Evidence map›Paper›PMID 23353550›Full record

ArticleDevelopmental biology2013

Loss of ascl1a prevents secretory cell differentiation within the zebrafish intestinal epithelium resulting in a loss of distal intestinal motility.

Gillian Roach, Rachel Heath Wallace, Amy Cameron, Rifat Emrah Ozel, Cintia F Hongay, Reshica Baral, Silvana Andreescu, Kenneth N Wallace

Abstract read
In one paragraph

Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  5. Developmental regulation of intestinalbioRxiv : the preprint server for biology · 2025
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  20. Type II NaPflugers Archiv : European journal of physiology · 2019
    Review
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 1 institution in 1 country.

Gillian RoachDepartment of Biology, Clarkson University, 8 Clarkson Ave., Potsdam, NY 13699, USA.
Rachel Heath Wallace
Amy Cameron
Rifat Emrah Ozel
Cintia F Hongay
Reshica Baral
Silvana Andreescu
Kenneth N Wallace
Clarkson University · US

Funding

Development and Functional Analysis of Components of the Zebrafish Serotonin SignR15DK089474 · NIDDK · CLARKSON UNIVERSITY · PI WALLACE, KENNETH N · 2010 to 2012
$470k
NIDDK NIH HHS 1R15DK089474-01NIDDK NIH HHS R15 DK089474
6 · The paper itself

Abstract

The vertebrate intestinal epithelium is renewed continuously from stem cells at the base of the crypt in mammals or base of the fold in fish over the life of the organism. As stem cells divide, newly formed epithelial cells make an initial choice between a secretory or enterocyte fate. This choice has previously been demonstrated to involve Notch signaling as well as Atonal and Her transcription factors in both embryogenesis and adults. Here, we demonstrate that in contrast to the atoh1 in mammals, ascl1a is responsible for formation of secretory cells in zebrafish. ascl1a-/- embryos lack all intestinal epithelial secretory cells and instead differentiate into enterocytes. ascl1a-/- embryos also fail to induce intestinal epithelial expression of deltaD suggesting that ascl1a plays a role in initiation of Notch signaling. Inhibition of Notch signaling increases the number of ascl1a and deltaD expressing intestinal epithelial cells as well as the number of developing secretory cells during two specific time periods: between 30 and 34hpf and again between 64 and 74hpf. Loss of enteroendocrine products results in loss of anterograde motility in ascl1a-/- embryos. 5HT produced by enterochromaffin cells is critical in motility and secretion within the intestine. We find that addition of exogenous 5HT to ascl1a-/- embryos at near physiological levels (measured by differential pulse voltammetry) induce anterograde motility at similar levels to wild type velocity, distance, and frequency. Removal or doubling the concentration of 5HT in WT embryos does not significantly affect anterograde motility, suggesting that the loss of additional enteroendocrine products in ascl1a-/- embryos also contributes to intestinal motility. Thus, zebrafish intestinal epithelial cells appear to have a common secretory progenitor from which all subtypes form. Loss of enteroendocrine cells reveals the critical need for enteroendocrine products in maintenance of normal intestinal motility.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationCell LineageEnterochromaffin CellsEnterocytesEpithelial CellsGastrointestinal MotilityGene Expression Regulation, DevelopmentalGoblet CellsIntestinesModels, BiologicalModels, GeneticMutationSignal TransductionTranscription FactorsAscl1a protein, zebrafishBasic Helix-Loop-Helix ProteinsTranscription FactorsZebrafish Proteins

Identifiers

PMID23353550
PMCPMC3636723
OpenAlexW2092458252

What OpenQuestion holds

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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.