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DOI10.1073/pnas.2017636118
Endoplasmic reticulum membrane receptors of the GET pathway are conserved throughout eukaryotes
Asseck L.Y.; Mehlhorn D.G.; Monroy J.R.; Ricardi M.M.; Breuninger H.; Wallmeroth N.; Berendzen K.W.; Nowrousian M.; Xing S.; Schwappach B.; Bayer M.; Grefen C.
发表日期2021
ISSN00278424
卷号118期号:1
英文摘要Type II tail-anchored (TA) membrane proteins are involved in diverse cellular processes, including protein translocation, vesicle trafficking, and apoptosis. They are characterized by a single C-terminal transmembrane domain that mediates posttranslational targeting and insertion into the endoplasmic reticulum (ER) via the Guided-Entry of TA proteins (GET) pathway. The GET system was originally described in mammals and yeast but was recently shown to be partially conserved in other eukaryotes, such as higher plants. A newly synthesized TA protein is shielded from the cytosol by a pretargeting complex and an ATPase that delivers the protein to the ER, where membrane receptors (Get1/WRB and Get2/CAML) facilitate insertion. In the model plant Arabidopsis thaliana, most components of the pathway were identified through in silico sequence comparison, however, a functional homolog of the coreceptor Get2/CAML remained elusive. We performed immunoprecipitation- mass spectrometry analysis to detect in vivo interactors of AtGET1 and identified a membrane protein of unknown function with low sequence homology but high structural homology to both yeast Get2 and mammalian CAML. The protein localizes to the ER membrane, coexpresses with AtGET1, and binds to Arabidopsis GET pathway components. While loss-of-function lines phenocopy the stunted root hair phenotype of other Atget lines, its heterologous expression together with the coreceptor AtGET1 rescues growth defects of Δget1get2 yeast. Ectopic expression of the cytosolic, positively charged N terminus is sufficient to block TA protein insertion in vitro. Our results collectively confirm that we have identified a plant-specific GET2 in Arabidopsis, and its sequence allows the analysis of cross-kingdom pathway conservation. © 2021 National Academy of Sciences. All rights reserved.
英文关键词ER membrane; GET pathway; Root hairs; SNAREs; Tail-anchored proteins
语种英语
scopus关键词adenosine triphosphatase; membrane protein; membrane receptor; tail anchored protein; unclassified drug; amino terminal sequence; Arabidopsis thaliana; Article; computer model; controlled study; ectopic expression; endoplasmic reticulum; eukaryote; genetic conservation; guided entry of tail anchored protein pathway; heterologous expression; immunoprecipitation; in vitro study; in vivo study; mass spectrometry; nonhuman; priority journal; protein localization; protein protein interaction; protein targeting; root hair; sequence homology; structural homology
来源期刊Proceedings of the National Academy of Sciences of the United States of America
文献类型期刊论文
条目标识符http://gcip.llas.ac.cn/handle/2XKMVOVA/181142
作者单位Developmental Genetics, Centre for Plant Molecular Biology, University of Tubingen, Tubingen, 72076, Germany; Department of Molecular and Cellular Botany, Ruhr-University Bochum, Bochum, 44780, Germany; Department of Molecular Biology, University Medical Center Gottingen, Gottingen, 37073, Germany; High-Complexity Instrument Laboratory, Universidad de La Salle, Bogota, 110231, Colombia; Department of Cell Biology, Max Planck Institute for Developmental Biology, Tubingen, 72076, Germany
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Asseck L.Y.,Mehlhorn D.G.,Monroy J.R.,et al. Endoplasmic reticulum membrane receptors of the GET pathway are conserved throughout eukaryotes[J],2021,118(1).
APA Asseck L.Y..,Mehlhorn D.G..,Monroy J.R..,Ricardi M.M..,Breuninger H..,...&Grefen C..(2021).Endoplasmic reticulum membrane receptors of the GET pathway are conserved throughout eukaryotes.Proceedings of the National Academy of Sciences of the United States of America,118(1).
MLA Asseck L.Y.,et al."Endoplasmic reticulum membrane receptors of the GET pathway are conserved throughout eukaryotes".Proceedings of the National Academy of Sciences of the United States of America 118.1(2021).
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