ArticleCell cycle (Georgetown, Tex.)2016
Loss of all 3 Extended Synaptotagmins does not affect normal mouse development, viability or fertility.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Stay in touch with the endoplasmic reticulum.Science China. Life sciences · 2024Pooled it
- MCTP1 and MCTP2 promote ER-PM contact sites and regulate PI4P homeostasis and cell migration.Molecular biology of the cell · 2026Article
- Sphingosine-1-phosphate signalling activates E-Syt1 to facilitate HDL-derived cholesterol transport.Nature cell biology · 2025Article
- ER-plasma membrane contact sites deliver ER lipids and proteins for rapid cell surface expansion.The Journal of cell biology · 2024Article
- The Endoplasmic Reticulum and Its Contacts: Emerging Roles in Axon Development, Neurotransmission, and Degeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Article
- ESYT1 tethers the ER to mitochondria and is required for mitochondrial lipid and calcium homeostasis.Life science alliance · 2024Article
- Extended-Synaptotagmin-1 and -2 control T cell signaling and function.EMBO reports · 2024Article
- The role of extended synaptotagmin at membrane contact sites in cancer research.Frontiers in cell and developmental biology · 2023Review
- Tricalbin proteins regulate plasma membrane phospholipid homeostasis.Life science alliance · 2022Article
- INPP5K and Atlastin-1 maintain the nonuniform distribution of ER-plasma membrane contacts in neurons.Life science alliance · 2021Article
- Structural studies of the shortest extended synaptotagmin with only two C2 domains fromiScience · 2021Article
- Endoplasmic Reticulum-Plasma Membrane Contact Sites: Regulators, Mechanisms, and Physiological Functions.Frontiers in cell and developmental biology · 2021Review
- Extended synaptotagmin regulates membrane contact site structure and lipid transfer function in vivo.EMBO reports · 2020Article
- Hypothalamic extended synaptotagmin-3 contributes to the development of dietary obesity and related metabolic disorders.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- 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
- Tricalbins Contribute to Cellular Lipid Flux and Form Curved ER-PM Contacts that Are Bridged by Rod-Shaped Structures.Developmental cell · 2019Article
- Tricalbin-Mediated Contact Sites Control ER Curvature to Maintain Plasma Membrane Integrity.Developmental cell · 2019Article
- Recent insights into mammalian ER-PM junctions.Current opinion in cell biology · 2019Review
- Phospholipid transport protein function at organelle contact sites.Current opinion in cell biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extended synaptotagmins, E-Syt1, 2 and 3, are multiple C2 domain membrane proteins that are tethered to the endoplasmic reticulum and interact in a calcium dependent manner with plasma membrane phospholipids to form endoplasmic reticulum - plasma membrane junctions. These junctions have been implicated in the exchange of phospholipids between the 2 organelles. The E-Syts have further been implicated in receptor signaling and endocytosis and can interact directly with fibroblast growth factor and other cell surface receptors. Despite these multiple functions, the search for a requirement in vivo has been elusive. Most recently, we found that the genes for E-Syt2 and 3 could be inactivated without effect on mouse development, viability, fertility or morphology. We have now created insertion and deletion mutations in the last of the mouse E-Syt genes. We show that E-Syt1 is specifically expressed throughout the embryonic skeleton during the early stages of chrondrogenesis in a pattern quite distinct from that of E-Syt2 or 3. Despite this, E-Syt1 is also not required for mouse development and propagation. We further show that even the combined inactivation of all 3 E-Syt genes has no effect on mouse viability or fertility in the laboratory. However, this inactivation induces an enhancement in the expression of the genes encoding Orp5/8, Orai1, STIM1 and TMEM110, endoplasmic reticulum - plasma membrane junction proteins that potentially could compensate for E-Syt loss. Given the multiple functions suggested for the E-Syts and their evolutionary conservation, our unexpected findings suggest that they may only provide a survival advantage under specific conditions that have as yet to be identified.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.