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ABSTRACT: LUHMES epigenetic data

PROVIDER: PRJNA1076600 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27970100.fastq.gz	Fastqsanger.gz
	SRR27970101.fastq.gz	Fastqsanger.gz
	SRR27970102.fastq.gz	Fastqsanger.gz
	SRR27970103_1.fastq.gz	Fastqsanger.gz
	SRR27970104_1.fastq.gz	Fastqsanger.gz

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RNA-seq of CSMD1 enhancer CRISPRi in LUHMES cells and differentiated neurons

Project description:we performed lentiviral CRISPR interference (CRISPRi) by recruiting dCas9 fused with the KRAB domain to the CSMD1 enhancer (fam3) in the neuronal precursor cell line – Lund human mesencephalic (LUHMES). Given that the expression of CSMD1 was not detectable in LUHMES cells we differentiated these cells into neurons. Differentiated neurons with CRISPRi of CSMD1 enhancer showed significantly higher expression of CSMD1 than control.

2022-06-30 | E-MTAB-8027 | biostudies-arrayexpress

Project description:LUHMES baseline Konstanz

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Neuronal differentiation of LUHMES cells is accompanied by substantial changes of the proteome

Project description:To study mechanisms of neurodegenerative diseases, neuronal cell lines are important model systems and are often differentiated into postmitotic neuron-like cells to resemble more closely primary neurons obtained from brains. One such cell line is the Lund Human Mesencephalic (LUHMES) cell line which can be differentiated into dopamine-like neurons and is frequently used to study mechanisms of Parkinson’s disease (PD) and neurotoxicity. Neuronal differentiation of LUHMES cells is commonly verified by measurement of selected neuronal markers, but little is known about proteome-wide protein abundance changes during differentiation. Using mass spectrometry and label-free quantification (LFQ) we compared the proteome of differentiated and undifferentiated LUHMES cells as well as of cultured primary murine midbrain neurons, which are mainly dopaminergic. Neuronal differentiation induced substantial changes of the LUHMES cell proteome (18.4% reveal protein abundance changes of more than 4-fold), with proliferation-related proteins (e.g. MCMs) being strongly down-regulated and neuronal and dopaminergic proteins being up to 1000-fold upregulated, such as L1CAM and SNCA. Several of these proteins, including MAPT and SYN1, may be useful new markers to experimentally validate neuronal differentiation of cultured LUHMES cells. Primary midbrain neurons were more closely related to differentiated than to undifferentiated LUHMES cells with respect to the abundance of proteins related to neurodegeneration or to genetic forms of PD. In summary, our comparative proteomic analysis demonstrates that differentiated LUHMES cells are a suitable model for studies on PD and neurodegeneration and provides a resource of the proteome-wide changes during neuronal differentiation.

2020-09-24 | PXD020044 | Pride

Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synuclein

Project description:Differential transcriptome analysis in LUHMES cells overexpressing human wild-type alpha-synuclein or GFP

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Time-course transcriptome analysis of a human neuronal cell line

Project description:RNA-seq analysis on a human neuronal cell line derived from fetal mesencephalon (LUHMES) from day 0 to day 6.

2021-07-31 | E-MTAB-8908 | biostudies-arrayexpress

Transcriptome and proteome analysis in LUHMES cells overexpressing alpha-synculein

Project description:LUHMES cells share many characteritics with human dopamingeric neurons in the substantia nigra, the cells whose demise is responsible for the motor symptoms in Parkinson’s disease (PD). LUHMES cells can therefore be used bona fide as a model to study pathophysiological processes involved in PD. Previously, we showed that LUHMES cell degenerate after six days upon overexpression of wild type alpha-synuclein. In the present study we performed a transcriptome and proteome expression analysis in alpha-synuclein-overexpressing cells and GFP-expressing control cells in order to identify genes and proteins that are differentially regulated upon overexpression of alpha-synuclein. The analysis was performed four days after the initiation of alpha-synuclein or GFP overexpression, before the cells died in order to identify processes that preceded cell death.

2022-05-19 | PXD028322 | Pride

Time-course transcriptome analysis of a human neuronal cell line with RFX2 KO

Project description:RNA-seq analysis on a human neuronal cell line derived from fetal mesencephalon (LUHMES) wild type and RFX2 knockout from day 0 to day 6.

2024-01-31 | E-MTAB-11546 | biostudies-arrayexpress

Long-term treatment with bortezomib induces specific methylation changes in differentiated neuronal cells

Project description:Genome-wide patterns of DNA methylation were quantified using the Illumina Infinium HumanMethylationEPIC BeadChip in DNA samples extracted from LUHMES cell line cells repeatedly treated with bortezomib (BTZ).

2022-08-03 | GSE202792 | GEO

Capture Hi-C (HiCap) experiments performed on LUHMES cell line differentiated in three (D3) and six days (D6). We fragmented the genome using DpnII. HiCap experiments at each time point (D1, D3 and D6) are performed in two replicates

Project description:LUHMES cells are non-tumorigenic model of human dopaminergic neurons. Their physiology and phenotypic changes upon differentiation can provide clues into the pathology of neurological diseases such as dyslexia, autism, schizophrenia.

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Alpha-synuclein overexpression is associated with epigenomic dysregulation of glutamate signaling and locomotor pathways

Project description:Although Parkinson’s disease (PD) is one of the most rapidly growing neurological disorders, interindividual differences in PD etiology related to genetics are not fully understood. Here, we demonstrate genome-wide DNA methylation and hydroxymethylation alterations associated with overexpression of two PD-linked alpha-synuclein variants (wild type and A30P) in LUHMES cells differentiated to dopaminergic neurons. Alpha-synuclein altered DNA methylation at thousands of CpGs and DNA hydroxymethylation at hundreds of CpGs in both genotypes, and primarily at locomotor and glutamate signaling pathway genes. In some cases, epigenetic changes were associated with transcription. SMITE network analysis incorporating H3K4me1 ChIP-seq to score DNA methylation and hydroxymethylation changes across promoters, enhancers, and gene bodies confirmed epigenetic and transcriptional deregulation of glutamate signaling modules in both genotypes. Our results identify distinct and shared impacts of alpha-synuclein variants on the epigenome, and associate alpha-synuclein in the epigenetic etiology of PD.

2021-08-02 | GSE181126 | GEO

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