Evidence map›Paper›PMID 28155855›Full record

ArticleNature communications2017

Evolution of Shh endoderm enhancers during morphological transition from ventral lungs to dorsal gas bladder.

Tomoko Sagai, Takanori Amano, Akiteru Maeno, Tetsuaki Kimura, Masatoshi Nakamoto, Yusuke Takehana, Kiyoshi Naruse, Norihiro Okada, Hiroshi Kiyonari, Toshihiko Shiroishi

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Enhancer adoption caused by genomic insertion elicits interdigitalProceedings of the National Academy of Sciences of the United States of America · 2018
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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

10 authors at 4 institutions in 2 countries.

Tomoko SagaiMammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan.
Takanori AmanoMammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan.
Akiteru MaenoMammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan.
Tetsuaki KimuraInteruniversity Bio-Backup Project Center, National Institute for Basic Biology, Okazaki, Aichi 444-8585, Japan.
Masatoshi NakamotoInteruniversity Bio-Backup Project Center, National Institute for Basic Biology, Okazaki, Aichi 444-8585, Japan.
Yusuke TakehanaInteruniversity Bio-Backup Project Center, National Institute for Basic Biology, Okazaki, Aichi 444-8585, Japan.
Kiyoshi NaruseInteruniversity Bio-Backup Project Center, National Institute for Basic Biology, Okazaki, Aichi 444-8585, Japan.ORCID 0000-0001-9185-3495
Norihiro OkadaDepartment of Life Sciences, National Cheng Kung University, Tainan 701, Taiwan.
Hiroshi KiyonariLaboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology (CDB), Kobe, Hyogo 650-0047, Japan.
Toshihiko ShiroishiMammalian Genetics Laboratory, Genetic Strains Research Center, National Institute of Genetics, Mishima, Shizuoka 411-8540, Japan.
National Institute for Basic Biology · JPNational Institute of Genetics · JPGenetic Resources Center · JPNational Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shh signalling plays a crucial role for endoderm development. A Shh endoderm enhancer, MACS1, is well conserved across terrestrial animals with lungs. Here, we first show that eliminating mouse MACS1 causes severe defects in laryngeal development, indicating that MACS1-directed Shh signalling is indispensable for respiratory organogenesis. Extensive phylogenetic analyses revealed that MACS1 emerged prior to the divergence of cartilaginous and bony fishes, and even euteleost fishes have a MACS1 orthologue. Meanwhile, ray-finned fishes evolved a novel conserved non-coding sequence in the neighbouring region. Transgenic assays showed that MACS1 drives reporter expression ventrally in laryngeal epithelium. This activity has been lost in the euteleost lineage, and instead, the conserved non-coding sequence of euteleosts acquired an enhancer activity to elicit dorsal epithelial expression in the posterior pharynx and oesophagus. These results implicate that evolution of these two enhancers is relevant to the morphological transition from ventral lungs to dorsal gas bladder.

Indexed as

Enhancer Elements, GeneticEvolution, MolecularAir SacsAnimalsAnimals, Genetically ModifiedBinding SitesCoenzyme A LigasesFishesForkhead Transcription FactorsGene Expression Regulation, DevelopmentalGenes, ReporterHedgehog ProteinsIntronsLarynxLungMiceAcsm1 protein, mouseCoenzyme A LigasesForkhead Transcription FactorsHedgehog ProteinsMitochondrial Proteins

Identifiers

PMID28155855
PMCPMC5296767
OpenAlexW2585085063

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.