Evidence map›Paper›PMID 27492621›Full record

ArticleNature communications2016

Sec16 alternative splicing dynamically controls COPII transport efficiency.

Ilka Wilhelmi, Regina Kanski, Alexander Neumann, Olga Herdt, Florian Hoff, Ralf Jacob, Marco Preußner, Florian Heyd

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. ER exit in physiology and disease.Frontiers in molecular biosciences · 2024
    Review
  6. Article
  7. Article
  8. Frontiers in immunology · 2022
    Article
  9. Article
  10. Enriched Alternative Splicing in Islets of Diabetes-Susceptible Mice.International journal of molecular sciences · 2021
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Ilka WilhelmiDepartment of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Institute of Chemistry and Biochemistry, Laboratory of RNA Biochemistry, Takustrasse 6, 14195 Berlin, Germany.
Regina KanskiDepartment of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Institute of Chemistry and Biochemistry, Laboratory of RNA Biochemistry, Takustrasse 6, 14195 Berlin, Germany.
Alexander NeumannDepartment of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Institute of Chemistry and Biochemistry, Laboratory of RNA Biochemistry, Takustrasse 6, 14195 Berlin, Germany.
Olga HerdtDepartment of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Institute of Chemistry and Biochemistry, Laboratory of RNA Biochemistry, Takustrasse 6, 14195 Berlin, Germany.
Florian HoffDepartment of Cell Biology and Cell Pathology, Philipps-University Marburg, Robert Koch Strae 6, 35037 Marburg, Germany.
Ralf JacobDepartment of Cell Biology and Cell Pathology, Philipps-University Marburg, Robert Koch Strae 6, 35037 Marburg, Germany.
Marco PreußnerDepartment of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Institute of Chemistry and Biochemistry, Laboratory of RNA Biochemistry, Takustrasse 6, 14195 Berlin, Germany.
Florian HeydDepartment of Biology, Chemistry, Pharmacy, Freie Universität Berlin, Institute of Chemistry and Biochemistry, Laboratory of RNA Biochemistry, Takustrasse 6, 14195 Berlin, Germany.
Freie Universität Berlin · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transport of secretory proteins from the endoplasmic reticulum (ER) to the Golgi depends on COPII-coated vesicles. While the basic principles of the COPII machinery have been identified, it remains largely unknown how COPII transport is regulated to accommodate tissue- or activation-specific differences in cargo load and identity. Here we show that activation-induced alternative splicing of Sec16 controls adaptation of COPII transport to increased secretory cargo upon T-cell activation. Using splice-site blocking morpholinos and CRISPR/Cas9-mediated genome engineering, we show that the number of ER exit sites, COPII dynamics and transport efficiency depend on Sec16 alternative splicing. As the mechanistic basis, we suggest the C-terminal Sec16 domain to be a splicing-controlled protein interaction platform, with individual isoforms showing differential abilities to recruit COPII components. Our work connects the COPII pathway with alternative splicing, adding a new regulatory layer to protein secretion and its adaptation to changing cellular environments.

Indexed as

Alternative SplicingBiological TransportClustered Regularly Interspaced Short Palindromic RepeatsCOP-Coated VesiclesEndoplasmic ReticulumExonsGolgi ApparatusHEK293 CellsHeLa CellsHumansProtein IsoformsProtein TransportT-LymphocytesVesicular Transport ProteinsProtein IsoformsSEC16A protein, humanVesicular Transport Proteins

Identifiers

PMID27492621
PMCPMC4980449
OpenAlexW2488214542

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.