Evidence map›Paper›PMID 21283795›Full record

ArticlePloS one2011

Dissecting genetic networks underlying complex phenotypes: the theoretical framework.

Fan Zhang, Hu-Qu Zhai, Andrew H Paterson, Jian-Long Xu, Yong-Ming Gao, Tian-Qing Zheng, Rong-Ling Wu, Bin-Ying Fu, Jauhar Ali, Zhi-Kang Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Genetic Dissection of Salt Tolerance and Yield Traits ofCurrent issues in molecular biology · 2023
    Article
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  3. A Genetic Network Underlying Rhizome Development inFrontiers in plant science · 2022
    Article
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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 5 institutions in 3 countries.

Fan ZhangInstitute of Crop Sciences/National Key Facility for Crop Gene Resources and Genetic Improvement, Chinese Academy of Agricultural Sciences, Beijing, China.
Hu-Qu Zhai
Andrew H Paterson
Jian-Long Xu
Yong-Ming Gao
Tian-Qing Zheng
Rong-Ling Wu
Bin-Ying Fu
Jauhar Ali
Zhi-Kang Li
Chinese Academy of Agricultural Sciences · CNInstitute of Crop Sciences · CNUniversity of Georgia · USInternational Rice Research Institute · PHPennsylvania State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Great progress has been made in genetic dissection of quantitative trait variation during the past two decades, but many studies still reveal only a small fraction of quantitative trait loci (QTLs), and epistasis remains elusive. We integrate contemporary knowledge of signal transduction pathways with principles of quantitative and population genetics to characterize genetic networks underlying complex traits, using a model founded upon one-way functional dependency of downstream genes on upstream regulators (the principle of hierarchy) and mutual functional dependency among related genes (functional genetic units, FGU). Both simulated and real data suggest that complementary epistasis contributes greatly to quantitative trait variation, and obscures the phenotypic effects of many 'downstream' loci in pathways. The mathematical relationships between the main effects and epistatic effects of genes acting at different levels of signaling pathways were established using the quantitative and population genetic parameters. Both loss of function and "co-adapted" gene complexes formed by multiple alleles with differentiated functions (effects) are predicted to be frequent types of allelic diversity at loci that contribute to the genetic variation of complex traits in populations. Downstream FGUs appear to be more vulnerable to loss of function than their upstream regulators, but this vulnerability is apparently compensated by different FGUs of similar functions. Other predictions from the model may account for puzzling results regarding responses to selection, genotype by environment interaction, and the genetic basis of heterosis.

Indexed as

Epistasis, GeneticGene Regulatory NetworksModels, GeneticAllelesGenetic VariationHumansHybrid VigorPhenotypeQuantitative Trait Loci

Identifiers

PMID21283795
PMCPMC3024316
OpenAlexW2068944437

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.