Evidence map›Paper›PMID 35410466›Full record

ArticleNature communications2022

Multidimensional chromatin profiling of zebrafish pancreas to uncover and investigate disease-relevant enhancers.

Renata Bordeira-Carriço, Joana Teixeira, Marta Duque, Mafalda Galhardo, Diogo Ribeiro, Rafael D Acemel, Panos N Firbas, Juan J Tena, Ana Eufrásio, Joana Marques and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

3 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

15 authors at 2 institutions in 2 countries.

Renata Bordeira-Carriço *Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.
Joana Teixeira *Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.ORCID http://orcid.org/0000-0003-3605-3035
Marta Duque *Instituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.
Mafalda GalhardoInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.ORCID http://orcid.org/0000-0001-8911-1660
Diogo RibeiroInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.
Rafael D AcemelCentro Andaluz de Biología del Desarrollo (CABD), Universidad Pablo de Olavide, Sevilla, 41013, Spain.
Panos N FirbasCentro Andaluz de Biología del Desarrollo (CABD), Universidad Pablo de Olavide, Sevilla, 41013, Spain.
Juan J TenaCentro Andaluz de Biología del Desarrollo (CABD), Universidad Pablo de Olavide, Sevilla, 41013, Spain.ORCID http://orcid.org/0000-0001-8165-7984
Ana EufrásioInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.
Joana MarquesInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.
Fábio J FerreiraInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.ORCID http://orcid.org/0000-0001-9958-9238
Telmo FreitasInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal.
Fátima CarneiroDepartamento de Patologia, Faculdade de Medicina da Universidade do Porto (FMUP), Porto, 4200-319, Portugal.ORCID http://orcid.org/0000-0002-1964-1006
José Luís Goméz-SkarmetaCentro Andaluz de Biología del Desarrollo (CABD), Universidad Pablo de Olavide, Sevilla, 41013, Spain.
José BessaInstituto de Biologia Molecular e Celular (IBMC), Universidade do Porto, Porto, 4200-135, Portugal. jose.bessa@ibmc.up.pt.ORCID http://orcid.org/0000-0002-8591-7138
Universidade do Porto · PTCentro Andaluz de Biología del Desarrollo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pancreas is a central organ for human diseases. Most alleles uncovered by genome-wide association studies of pancreatic dysfunction traits overlap with non-coding sequences of DNA. Many contain epigenetic marks of cis-regulatory elements active in pancreatic cells, suggesting that alterations in these sequences contribute to pancreatic diseases. Animal models greatly help to understand the role of non-coding alterations in disease. However, interspecies identification of equivalent cis-regulatory elements faces fundamental challenges, including lack of sequence conservation. Here we combine epigenetic assays with reporter assays in zebrafish and human pancreatic cells to identify interspecies functionally equivalent cis-regulatory elements, regardless of sequence conservation. Among other potential disease-relevant enhancers, we identify a zebrafish ptf1a distal-enhancer whose deletion causes pancreatic agenesis, a phenotype previously found to be induced by mutations in a distal-enhancer of PTF1A in humans, further supporting the causality of this condition in vivo. This approach helps to uncover interspecies functionally equivalent cis-regulatory elements and their potential role in human disease.

Indexed as

Enhancer Elements, GeneticZebrafishAnimalsChromatinGenome-Wide Association StudyPancreasChromatin

Identifiers

PMID35410466
PMCPMC9001708
OpenAlexW4223449479

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.