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Deletion of the Alzheimer’s disease risk associated Abi3 gene locus in mice results in obesity and systemic metabolic disruption

ABSTRACT: Deletion of the Alzheimer’s disease risk associated Abi3 gene locus in mice results in obesity and systemic metabolic disruption

PROVIDER: PRJNA874925 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21314832.fastq.gz	Fastqsanger.gz
	SRR21314833.fastq.gz	Fastqsanger.gz
	SRR21314834.fastq.gz	Fastqsanger.gz
	SRR21314835.fastq.gz	Fastqsanger.gz
	SRR21314836.fastq.gz	Fastqsanger.gz

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Deletion of the Alzheimer’s disease risk associated Abi3 gene locus in mice results in obesity and systemic metabolic disruption

Project description:A rare coding variant was identified within the human ABI3 gene that is associated with increased risk of Alzheimer’s disease (AD). Following this discovery, we recently demonstrated that deletion of Abi3 gene locus notably exacerbates AD neuropathology in the 5xFAD transgenic mouse model of amyloidosis. In the course of a related investigation into the functional impact of Abi3 deletion in mice, we made an unexpected discovery regarding the impact of Abi3 deletion on the non-transgenic littermates of those 5xFAD mice. In those mice, we found that deletion of Abi3 gene locus resulted in an obese phenotype. Therefore, we investigated this serendipitous discovery. In this report, we demonstrate that mice lacking Abi3 have dramatically increased body weight and body fat. Further, we determined that these mice without Abi3 have reduced energy expenditure. Additionally, we found that deletion of the Abi3 gene locus altered gene expression, particularly within immune pathways, within the hypothalamus. Subsequent immunohistological analysis of the central nervous system (CNS) revealed that microglia number and area were decreased specifically within the mediobasal hypothalamus of mice without Abi3. Altogether, this investigation establishes the functional importance of the Abi3 gene locus, particularly within the CNS, in the regulation of systemic metabolism and maintenance of healthy weight.

2022-12-13 | GSE212299 | GEO

Deletion of Abi3 gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis

Project description:Recently, large-scale human genetics studies identified a rare coding variant in the ABI3 gene that is associated with an increased risk of late-onset Alzheimer’s disease (AD). However, pathways by which ABI3 contributes to the pathogenesis of AD are unknown. To address this critical question, we determined whether loss of ABI3 function affects pathological features of AD in the 5XFAD mouse model. We demonstrate that the deletion of Abi3 locus significantly increases amyloid-b (Ab) accumulation and decreases microglia clustering around the plaques. Furthermore, long-term potentiation is impaired in 5XFAD;Abi3 knock-out (“Abi3-/-”) mice. Moreover, we identified dramatic changes in the proportion of microglia subpopulations in Abi3-/- mice using a single-cell RNA sequencing approach. Mechanistic studies demonstrate that Abi3 knockdown in microglia impairs migration and phagocytosis. Taken together, our study provides the first in vivo functional evidence that loss of ABI3 function may increase the risk of developing AD by affecting Ab accumulation and neuroinflammation.

2021-11-10 | GSE175389 | GEO

Deletion of Abi3 gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis

Project description:Recently, large-scale human genetics studies identified a rare coding variant in the ABI3 gene that is associated with an increased risk of late-onset Alzheimer’s disease (AD). However, pathways by which ABI3 contributes to the pathogenesis of AD are unknown. To address this critical question, we determined whether loss of ABI3 function affects pathological features of AD, such as amyloid- (A) accumulation, inflammation, and synaptic dysfunction, in the 5XFAD mouse model. We demonstrate that the deletion of Abi3 locus significantly increases levels of soluble and insoluble A and amyloid plaques and decreases microglia clustering around the plaques. Furthermore, long-term potentiation is impaired in Abi3 knock-out (Abi3-/-) mice. Nanostring-based transcriptomic analyses indicate that genes involved in microglial phagocytosis and immune response pathways are dysregulated in Abi3-/-mice. Moreover, we identified dramatic changes in microglia subpopulations in Abi3-/- mice using a single-cell RNA sequencing approach. Taken together, our study provides the first in vivo functional evidence that loss of ABI3 function may increase the risk of developing AD by affecting A pathway and neuroinflammation.

2021-11-04 | GSE159866 | GEO

Identification of target genes of ABI3 [Agilent 44k]

Project description:ABI3 is a key regulator of seed development in Arabidopsis and other plants.To identify genes regulated by ABI3 we performed array based transcriptome analysis of Dexamethasone inducible ABI3 transgenic seedlings. ABI3 mostly in concert with abscisic acid (ABA) was found to activate genes specifically expressed during the maturation phase of seed development.

2012-06-01 | GSE33951 | GEO

Deletion of Abi3 gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis

Project description:Deletion of Abi3 gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis

| PRJNA670808 | ENA

Deletion of Abi3 gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis

Project description:Deletion of Abi3 gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis

| PRJNA732208 | ENA

Medicago abi3 mutant analysis

Project description:Comparison of transcriptomes of WT and abi3 mutant lines at 32 and 40 days after pollination Transcriptome of Medicago WT lines (3 replicates) compared with Medicago abi3 mutant lines (NF6003) using Medicago_v1 NimbleGen chip

2014-05-09 | E-GEOD-57457 | biostudies-arrayexpress

ABI3 Network Walking

Project description:Deciphering gene regulatory networks (GRNs) is a key for understanding gene expression regulations in living systems. Here, we describe the investigation of the ABSCISIC ACID INSENSITIVE 3 (ABI3) plant transcription factor GRN vicinity by a technique called Network Walking. The method involves transient transformation of protoplasts and inducible nuclear re-localization of transcription factors along with transcriptomic analysis. This genome-wide approach allowed the de novo recovery of i) direct and indirect ABI3 target genes, ii) cis-binding site preference, and iii) biological processes regulated by this canonical abscisic acid response factor. This work improves our knowledge of ABI3 action by inferring network motifs (such as Feed Forwar Loops) under its influence. The novel high-throughput-oriented technique will help accelerate GRN systems investigations in plants, as well as in other organisms. This work studies ABI3 direct and indirect targets by a technique named Network Walking. Root/protoplasts were treated with or without dexamethasone (DEX) and cycloheximide (CHX). 3 reps each.

2013-01-01 | E-GEOD-33344 | biostudies-arrayexpress

Identification of target genes of ABI3

Project description:This SuperSeries is composed of the following subset Series: GSE33951: Identification of target genes of ABI3 [Agilent 44k] GSE34033: Identification of target genes of ABI3 [Agilent 2x244k] GSE34041: Identification of target genes of ABI3 [SAP] Refer to individual Series

2012-05-31 | E-GEOD-34043 | biostudies-arrayexpress

ABI3 TARGET approach

2013-01-01 | GSE33344 | GEO