Evidence map›Paper›PMID 29216297›Full record

ArticlePloS one2017

Skn-1a/Pou2f3 functions as a master regulator to generate Trpm5-expressing chemosensory cells in mice.

Junpei Yamashita, Makoto Ohmoto, Tatsuya Yamaguchi, Ichiro Matsumoto, Junji Hirota

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
–field-weighted citation impact
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

103 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Influenza-induced tuft cell expansion alters ILC-mediated inflammation.bioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Tuft Cells in the Gut Limit Cognitive Disorders by Regulating Gut Homeostasis.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

43 more citing papers are in PubMed but not listed here.

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

5 authors.

Junpei YamashitaDepartment of Life Science and Technology, Graduate School of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Makoto OhmotoMonell Chemical Senses Center, Philadelphia, United States of America.
Tatsuya YamaguchiDepartment of Life Science and Technology, Graduate School of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.
Ichiro MatsumotoMonell Chemical Senses Center, Philadelphia, United States of America.
Junji HirotaDepartment of Life Science and Technology, Graduate School of Life Science and Technology, Tokyo Institute of Technology, Yokohama, Japan.ORCID http://orcid.org/0000-0002-5741-0655

Funding

Roles of Ascl1 for generation and differentiation of taste cellsR01DC015491 · NIDCD · MONELL CHEMICAL SENSES CENTER · PI MATSUMOTO, ICHIRO · 2016 to 2020
$1.6M
NIDCD NIH HHS R01 DC015491
6 · The paper itself

Abstract

Transient receptor potential channel M5 (Trpm5)-expressing cells, such as sweet, umami, and bitter taste cells in the oropharyngeal epithelium, solitary chemosensory cells in the nasal respiratory epithelium, and tuft cells in the small intestine, that express taste-related genes function as chemosensory cells. Previous studies demonstrated that Skn-1a/Pou2f3, a POU homeodomain transcription factor is expressed in these Trpm5-expressing chemosensory cells, and is necessary for their generation. Trpm5-expressing cells have recently been found in trachea, auditory tube, urethra, thymus, pancreatic duct, stomach, and large intestine. They are considered to be involved in protective responses to potential hazardous compounds as Skn-1a-dependent bitter taste cells, respiratory solitary chemosensory cells, and intestinal tuft cells are. In this study, we examined the expression and function of Skn-1a/Pou2f3 in Trpm5-expressing cells in trachea, auditory tube, urethra, thymus, pancreatic duct, stomach, and large intestine. Skn-1a/Pou2f3 is expressed in a majority of Trpm5-expressing cells in all tissues examined. In Skn-1a/Pou2f3-deficient mice, the expression of Trpm5 as well as marker genes for Trpm5-expressing cells were absent in all tested tissues. Immunohistochemical analyses demonstrated that two types of microvillous cells exist in trachea, urethra, and thymus, Trpm5-positive and Trpm5-negative cells. In Skn-1a/Pou2f3-deficient mice, a considerable proportion of Trpm5-negative and villin-positive microvillous cells remained present in these tissues. Thus, we propose that Skn-1a/Pou2f3 is the master regulator for the generation of the Trpm5-expressing microvillous cells in multiple tissues.

Indexed as

AnimalsDigestive SystemFemaleMaleMiceMice, Inbred C57BLMice, KnockoutOctamer Transcription FactorsTracheaTRPM Cation ChannelsOctamer Transcription FactorsPou2f3 protein, mouseTrpm5 protein, mouseTRPM Cation Channels

Identifiers

PMID29216297
PMCPMC5720759

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Registered trials

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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.