ArticleMolecular biology of the cell2014
ER-associated retrograde SNAREs and the Dsl1 complex mediate an alternative, Sey1p-independent homotypic ER fusion pathway.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Structure of a membrane tethering complex incorporating multiple SNAREs.Nature structural & molecular biology · 2024Article
- Evolution of factors shaping the endoplasmic reticulum.Traffic (Copenhagen, Denmark) · 2022Article
- Sticking With It: ER-PM Membrane Contact Sites as a Coordinating Nexus for Regulating Lipids and Proteins at the Cell Cortex.Frontiers in cell and developmental biology · 2020Review
- Roles of singleton tryptophan motifs in COPI coat stability and vesicle tethering.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Comparative genomics of nuclear envelope proteins.BMC genomics · 2018Article
- Fat storage-inducing transmembrane (FIT or FITM) proteins are related to lipid phosphatase/phosphotransferase enzymes.Microbial cell (Graz, Austria) · 2017Article
- Influence of the bud neck on nuclear envelope fission in Saccharomyces cerevisiae.Experimental cell research · 2017Article
- DnaJ/Hsc70 chaperone complexes control the extracellular release of neurodegenerative-associated proteins.The EMBO journal · 2016Article
- Physiological lipid composition is vital for homotypic ER membrane fusion mediated by the dynamin-related GTPase Sey1p.Scientific reports · 2016Article
- Structural basis for the binding of tryptophan-based motifs by δ-COP.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- SNAREs support atlastin-mediated homotypic ER fusion in Saccharomyces cerevisiae.The Journal of cell biology · 2015Article
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5 authors.
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Abstract
The peripheral endoplasmic reticulum (ER) network is dynamically maintained by homotypic (ER-ER) fusion. In Saccharomyces cerevisiae, the dynamin-like GTPase Sey1p can mediate ER-ER fusion, but sey1Δ cells have no growth defect and only slightly perturbed ER structure. Recent work suggested that ER-localized soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) mediate a Sey1p-independent ER-ER fusion pathway. However, an alternative explanation--that the observed phenotypes arose from perturbed vesicle trafficking--could not be ruled out. In this study, we used candidate and synthetic genetic array (SGA) approaches to more fully characterize SNARE-mediated ER-ER fusion. We found that Dsl1 complex mutations in sey1Δ cells cause strong synthetic growth and ER structure defects and delayed ER-ER fusion in vivo, additionally implicating the Dsl1 complex in SNARE-mediated ER-ER fusion. In contrast, cytosolic coat protein I (COPI) vesicle coat mutations in sey1Δ cells caused no synthetic defects, excluding perturbed retrograde trafficking as a cause for the previously observed synthetic defects. Finally, deleting the reticulons that help maintain ER architecture in cells disrupted for both ER-ER fusion pathways caused almost complete inviability. We conclude that the ER SNAREs and the Dsl1 complex directly mediate Sey1p-independent ER-ER fusion and that, in the absence of both pathways, cell viability depends upon membrane curvature-promoting reticulons.
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