Evidence map›Paper›PMID 21208429›Full record

ArticleBMC evolutionary biology2011

The tendency to recreate ancestral CG dinucleotides in the human genome.

Mingkun Li, Su-Shing Chen

Open access · goldAbstract read
In one paragraph

Article in BMC evolutionary biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 18 citations in OpenAlex.

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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

2 authors at 1 institution in 2 countries.

Mingkun LiCAS-MPG Partner Institute of Computational Biology, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, 200000 Shanghai, PR China. mingkun_li@eva.mpg.de
Su-Shing Chen
Shanghai Institutes for Biological Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe CG dinucleotides are known to be deficient in the human genome, due to a high mutation rate from 5-methylated CG to TG and its complementary pair CA. Meanwhile, many cellular functions rely on these CG dinucleotides, such as gene expression controlled by cytosine methylation status. Thus, CG dinucleotides that provide essential functional substrates should be retained in genomes. How these two conflicting processes regarding the fate of CG dinucleotides - i.e., high mutation rate destroying CG dinucleotides, vs. functional processes that require their preservation remains an unsolved question.

resultsBy analyzing the mutation and frequency spectrum of newly derived alleles in the human genome, a tendency towards generating more CGs was observed, which was mainly contributed by an excess number of mutations from CA/TG to CG. Simultaneously, we found a fixation preference for CGs derived from TG/CA rather than CGs generated by other dinucleotides. These tendencies were observed both in intergenic and genic regions. An analysis of Integrated Extended Haplotype Homozygosity provided no evidence of selection for newly derived CGs.

conclusionsAncestral CG dinucleotides that were subsequently lost by mutation tend to be recreated in the human genome, as indicated by a biased mutation and fixation pattern favoring new CGs that derived from TG/CA.

Indexed as

Dinucleotide RepeatsEvolution, MolecularGC Rich SequenceGenome, HumanAnimalsDNA MethylationGene FrequencyHumansMammalsMolecular Sequence DataMutationPhylogenyPolymorphism, Single Nucleotide

Identifiers

PMID21208429
PMCPMC3025853
OpenAlexW2146323990

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.