Evidence map›Paper›PMID 27611740›Full record

ArticleScientific reports2016

Molecular mechanism of male differentiation is conserved in the SRY-absent mammal, Tokudaia osimensis.

Tomofumi Otake, Asato Kuroiwa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. 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
4.8field-weighted citation impact, top 5% 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, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Turnover of mammal sex chromosomes in theProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Review
  6. Article
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  8. Article
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  11. Review
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  14. AAsian journal of andrology
    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

2 authors at 1 institution in 1 country.

Tomofumi OtakeFunctional Genome Science Biosystems Science Course, Graduate School of Life Science, Hokkaido University, Kita 10 Nishi 8, Kita-ku, Sapporo, Hokkaido 060-0810, Japan.
Asato KuroiwaFunctional Genome Science Biosystems Science Course, Graduate School of Life Science, Hokkaido University, Kita 10 Nishi 8, Kita-ku, Sapporo, Hokkaido 060-0810, Japan.
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The sex-determining gene SRY induces SOX9 expression in the testes of eutherian mammals via two pathways. SRY binds to testis-specific enhancer of Sox9 (TESCO) with SF1 to activate SOX9 transcription. SRY also up-regulates ER71 expression, and ER71 activates Sox9 transcription. After the initiation of testis differentiation, SOX9 enhances Amh expression by binding to its promoter with SF1. SOX8, SOX9 and SOX10, members of the SOXE gene family, also enhance the activities of the Amh promoter and TESCO. In this study, we investigated the regulation of these sexual differentiation genes in Tokudaia osimensis, which lacks a Y chromosome and the SRY gene. The activity of the AMH promoter was stimulated by SOXE genes and SF1. Mutant AMH promoters, with mutations in its SOX and SF1 binding sites, did not show significant activity by SOX9 and SF1. These results indicate that AMH expression was regulated by the binding of SOX9 and SF1. By contrast, SOXE genes could not enhance TESCO activity. These results indicate that TESCO enhancer activity was lost in this species. Furthermore, the activity of the SOX9 promoter was enhanced by ER71, indicating that ER71 may play an important role in the testis-specific expression of SOX9.

Indexed as

Sex Determination ProcessesAnimalsGene Expression RegulationMaleMurinaeSOX Transcription FactorsTestisY ChromosomeSOX Transcription Factors

Identifiers

PMID27611740
PMCPMC5017195
OpenAlexW2517446412

What OpenQuestion holds

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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.