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The neurotrophic factor MANF regulates autophagic flux and lysosome function to promote proteostasis in C. elegans

ABSTRACT: The neurotrophic factor MANF regulates autophagic flux and lysosome function to promote proteostasis in C. elegans

PROVIDER: PRJNA1168187 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30868807.fastq.gz	Fastqsanger.gz
	SRR30868808.fastq.gz	Fastqsanger.gz
	SRR30868809.fastq.gz	Fastqsanger.gz
	SRR30868810.fastq.gz	Fastqsanger.gz
	SRR30868811.fastq.gz	Fastqsanger.gz

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The neurotrophic factor MANF regulates autophagic flux and lysosome function to promote proteostasis in C. elegans

Project description:Mesencephalic astrocyte-derived neurotrophic factor (MANF) is the only neurotrophic factor to be conserved between C. elegans and humans. MANF is a unique neutrotophic factor, as it is a resident ER protein in cells that express it and has a role in regulating ER stress response to tunicamycin exposure and pathogenic Pseudomonas exposure. We sought to further understand the role of MANF by comparing a deletion allele, an overexpression line, and the wild-type in this RNAseq experiment.

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Colchicine Ameliorates Doxorubicin Cardiotoxicity Via Promoting Autophagic Flux

Project description:Doxorubicin (DOX) cardiotoxicity is an important factor of heart failure. The only clinically approved drug is dexrazoxane, while its side effect of secondary malignancies severely limited its application. It is urgent to find other alternative efficacious molecular for these chemotherapy patients. Colchicine is a safe and well tolerated anti-inflammation drug which also functions in attenuating the reactive oxygen species (ROS) generation. High dose of colchicine was reported block the autophagosome-lysosome fusion in cancer cells due to its destabilization effect to the microtubule system, while how colchicine affects the autophagic flux in cardiomyocytes is largely unknown. Recent years low dose of colchicine administration was reported helpful to the patients with pericarditis, postprocedural atrial fibrillation and coronary artery disease, most of the research attributed it to its anti-inflammation effect. Whether the autophagic flux regulated by colchicine also benefits to DOX induced heart failure remains unclear. Doxorubicin (DOX) administration was used to establish heart failure models in vivo and in vitro. Results showed that DOX blocked the autophagic vacuoles degradation, leading to damaged mitochondria and ROS accumulation. Heart failure characteristics were obviously improved after low dose of colchicine administration. Mechanistically, low dose of colchicine promoted the autolysosome degradation, cleared the damaged mitochondria, and ROS accumulation induced by the DOX and as a result attenuated DOX cardiotoxicity.

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Miz1 is required to maintain autophagic flux

Project description:Miz1 is required to maintain autophagic flux

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Colchicine Ameliorates Doxorubicin Cardiotoxicity Via Promoting Autophagic Flux

Project description:Colchicine Ameliorates Doxorubicin Cardiotoxicity Via Promoting Autophagic Flux

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Miz1 is required to maintain autophagic flux

Project description:Miz1 is a zinc finger protein that regulates expression of cell cycle inhibitors as part of a complex with Myc. Cell cycle-independent functions of Miz1 are poorly understood. Here, we use a Nestin-Cre transgene to delete an essential domain of Miz1 in the central nervous system (Miz1M-NM-^TPOZNes). Miz1M-NM-^TPOZNes mice display cerebellar neurodegeneration characterized by the progressive loss of Purkinje cells. Chromatin immunoprecipitation sequencing and biochemical analyses show that Miz1 activates transcription upon binding to a non-palindromic sequence present in core promoters. Target genes of Miz1 encode regulators of autophagy and proteins involved in vesicular transport that are required for autophagy. Miz1M-NM-^TPOZ neuronal progenitors and fibroblasts show reduced autophagic flux. Consistently, polyubiquitinated proteins and p62/Sqtm1 accumulate in the cerebella of Miz1M-NM-^TPOZNes mice, characteristic features of defective autophagy. Our data suggest that Miz1 may link cell growth and ribosome biogenesis to the transcriptional regulation of vesicular transport and autophagy. ChIP-Seq with H190 and G18 on an Illumina Genome Analyzer IIx.

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PIP4K2C inhibition reverses autophagic flux impairment induced by SARS-CoV-2

Project description:In search for broad-spectrum antivirals, we discovered a small molecule inhibitor, RMC-113, that potently suppresses the replication of multiple RNA viruses including SARS-CoV-2 in human lung organoids. We demonstrated selective dual inhibition of the lipid kinases PIP4K2C and PIKfyve by RMC-113 and target engagement by its clickable analog. Advanced lipidomics revealed alteration of SARS-CoV-2-induced phosphoinositide signature by RMC-113 and linked its antiviral effect with functional PIP4K2C and PIKfyve inhibition. We discovered PIP4K2C’s roles in SARS-CoV-2 entry, RNA replication, and assembly/egress, validating it as a druggable antiviral target. Integrating proteomics, single-cell transcriptomics, and functional assays revealed that PIP4K2C regulates virus-induced impairment of autophagic flux. Reversing this autophagic flux impairment via promoting degradation of viral protein is a mechanism of antiviral action of RMC-113. These findings reveal virus-induced autophagy regulation via PIP4K2C, an understudied kinase, and propose dual inhibition of PIP4K2C and PIKfyve as a candidate strategy to combat emerging viruses.

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PIP4K2C inhibition reverses autophagic flux impairment induced by SARS-CoV-2

Project description:PIP4K2C inhibition reverses autophagic flux impairment induced by SARS-CoV-2

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Monitoring Autophagic Flux in vivo Revealed its Physiological Response and Significance of Heterogeneity in Pancreatic Beta Cells

Project description:Autophagy plays an important role in preserving cellular homeostasis in pancreatic beta cells. However, the extent of autophagic flux induced in various physiological settings in vivo is unclear. In this study, we generated transgenic mice expressing pHluorin-LC3-mCherry reporter for monitoring systemic autophagic flux. Our findings revealed that autophagic flux in pancreatic islets enhanced after starvation, although suppression of the flux after short-term refeeding needs more prolonged restarvation in islets than in liver and skeletal muscle. Furthermore, heterogeneity of autophagic flux in beta cells manifested after increasing insulin resistance and intracellular calcium influx by glucose stimulation increased more in high- than low-flux beta cells, with differential gene expression based on the flux. Thus, our monitor mouse enables us to reveal physiological response and biological insight of heterogeneity in autophagic flux in pancreatic beta cells.

2023-03-15 | PXD036390 | JPOST Repository

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