Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

16s rDNA sequencing of feces from C9orf72 loss of function mice

ABSTRACT: 16s rDNA sequencing of feces from C9orf72 loss of function mice

PROVIDER: PRJNA614503 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11393730_1.fastq.gz	Fastqsanger.gz
	SRR11393730_2.fastq.gz	Fastqsanger.gz
	SRR11393731_1.fastq.gz	Fastqsanger.gz
	SRR11393731_2.fastq.gz	Fastqsanger.gz
	SRR11393732_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 100

Similar Datasets

16s rDNA sequencing of feces from C9orf72 loss of function mice

Project description:We report the sequencing of bacterial species across four environments in which C9orf72 loss of function mice were studied as well as mice that received fecal transplantation. Our study elucidates bacterial communities that associate with pro-inflammatory or pro-survival outcomes in this model of ALS/FTD with features of autoimmunity and systemic and neural inflammation.

2020-03-24 | GSE147325 | GEO

Mus musculus feces 16s rDNA sequencing

Project description:Mus musculus feces 16s rDNA sequencing Raw sequence reads

| PRJNA874477 | ENA

C9orf72 is required for proper macrophage and microglial function in mice

Project description:Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Decreased expression of C9orf72 is seen in expansion carriers, suggesting loss of function may play a role in disease. We find that two independent mouse lines lacking the C9orf72 ortholog (3110043O21Rik) in all tissues developed normally and aged without motor neuron disease. Instead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of engorged macrophage-like cells. C9orf72 expression was highest in myeloid cells, and loss of C9orf72 led to lysosomal accumulation and altered immune responses in macrophages and microglia, with age-related neuroinflammation similar to C9orf72 ALS but not sporadic ALS patient tissue. Thus, C9orf72 is required for normal function of myeloid cells, and altered microglial function may contribute to neurodegeneration in C9orf72 expansion carriers.

2016-03-24 | GSE77681 | GEO

C9orf72 deficiency promotes microglial mediated synaptic loss in aging and amyloid accumulation [scRNA-seq]

Project description:C9orf72 repeat expansions cause inherited amyotrophic lateral sclerosis/frontotemporal dementia (ALS/FTD) and result in both loss of C9orf72 protein expression and production of potentially toxic RNA and dipeptide repeat proteins. In addition to ALS/FTD, C9orf72 repeat expansions have been reported in a broad array of neurodegenerative syndromes including Alzheimer’s disease. Here we show that C9orf72 deficiency promotes loss of homeostatic signatures in microglia and transition to an inflammatory state characterized by an enhanced type I IFN signature. Furthermore, C9orf72-depleted microglia trigger age-dependent neuronal defects, in particular enhanced cortical synaptic pruning, leading to altered learning and memory behaviors in mice. Interestingly, C9orf72 deficient microglia also promote enhanced synapse loss and neuronal deficits in a mouse model of amyloid accumulation, while paradoxically improving plaque clearance. These findings suggest that altered microglial function due to decreased C9orf72 expression directly contributes to neurodegeneration in repeat expansion carriers independent of gain of function toxicities.

2022-06-15 | GSE164674 | GEO

Feces 16S rRNA seq of mice treated by AZ1 with 2.5% DSS or H2O

Project description:Feces 16s rRNA seq experiments is required to demonstrate the AZ1 doesn’t impact the intestinal microbiota.

2020-02-14 | GSE143003 | GEO

C9orf72 deficiency promotes microglial mediated synaptic loss in aging and amyloid accumulation [bulk RNA-seq]

2022-06-15 | GSE164675 | GEO

soil 16s rDNA

Project description:soil 16s rDNA Metagenome

| PRJNA756830 | ENA

iPSC derived motor neuron cultures from C9ORF72 carriers

Project description:Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative condition characterized by loss of motor neurons in the brain and spinal cord. Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9ORF72 gene are the most common cause of the familial form of ALS (C9-ALS), as well as frontotemporal lobar degeneration and other neurological diseases. How the repeat expansion causes disease remains unclear, with both loss of function (haploinsufficiency) and gain of function (either toxic RNA or protein products) proposed. We report a cellular model of C9-ALS with motor neurons differentiated from induced pluripotent stem cells (iPSCs) derived from ALS patients carrying the C9ORF72 repeat expansion. No significant loss of C9ORF72 expression was observed, and knockdown of the transcript was not toxic to cultured human motor neurons. Transcription of the repeat was increased, leading to accumulation of GGGGCC repeat–containing RNA foci selectively in C9-ALS iPSC-derived motor neurons. Repeat-containing RNA foci colocalized with hnRNPA1 and Pur-?, suggesting that they may be able to alter RNA metabolism. C9-ALS motor neurons showed altered expression of genes involved in membrane excitability including DPP6, and demonstrated a diminished capacity to fire continuous spikes upon depolarization compared to control motor neurons. Antisense oligonucleotides targeting the C9ORF72 transcript suppressed RNA foci formation and reversed gene expression alterations in C9-ALS motor neurons. These data show that patient-derived motor neurons can be used to delineate pathogenic events in ALS. Transcriptome profiling from iPSC derived motor neurons compared to controls

2013-11-07 | E-GEOD-52202 | biostudies-arrayexpress

16S rDNA sequencing

Project description:16S rDNA sequencing Raw sequence reads

| PRJNA882208 | ENA

16S rRNA gene sequence analysis of feces samples from rats treated with paclitaxel or vehicle controls

Project description:To address the role of gut microbiota in the development of paclitaxel-induced peripheral neuropathy (PIPN), we performed 16S rRNA sequencing analysis of feces samples at 14 days and 28 days after the initiation of paclitaxel or vehicle injections.

2023-10-16 | E-MTAB-13426 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data