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TMEM41B: An Evolutionarily Conserved Nexus in Thermogenic Regulation

ABSTRACT: TMEM41B: An Evolutionarily Conserved Nexus in Thermogenic Regulation

PROVIDER: PRJNA1214290 | ENA |

REPOSITORIES: ENA

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TMEM41B is a pan-flavivirus host factor

Project description:Flaviviruses pose a constant threat to human health. These RNA viruses are transmitted by the bite of infected mosquitoes and ticks and regularly cause outbreaks. To identify host factors required for flavivirus infection we performed full-genome loss of function CRISPR-Cas9 screens. Based on these results we focused our efforts on characterizing the roles that TMEM41B and VMP1 play in the virus replication cycle. Our mechanistic studies on TMEM41B revealed that all members of the Flaviviridae family that we tested require TMEM41B. We tested 12 additional virus families and found that SARS-CoV-2 of the Coronaviridae also required TMEM41B for infection. Remarkably, single nucleotide polymorphisms (SNPs) present at nearly twenty percent in East Asian populations reduce flavivirus infection. Based on our mechanistic studies we propose that TMEM41B is recruited to flavivirus RNA replication complexes to facilitate membrane curvature, which creates a protected environment for viral genome replication.

2020-11-24 | GSE162040 | GEO

A transphyletic approach to analyzing evolutionarily conserved β-catenin modules

Project description:To identify evolutionarily conserved Beta-catenin protein interactions, Beta-catenin mRNA from various metazoans was injected into Xenopus embryos and immunopurified at gastrula stage. Beta-catenin complexes were then separated on an SDS-PAGE gel and subjected mass spectrometric analysis

2023-07-08 | PXD035167 | JPOST Repository

TMEM41B is an endoplasmic reticulum Ca2+ release channel maintaining naive T cell quiescence and responsiveness

Project description:In mammalian cells, endoplasmic reticulum (ER) passively releases Ca2+ under steady state, but channels involved remain elusive. Here, we report that TMEM41B, an ER-resident membrane protein critical for autophagy, lipid metabolism, and viral infection, functions as an ER Ca2+ release channel. Biochemically, purified recombinant TMEM41B forms a concentration-dependent Ca2+ channel in single-channel electrophysiology assays. Cellularly, TMEM41B deficiency causes ER Ca2+ overload, while overexpression of TMEM41B depletes ER Ca2+. Immunologically, ER Ca2+ overload leads to upregulation of IL-2 and IL-7 receptors in naive T cells, which in turn increases basal signaling of JAK-STAT, AKT-mTOR, and MAPK pathways. This dysregulation drives TMEM41B-deficient naive T cells into a metabolically activated yet immunologically naive state. ER Ca2+ overload also downregulates CD5, lowering the activation threshold of TMEM41B-deficient T cells and leading to heightened T cell responses during infections. In summary, we identify TMEM41B as a concentration-dependent ER Ca2+ release channel, revealing an unexpected role of ER Ca2+ in naive T cell quiescence and responsiveness.

2025-03-01 | GSE285373 | GEO

An evolutionarily conserved ribosome-rescue pathway maintains epidermal homeostasis

Project description:An evolutionarily conserved ribosome-rescue pathway maintains epidermal homeostasis

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Identification of Evolutionarily Conserved VSX2 Enhancers in Retinal Development

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Isoform-specific translational control is evolutionarily conserved in primates

Project description:Isoform-specific translational control is evolutionarily conserved in primates

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TMEM41B is a novel regulator of autophagy and lipid mobilization

Project description:Autophagy maintains cellular homeostasis by targeting damaged organelles, pathogens or misfolded protein aggregates for lysosomal degradation. The autophagic process is initiated by the formation of autophagosomes, which can selectively enclose cargo via autophagy cargo receptors. A machinery of well-characterized autophagy-related proteins orchestrate the biogenesis of autophagosomes, however, the origin of the required membranes is incompletely understood. Here, we applied sensitized pooled CRISPR screens and identified the uncharacterized transmembrane protein TMEM41B as a novel regulator of autophagy. In the absence of TMEM41B, autophagosome biogenesis is stalled, LC3 accumulates at WIPI2- and DFCP1-positive isolation membranes, and lysosomal flux of autophagy cargo receptors and intracellular bacteria is impaired. In addition to defective autophagy, we found that TMEM41B knockout cells display significantly enlarged lipid droplets and reduced mobilization and β-oxidation of fatty acids. TMEM41B localizes to the endoplasmic reticulum (ER) and interacts with SIGMAR1, a chaperone which regulates calcium and lipid transfer at ER contact sites with mitochondria and lipid droplets. Taken together, we propose that TMEM41B is a novel regulator of autophagosome biogenesis and ER lipid mobilization.

2018-08-20 | PXD010207 | Pride

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Successful axonal regeneration is driven by evolutionarily conserved metabolic reprogramming

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