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Wnt Signaling Rescues Amyloid Beta-Induced Gut Stem Cell Loss

ABSTRACT: Wnt Signaling Rescues Amyloid Beta-Induced Gut Stem Cell Loss

PROVIDER: PRJNA753593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15411682_1.fastq.gz	Fastqsanger.gz
	SRR15411682_2.fastq.gz	Fastqsanger.gz
	SRR15411683_1.fastq.gz	Fastqsanger.gz
	SRR15411683_2.fastq.gz	Fastqsanger.gz
	SRR15411684_1.fastq.gz	Fastqsanger.gz

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Wnt Signaling Rescues Amyloid Beta-Induced Gut Stem Cell Loss

Project description:Wnt signaling has well established roles in development and cancer progression. Its roles during normal adult homeostasis are less well studied, but Wnt is a major stem cell regulating factor in adult tissues. Here we use an optogenetic model of amyloid beta aggregation to examine the effect of Wnt signaling on protein aggregation. We observe that Wnt activation rescues the detrimental effects of Amyloid. We analyze the gene expression changes downstream of Wnt that contribute to this rescue and find a protein misfolding response and a metabolic response, but the major factor we focus on is inflammation. Wnt expression reduces inflammation through repression of Toll activating factors, and chronic Toll activation reduces lifespan. We propose that the protective effect observed for lithium treatment functions at least in part through Wnt activation and inhibition of inflammation.

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Wnt Signaling Rescues Amyloid Beta-Induced Gut Stem Cell Loss.

Project description:Patients with Alzheimer's disease suffer from a decrease in brain mass and a prevalence of amyloid-β plaques. These plaques are thought to play a role in disease progression, but their exact role is not entirely established. We developed an optogenetic model to induce amyloid-β intracellular oligomerization to model distinct disease etiologies. Here, we examine the effect of Wnt signaling on amyloid in an optogenetic, Drosophila gut stem cell model. We observe that Wnt activation rescues the detrimental effects of amyloid expression and oligomerization. We analyze the gene expression changes downstream of Wnt that contribute to this rescue and find changes in aging related genes, protein misfolding, metabolism, and inflammation. We propose that Wnt expression reduces inflammation through repression of Toll activating factors. We confirm that chronic Toll activation reduces lifespan, but a decrease in the upstream activator Persephone extends it. We propose that the protective effect observed for lithium treatment functions, at least in part, through Wnt activation and the inhibition of inflammation.

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