Evidence map›Paper›PMID 18077390›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Genomic drift and copy number variation of sensory receptor genes in humans.

Masafumi Nozawa, Yoshihiro Kawahara, Masatoshi Nei

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

81 citing papers in PubMed.

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  16. Expansion of vomeronasal receptor genes (Communications biology · 2019
    Article
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21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Masafumi NozawaInstitute of Molecular Evolutionary Genetics and Department of Biology, Pennsylvania State University, 328 Mueller Laboratory, University Park, PA 16802, USA.
Yoshihiro Kawahara
Masatoshi Nei

Funding

THEORETICAL POPULATION GENETICS AND ITS APPLICATIONSR01GM020293 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI NEI, MASATOSHI · 1985 to 2009
$1.8M
NIGMS NIH HHS GM020293NIGMS NIH HHS R01 GM020293
6 · The paper itself

Abstract

The number of sensory receptor genes varies extensively among different mammalian species. This variation is believed to be caused partly by physiological requirements of animals and partly by genomic drift due to random duplication and deletion of genes. If the contribution of genomic drift is substantial, each species should contain a significant amount of copy number variation (CNV). We therefore investigated CNVs in sensory receptor genes among 270 healthy humans by using published CNV data. The results indicated that olfactory receptor (OR), taste receptor type 2, and vomeronasal receptor type 1 genes show a high level of intraspecific CNVs. In particular, >30% of the approximately 800 OR gene loci in humans were polymorphic with respect to copy number, and two randomly chosen individuals showed a copy number difference of approximately 11 in functional OR genes on average. There was no significant difference in the amount of CNVs between functional and nonfunctional OR genes. Because pseudogenes are expected to evolve in a neutral fashion, this observation suggests that functional OR genes also have evolved in a similar manner with respect to copy number change. In addition, we found that the evolutionary change of copy number of OR genes approximately follows the Gaussian process in probability theory, and the copy number divergence between populations has increased with evolutionary time. We therefore conclude that genomic drift plays an important role for generating intra- and interspecific CNVs of sensory receptor genes. Similar results were obtained when all annotated genes were analyzed.

Indexed as

Gene DosageGenetic DriftGenetic VariationSensory Receptor CellsGenome, HumanHumans

Identifiers

PMID18077390
PMCPMC2154446

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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.