Evidence map›Paper›PMID 31830033›Full record

ArticlePLoS genetics2019

Coacting enhancers can have complementary functions within gene regulatory networks and promote canalization.

Leslie Dunipace, Zsuzsa Ákos, Angelike Stathopoulos

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

  1. Temporal loss ofGenes & development · 2026
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  16. Enhancer redundancy in development and disease.Nature reviews. Genetics · 2021
    Review
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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.

Leslie DunipaceCalifornia Institute of Technology, Pasadena, CA, United States of America.ORCID 0000-0002-1739-6537
Zsuzsa ÁkosCalifornia Institute of Technology, Pasadena, CA, United States of America.
Angelike StathopoulosCalifornia Institute of Technology, Pasadena, CA, United States of America.ORCID 0000-0001-6597-2036
California Institute of Technology · US

Funding

Temporal control of cell patterning, signaling, and movement in early embryosR35GM118146 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI STATHOPOULOS, ANGELIKE · 2016 to 2025
$5.8M
NIGMS NIH HHS R35 GM118146
6 · The paper itself

Abstract

Developmental genes are often regulated by multiple enhancers exhibiting similar spatiotemporal outputs, which are generally considered redundantly acting though few have been studied functionally. Using CRISPR-Cas9, we created deletions of two enhancers, brk5' and brk3', that drive similar but not identical expression of the gene brinker (brk) in early Drosophila embryos. Utilizing both in situ hybridization and quantitative mRNA analysis, we investigated the changes in the gene network state caused by the removal of one or both of the early acting enhancers. brk5' deletion generally phenocopied the gene mutant, including expansion of the BMP ligand decapentaplegic (dpp) as well as inducing variability in amnioserosa tissue cell number suggesting a loss of canalization. In contrast, brk3' deletion presented unique phenotypes including dorsal expansion of several ventrally expressed genes and a decrease in amnioserosa cell number. Similarly, deletions were made for two enhancers associated with the gene short-gastrulation (sog), sog.int and sog.dist, demonstrating that they also exhibit distinct patterning phenotypes and affect canalization. In summary, this study shows that similar gene expression driven by coacting enhancers can support distinct, and sometimes complementary, functions within gene regulatory networks and, moreover, that phenotypes associated with individual enhancer deletion mutants can provide insight into new gene functions.

Indexed as

Gene Regulatory NetworksAnimalsBody PatterningCRISPR-Cas SystemsDrosophilaDrosophila ProteinsEnhancer Elements, GeneticGene Expression ProfilingGene Expression Regulation, DevelopmentalPhenotypeRepressor ProteinsSequence Deletionbrk protein, DrosophilaDrosophila ProteinsRepressor Proteinssog protein, Drosophila

Identifiers

PMID31830033
PMCPMC6932828
OpenAlexW2996507128

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.