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Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Keratinocytes ssRNA-Seq]

ABSTRACT: Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Keratinocytes ssRNA-Seq]

PROVIDER: PRJNA419517 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6315890.fastq.gz	Fastqsanger.gz
	SRR6315888.fastq.gz	Fastqsanger.gz
	SRR6315889.fastq.gz	Fastqsanger.gz

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Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Epidermis ssRNA-Seq]

Project description:Arp2/3 complex assembles branched actin filaments key to many cellular processes, but its organismal roles remain poorly understood. Here we employed conditional arpc4 knockout mice to study the function of the Arp2/3 complex in the epidermis.We found that depletion of the Arp2/3 complex by knockout of arpc4 results in skin abnormalities at birth that evolve into a severe psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2. Knockout of arpc4 in cultured keratinocytes was sufficient to induce nuclear accumulation of Nrf2, upregulation of Nrf2-target genes and decreased filamentous actin levels. Furthermore, pharmacological inhibition of the Arp2/3 complex unmasked the role of branched actin filaments in Nrf2 regulation. Consistently, we unveiled that Nrf2 associates with the actin cytoskeleton in cells and binds to filamentous actin in vitro Finally, we discovered that Arpc4 is downregulated in both human and mouse psoriatic epidermis. Thus, the Arp2/3 complex affects keratinocytes' shape and transcriptome through an actin-based cell-autonomous mechanism that influences epidermal morphogenesis and homeostasis.

2017-11-23 | GSE107265 | GEO

Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Keratinocytes ssRNA-Seq]

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Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Epidermis ssRNA-Seq]

Project description:Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2 [Epidermis ssRNA-Seq]

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Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2

Project description:Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2

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Knockout of the Arp2/3 complex in epidermis causes a psoriasis-like disease hallmarked by hyperactivation of transcription factor Nrf2

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Project description:Microglia are the major brain-resident immune cell subsetthat areessential during pathology and physiology in the central nervous system. The regulation of functional elementsrequired for microglialhomeostasis needsto be precisely orchestrated.To date, the underlying mechanismshave not been fully investigated. Here,we show that actin network dynamics mediated by the Arp2/3 complex play a crucial role in microglial cell function. Upon interruption of Arp2/3 complex integrity in the conditional knockoutmouse model, we found significant alterations in microglial cell morphology, motility, and chemotaxisfunction.Transcriptomics analysis revealedthat Arp2/3-deficient microglia downregulatehomeostatic signature and upregulatecell activationthat isassociated with APOE induction, Ms4a7upregulation,and TGFsignaling impairment. In vitrostudies confirm that the Arp2/3 downstream actin-related molecules are required for mediating the TGFsignaling pathway in microglia. Our resultsshow that the Arp2/3complexis required for microglia cell dynamics and plays a key role in maintaining microglial cell homeostasis by regulating the TGF-β signaling.

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