Evidence map›Paper›PMID 26254189›Full record

ArticleDevelopmental biology2015

The V-ATPase accessory protein Atp6ap1b mediates dorsal forerunner cell proliferation and left-right asymmetry in zebrafish.

Jason J Gokey, Agnik Dasgupta, Jeffrey D Amack

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Macrophage vacuolar ATPase (v-ATPase) function controlsbioRxiv : the preprint server for biology · 2025
    Article
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  14. CDG Therapies: From Bench to Bedside.International journal of molecular sciences · 2018
    Review
  15. Cilia in vertebrate left-right patterning.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    Review
  16. Copy number variation as a genetic basis for heterotaxy and heterotaxy-spectrum congenital heart defects.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016
    Article
  17. Kupffer's vesicle size threshold for robust left-right patterning of the zebrafish embryo.Developmental dynamics : an official publication of the American Association of Anatomists · 2016
    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

3 authors at 1 institution in 1 country.

Jason J GokeyDepartment of Cell and Developmental Biology, State University of New York, Upstate Medical University, Syracuse, NY, USA.
Agnik DasguptaDepartment of Cell and Developmental Biology, State University of New York, Upstate Medical University, Syracuse, NY, USA.
Jeffrey D AmackDepartment of Cell and Developmental Biology, State University of New York, Upstate Medical University, Syracuse, NY, USA. Electronic address: amackj@upstate.edu.
SUNY Upstate Medical University · US

Funding

Regulation of Ciliated Cells that Control Cardiac LateralityR01HL095690 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI AMACK, JEFFREY D · 2009 to 2014
$1.7M
NHLBI NIH HHS R01 HL095690NHLBI NIH HHS R01HL095690
6 · The paper itself

Abstract

Asymmetric fluid flows generated by motile cilia in a transient 'organ of asymmetry' are involved in establishing the left-right (LR) body axis during embryonic development. The vacuolar-type H(+)-ATPase (V-ATPase) proton pump has been identified as an early factor in the LR pathway that functions prior to cilia, but the role(s) for V-ATPase activity are not fully understood. In the zebrafish embryo, the V-ATPase accessory protein Atp6ap1b is maternally supplied and expressed in dorsal forerunner cells (DFCs) that give rise to the ciliated organ of asymmetry called Kupffer's vesicle (KV). V-ATPase accessory proteins modulate V-ATPase activity, but little is known about their functions in development. We investigated Atp6ap1b and V-ATPase in KV development using morpholinos, mutants and pharmacological inhibitors. Depletion of both maternal and zygotic atp6ap1b expression reduced KV organ size, altered cilia length and disrupted LR patterning of the embryo. Defects in other ciliated structures-neuromasts and olfactory placodes-suggested a broad role for Atp6ap1b during development of ciliated organs. V-ATPase inhibitor treatments reduced KV size and identified a window of development in which V-ATPase activity is required for proper LR asymmetry. Interfering with Atp6ap1b or V-ATPase function reduced the rate of DFC proliferation, which resulted in fewer ciliated cells incorporating into the KV organ. Analyses of pH and subcellular V-ATPase localizations suggested Atp6ap1b functions to localize the V-ATPase to the plasma membrane where it regulates proton flux and cytoplasmic pH. These results uncover a new role for the V-ATPase accessory protein Atp6ap1b in early development to maintain the proliferation rate of precursor cells needed to construct a ciliated KV organ capable of generating LR asymmetry.

Indexed as

Body PatterningCell ProliferationAnimalsCiliaHydrogen-Ion ConcentrationProton-Translocating ATPasesZebrafishZebrafish Proteinsatp6ap1b protein, zebrafishProton-Translocating ATPasesZebrafish ProteinsDorsal forerunner cellsKupffer’s vesicleLeft–right patterningpH and ion fluxProliferationV-ATPaseZebrafish

Identifiers

PMID26254189
PMCPMC4641761
OpenAlexW1086374798

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.