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Exocyst protein subnetworks integrate Hippo and mTOR signaling to promote virus detection and cancer

ABSTRACT: Exocyst protein subnetworks integrate Hippo and mTOR signaling to promote virus detection and cancer

PROVIDER: PRJNA736436 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14768590.fastq.gz	Fastqsanger.gz
	SRR14768591.fastq.gz	Fastqsanger.gz
	SRR14768592.fastq.gz	Fastqsanger.gz

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Exocyst protein subnetworks integrate Hippo and mTOR signaling to promote virus detection and cancer.

Project description:The exocyst is an evolutionarily conserved protein complex that regulates vesicular trafficking and scaffolds signal transduction. Key upstream components of the exocyst include monomeric RAL GTPases, which help mount cell-autonomous responses to trophic and immunogenic signals. Here, we present a quantitative proteomics-based characterization of dynamic and signal-dependent exocyst protein interactomes. Under viral infection, an Exo84 exocyst subcomplex assembles the immune kinase Protein Kinase R (PKR) together with the Hippo kinase Macrophage Stimulating 1 (MST1). PKR phosphorylates MST1 to activate Hippo signaling and inactivate Yes Associated Protein 1 (YAP1). By contrast, a Sec5 exocyst subcomplex recruits another immune kinase, TANK binding kinase 1 (TBK1), which interacted with and activated mammalian target of rapamycin (mTOR). RALB was necessary and sufficient for induction of Hippo and mTOR signaling through parallel exocyst subcomplex engagement, supporting the cellular response to virus infection and oncogenic signaling. This study highlights RALB-exocyst signaling subcomplexes as mechanisms for the integrated engagement of Hippo and mTOR signaling in cells challenged by viral pathogens or oncogenic signaling.

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Exocyst protein subnetworks integrate Hippo and mTOR signaling to promote virus detection and cancer

Project description:We report the transcriptomic landscape of HeLa cells in reponse to immune stimulus. We use this data to identify the genes that are commonly upregulated in response to the immunogenic stimuli. The data represent RNAseq reads/abundance for the genes listed in the processed data.

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Human Hippo cancer mutation proteins TAP-LC-MS

Project description:The Hippo pathway is a commonly altered signaling pathway involved in cancer initiation and progression; however, exactly how this pathway becomes dysregulated to promote human cancer development has not been fully understood. In this study, we systematically analyzed the Hippo somatic mutations derived from human cancer genome and functionally annotated their roles in targeting the Hippo pathway. We identified a total of 85 driver missense mutations for the major Hippo pathway genes and elucidated the mechanisms by which these mutations altered their functions in the Hippo pathway. Through these analyses, we revealed zinc-finger domain (ZNF) as an integral structure required for MOB1 function, whose driver mutations promoted head and neck cancer development. Moreover, we discovered that the schwannoma/meningioma-derived NF2 driver mutations gained an oncogenic role by activating the VANGL-JNK pathway. Taken together, our study offers a rich somatic mutation resource for further investigating the Hippo pathway in human cancer, providing a molecular basis for the development of Hippo-related personalized cancer therapy.

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mTOR promotes zebrafish larvae fin regeneration through regulating macrophages activation and CaM-mTOR-dnm1l axis

Project description:To investigate the functional and mechanistic roles of mTOR in zebrafish larvae fin regeneration, we firstly examined the spatiotemporal expression of mTOR in larvae fin and established a mTOR knockout (mTOR-KO) transgenic fish line using CRISPER / Cas9 gene editing technology. Moreover, mTOR was essential for the activation of macrophages, which is a key factor in maintaining the regenerative repair process. We also demonstrated that mTOR knockdown attenuated the proliferative capacity of bud embryo cell during the regenerative phase, while cell apoptosis was not affected. RNA-sequence analysis showed changes in mitochondrial function and dnm1l was identified as the main regulatory factor during the fin regeneration stage. We further suggested that mTOR may promote mitochondrial fission to support bud embryo cell regeneration via CaM-mTOR-dnm1l axis.

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Project description:The over-activation of Hippo/YAP axis was often observed in pancreatic adenocarcinoma (PAAD), while the detailed mechanism is not totally understood. Recent studies demonstrated that the ubiquitin modification, which controlled the protein stability of YAP, played important roles in Hippo signaling and PAAD progression. In order to understand the underlying link between YAP protein stability and Hippo activity in PAAD progression, we carried out GSEA bioinformatic analysis coupled with siRNA screening and identified OTUD4 as an important effector for Hippo signaling in PAAD. OTUD4, which was highly expressed in PAAD tissue, correlated with Hippo target gene expression in PAAD tissues. Depletion of OTUD4 significantly reduced the activity of Hippo/YAP axis and hampered PAAD progression. Mechanism studies revealed that OTUD4 could interact with YAP and promote YAP K48-linked poly-ubiquitination and degradation in PAAD. In conclusion, our study identified an interesting regulation mechanism between OTUD4 and Hippo signaling in PAAD, while targeting OTUD4 could be a plausible strategy for PAAD therapy.

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