Evidence map›Paper›PMID 32733539›Full record

ArticleFrontiers in genetics2020

Balanced Genome Triplication in Wheat Causes Premature Growth Arrest and an Upheaval of Genome-Wide Gene Regulation.

Xiaowan Gou, Ruili Lv, Changyi Wang, Tiansi Fu, Yan Sha, Lei Gong, Huakun Zhang, Bao Liu

Abstract read
In one paragraph

Article in Frontiers in genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

8 authors.

Xiaowan GouSchool of Life Sciences, Jiangsu Normal University, Xuzhou, China.
Ruili LvKey Laboratory of Molecular Epigenetics, Northeast Normal University, Changchun, China.
Changyi WangKey Laboratory of Molecular Epigenetics, Northeast Normal University, Changchun, China.
Tiansi FuKey Laboratory of Molecular Epigenetics, Northeast Normal University, Changchun, China.
Yan ShaKey Laboratory of Molecular Epigenetics, Northeast Normal University, Changchun, China.
Lei GongKey Laboratory of Molecular Epigenetics, Northeast Normal University, Changchun, China.
Huakun ZhangKey Laboratory of Molecular Epigenetics, Northeast Normal University, Changchun, China.
Bao LiuKey Laboratory of Molecular Epigenetics, Northeast Normal University, Changchun, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polyploidy, or whole genome duplication (WGD), is a driving evolutionary force across the tree of life and has played a pervasive role in the evolution of the plant kingdom. It is generally believed that a major genetic attribute contributing to the success of polyploidy is increased gene and genome dosage. The evolution of polyploid wheat has lent support to this scenario. Wheat has evolved at three ploidal levels: diploidy, tetraploidy, and hexaploidy. Ample evidence testifies that the evolutionary success, be it with respect to evolvability, natural adaptability, or domestication has dramatically increased with each elevation of the ploidal levels. A long-standing question is what would be the outcome if a further elevation of ploidy is superimposed on hexaploid wheat? Here, we characterized a spontaneously occurring nonaploid wheat individual in selfed progenies of synthetic hexaploid wheat and compared it with its isogenic hexaploid siblings at the phenotypic, cytological, and genome-wide gene-expression levels. The nonaploid manifested severe defects in growth and development, albeit with a balanced triplication of the three wheat subgenomes. Transcriptomic profiling of the second leaf of nonaploid, taken at a stage when phenotypic abnormality was not yet discernible, already revealed significant dysregulation in global-scale gene expression with

Indexed as

dysregulationgenome multiplicationploidy levelploidy syndrometranscriptome shockTriticum aestivum

Identifiers

PMID32733539
PMCPMC7360807

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