Evidence map›Paper›PMID 34019822›Full record

ArticleCurrent biology : CB2021

Vmp1, Vps13D, and Marf/Mfn2 function in a conserved pathway to regulate mitochondria and ER contact in development and disease.

James L Shen, Tina M Fortier, Yan G Zhao, Ruoxi Wang, Margit Burmeister, Eric H Baehrecke

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-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

26 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. A nerve-wracking buzz: lessons fromFrontiers in aging neuroscience · 2023
    Review
  15. Article
  16. Review
  17. In situ architecture of the lipid transport protein VPS13C at ER-lysosome membrane contacts.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

James L ShenDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Tina M FortierDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Yan G ZhaoDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Ruoxi WangDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Margit BurmeisterMichigan Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USA; Department of Computational Medicine & Bioinformatics, University of Michigan, Ann Arbor, MI 48109, USA.
Eric H BaehreckeDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: eric.baehrecke@umassmed.edu.
University of Massachusetts Chan Medical School · USUniversity of Michigan · US

Funding

Regulation of autophagy during animal developmentR35GM131689 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Eric H Baehrecke · 2019 to 2026
$4.9M
Discovery of a novel role of VPS13D in AutophagyF30CA239374 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHEN, JAMES L · 2019 to 2023
$140k
NCI NIH HHS F30 CA239374NIGMS NIH HHS R35 GM131689
6 · The paper itself

Abstract

Mutations in Vps13D cause defects in autophagy, clearance of mitochondria, and human movement disorders. Here, we discover that Vps13D functions in a pathway downstream of Vmp1 and upstream of Marf/Mfn2. Like vps13d, vmp1 mutant cells exhibit defects in autophagy, mitochondrial size, and clearance. Through the relationship between vmp1 and vps13d, we reveal a novel role for Vps13D in the regulation of mitochondria and endoplasmic reticulum (ER) contact. Significantly, the function of Vps13D in mitochondria and ER contact is conserved between fly and human cells, including fibroblasts derived from patients suffering from VPS13D mutation-associated neurological symptoms. vps13d mutants have increased levels of Marf/MFN2, a regulator of mitochondrial fusion. Importantly, loss of marf/MFN2 suppresses vps13d mutant phenotypes, including mitochondria and ER contact. These findings indicate that Vps13d functions at a regulatory point between mitochondria and ER contact, mitochondrial fusion and autophagy, and help to explain how Vps13D contributes to disease.

Indexed as

Endoplasmic ReticulumMitochondriaAutophagyGTP PhosphohydrolasesHumansMembrane ProteinsMitochondrial DynamicsMitochondrial ProteinsMitochondrial SizeProteinsGTP PhosphohydrolasesMembrane ProteinsMFN2 protein, humanMitochondrial ProteinsProteinsVMP1 protein, humanVPS13D protein, humanautophagyDrosophilamembrane contactmitochondriaVmp1Vps13D

Identifiers

PMID34019822
PMCPMC8319081
OpenAlexW3161052958

What OpenQuestion holds

Textmetadata
LicenceTDM
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.