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Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral induced cellular damage

ABSTRACT: Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral induced cellular damage

PROVIDER: PRJNA1103879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28785876.fastq.gz	Fastqsanger.gz
	SRR28785877.fastq.gz	Fastqsanger.gz
	SRR28785878.fastq.gz	Fastqsanger.gz
	SRR28785879.fastq.gz	Fastqsanger.gz
	SRR28785880.fastq.gz	Fastqsanger.gz

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Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral induced cellular damage

Project description:RNA viruses co-opt host intracellular structures to create specialized replication sites and advance infection. The response of the host to this membrane disruption is poorly understood. In this study, we explore Arabidopsis thaliana's reaction to three distinct viruses that commandeer varying cellular compartments. Our findings reveal autophagy is significantly induced within systemically infected tissues, with autophagy disruption rendering plants highly sensitive to infection. Contrary to being an antiviral defense, quantitative analyses of viral RNA and proteomes establish autophagy as a critical component of the host's tolerance mechanism. Further analysis of mitochondrial hijacking by the Turnip Crinkle Virus has shown that despite perturbing mitochondrial integrity, the virus does not trigger a typical mitophagy response. Instead, viral infection activates a distinct selective autophagy mechanism, where oligomeric metabolic enzymes moonlight as selective autophagy receptors and degrade key executors of defense and cell death. Altogether, our study reveals an autophagy-regulated metabolic rheostats that gauges cellular integrity during viral infection.

2024-07-23 | GSE264734 | GEO

HO1 activates autophagy to protect intervertebral disc degeneration

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GNPS Metabolome profiling of S cerevisiae with drugs targeting receptors and enzymes

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Overexpression of the selective autophagy receptor AtNBR1

Project description:Cargo receptors are well established elements of the selective autophagy in all eukaryotes. The NBR1-like family of such receptors is evolutionarily conserved, however plants have only one member of the family, which is a functional and structural hybrid of its two animal counterparts, p62 (SQSTM1) and NBR1. Examination of plants overexpressing NBR1 indicates that they are oversensitive to TOR inhibitors and have more autophagosomes than the parental lines. The observed changes in shoots suggested induction of ABA signalling pathway, what was further corroborated by the germination tests and the assay of ABA level. The transcriptome changes in roots, such as lower level of snoRNA and some tRNAs, suggested inhibition of ribosome biogenesis, what is supported by identification of RPS6, an important component of TOR-dependent translational control, as a novel partner of NBR1. Grant number: 2014/15/B/NZ3/04854 Grant funding source: National Science Centre (Poland) Grantee Name: Agnieszka Sirko Grant title: Upstream regulators and cellular targets of the selective autophagy cargo receptor AtNBR1 in different phases of sulfur deficiency in plants.

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A selective autophagy pathway for endocytic protein condensates

Project description:Autophagy eliminates cytoplasmic content selected by autophagy receptors, which link cargoes to the membrane bound autophagosomal ubiquitin-like protein Atg8/LC3. Here, we discover a selective autophagy pathway for protein condensates formed by endocytic proteins. In this pathway, the endocytic yeast protein Ede1 functions as a selective autophagy receptor. Distinct domains within Ede1 bind Atg8 and mediate phase separation into condensates. Both properties are necessary for an Ede1-dependent autophagy pathway for endocytic proteins, which differs from regular endocytosis, does not involve other known selective autophagy receptors, but requires the core autophagy machinery. Cryo-electron tomography of Ede1-containing condensates – at the plasma membrane and in autophagic bodies – shows a phase-separated compartment at the beginning and end of the Ede1-mediated selective autophagy pathway. Our results imply an important role of autophagy in surveillance of membraneless compartments

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Metabolome profiling of S cerevisiae with drugs targeting receptors and enzymes

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THC Protect

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HO1 activates autophagy to protect intervertebral disc degeneration

Project description:Intervertebral disc degeneration (IDD) is majorly resulted from disordered extracellular matrix (ECM) metabolism, including decreased anabolism and increased catabolism activities in the nucleus pulposus (NP) cells of discs. Pro-inflammatory cytokines such as interleukin-1β (IL-1β) are considered to be potent mediators of ECM loss. We reported previously that hemeoxygenase-1 (HO-1) inducer cobalt protoporphyrin IX (CoPP) could attenuate the ECM breakdown which induced by IL-1β, however, the underlying mechanism remains elusive. Here we found that autophagy family genes were involved in the HO-1 mediated anti-inflammatory processes in human NP cells by using high throughput RNA-Seq technique. These findings suggest that autophagy might play a role in inflammation related ECM metabolism disorder, thus offering a direction of our in-depth study and providing a framework for the searching of potential therapeutic targets in the treatment of IDD

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2022-03-03 | PXD031527 | Pride

Selective inhibitors of autophagy reveal new link between the cell cycle and autophagy and lead to discovery of novel synergistic drug combinations

Project description:Autophagy is a conserved metabolic pathway that is central to many diseases. Recently, there has been a lot of interest in targeting autophagy with small molecule inhibitors as a possible therapeutic strategy. However, many of the compounds used for autophagy are non-selective. Here, we explored the inhibition of autophagy in pancreatic cancer cells using established selective small molecule inhibitors and discovered an unexpected link between the autophagy pathway and progression through the cell cycle. RNA-Seq analysis revealed that treatments with inhibitors that have different autophagy pathway targets block cell replication and activate other metabolic pathways to compensate for the blockade in autophagy. An unbiased screen looking for known drugs that might synergize with autophagy inhibition revealed new combination treatments that might provide a blueprint for therapeutic approaches to pancreatic cancer. The drugs quizartinib and THZ1 showed a strong synergistic effect in pancreatic cells with autophagy inhibition.

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