentiation of HOXA6/HOXB6/UBE3A mutants cells

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Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.

Project description:Angelman syndrome is a neurodevelopmental disorder caused by (epi)genetic lesions of maternal UBE3A. Research has focused largely on the role of UBE3A in neurons due to its imprinting in that cell type. Yet, evidence suggests there may be broader neurodevelopmental impacts of UBE3A dysregulation. Human cerebral organoids can investigate these understudied aspects of UBE3A as they recapitulate diverse cell types of the developing human brain. We performed single-cell RNA-sequencing on organoids to reveal the effects of UBE3A disruption on cell type-specific transcriptomic alterations and compositions. In the absence of UBE3A, progenitor proliferation and structures were disrupted while organoid composition shifted away from proliferative cell types. We observed impacts on non-neuronal cells including choroid plexus enrichment. Furthermore, EMX1+ cortical progenitors were negatively impacted, disrupting corticogenesis, and potentially delaying neuron maturation. This work reveals novel impacts of UBE3A on understudied cell types and related neurodevelopmental processes and elucidates potential new therapeutic targets.

2024-03-13 | GSE253230 | GEO

Ube3a-ATS characterization with strand-speicific microarray

Project description:This strand-specific array is performed to characterize expression features of Ube3a-ATS, including its imprinting status, its exon-intron structure, its transcriptional initiation and termination site as well as its polyadenylation status. The array contains reverse-complementary probes detecting transcripts from both strands and therefore we are able to pick up signal from both Ube3a sense and antisense. By comparing wild-type with various mutants, and total RNA with polyA RNA, we concluded that Ube3a-ATS is a paternally imprinted gene covering the whole gene body of Ube3a in the antisense orientation. It does not have an obvious exon-intron structure. Its transcription initiates at Snrpn major promoter and terminates ~40kb upstream of Ube3a transcriptional start site. Total RNA from Snrpn-Ube3a maternal deletion mutant (del s-u/+), its wild-type littermate, paternal deletion mutant and its wildtype littermate were analyzed. Mutant mice with S-U maternal deletion and Snrpn promoter paternal deleiton which leads to depletion of Ube3a-ATS (del s-u/0.9 and del s-u/4.8) were also analyzed. polyA RNA was purified from the sample 2 and sample 4. All eight samples were hybridized to the custom 8X60k Agilent CGH array.

2012-05-02 | E-GEOD-29254 | biostudies-arrayexpress

Ube3a-ATS characterization with strand-speicific microarray

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Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.

Project description:Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.

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RNA-sequencing of C.elegans isp-1 mutant and superoxide dismutase-isp-1 double mutants

Project description:isp-1;sod double mutants have decreased lifespan, increased resistance to oxidative stress and slow physiologic rates. We performed RNA sequencing to compare gene expression between isp-1 mutants and isp-1;sod-3 and isp-1;sod-5 double mutants

2017-08-30 | GSE95240 | GEO

Double-strand breaks in spo11 mutants

Project description:Double-strand breaks in spo11 mutants

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Imprinting effects of UBE3A loss on synaptic gene networks and Wnt signaling pathways

Project description:UBE3A encodes a E3 ubiquitin ligase whose loss from the maternal allele causes the neurodevelopmental disorder Angelman syndrome. Previous studies of UBE3A function have not examined full Ube3a deletion in mouse, the complexity of imprinted gene networks in brain, nor the molecular basis of systems-level cognitive dysfunctions in Angelman syndrome. We therefore utilized a systems biology approach to elucidate how UBE3A loss impacts the early postnatal brain in a novel CRISPR/Cas9 engineered rat Angelman model of a complete Ube3a deletion. Strand-specific transcriptome analysis of offspring from maternally or paternally inherited Ube3a deletions revealed the expected parental expression patterns of Ube3a sense and antisense transcripts by postnatal day 2 (P2) in hypothalamus and day 9 (P9) in cortex, compared to wild-type littermates. The dependency of genome-wide effects on parent-of-origin, Ube3a genotype, and time (P2, P9) was investigated through transcriptome (RNA-seq of cortex and hypothalamus) and methylome (whole genome bisulfite sequencing of hypothalamus). Weighted gene co-expression and co-methylation network analyses identified co-regulated networks in maternally inherited Ube3a deletion offspring enriched in postnatal developmental processes including Wnt signaling, synaptic regulation, neuronal and glial functions, epigenetic regulation, ubiquitin, circadian entrainment, and splicing. Furthermore, we showed that loss of the paternal Ube3a antisense transcript resulted in both unique and overlapping dysregulated gene pathways with maternal loss, predominantly at the level of differential methylation. Together, these results provide a holistic examination of the molecular impacts of UBE3A loss in brain, supporting the existence of interactive epigenetic networks between maternal and paternal transcripts at the Ube3a locus.

2020-03-01 | GSE137217 | GEO

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