Evidence map›Paper›PMID 24945811›Full record

ArticlePloS one2014

Rapid birth-and-death evolution of imprinted snoRNAs in the Prader-Willi syndrome locus: implications for neural development in Euarchontoglires.

Yi-Jun Zhang, Jian-Hua Yang, Qiao-Su Shi, Ling-Ling Zheng, Jun Liu, Hui Zhou, Hui Zhang, Liang-Hu Qu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.4field-weighted citation impact, top 17% 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, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Epigenetics in Prader-Willi Syndrome.Frontiers in genetics · 2021
    Review
  5. Review
  6. Functional diversity of small nucleolar RNAs.Nucleic acids research · 2020
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. 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 at 1 institution in 1 country.

Yi-Jun ZhangKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, and School of Life Sciences, Sun Yat-sen University, Guangzhou, P. R. China.
Jian-Hua YangKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, and School of Life Sciences, Sun Yat-sen University, Guangzhou, P. R. China.
Qiao-Su ShiLaboratory of Liver Disease Hospital, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, P. R. China.
Ling-Ling ZhengKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, and School of Life Sciences, Sun Yat-sen University, Guangzhou, P. R. China.
Jun LiuInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, P. R. China.
Hui ZhouKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, and School of Life Sciences, Sun Yat-sen University, Guangzhou, P. R. China.
Hui ZhangInstitute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, P. R. China.
Liang-Hu QuKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, and School of Life Sciences, Sun Yat-sen University, Guangzhou, P. R. China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Imprinted small nucleolar RNAs (snoRNAs) are only found in eutherian genomes and closely related to brain functions. A complex human neurological disease, Prader-Willi syndrome (PWS), is primarily attributed to the deletion of imprinted snoRNAs in chromosome 15q11-q13. Here we investigated the snoRNA repertoires in the PWS locus of 12 mammalian genomes and their evolution processes. A total of 613 imprinted snoRNAs were identified in the PWS homologous loci and the gene number was highly variable across lineages, with a peak in Euarchontoglires. Lineage-specific gene gain and loss events account for most extant genes of the HBII-52 (SNORD115) and the HBII-85 (SNORD116) gene family, and remarkable high gene-birth rates were observed in the primates and the rodents. Meanwhile, rapid sequence substitution occurred only in imprinted snoRNA genes, rather than their flanking sequences or the protein-coding genes located in the same imprinted locus. Strong selective constraints on the functional elements of these imprinted snoRNAs further suggest that they are subjected to birth-and-death evolution. Our data suggest that the regulatory role of HBII-52 on 5-HT2CR pre-mRNA might originate in the Euarchontoglires through adaptive process. We propose that the rapid evolution of PWS-related imprinted snoRNAs has contributed to the neural development of Euarchontoglires.

Indexed as

Evolution, MolecularAnimalsGenetic LociGenomic ImprintingHumansMammalsNeurogenesisOpen Reading FramesPhylogenyPrader-Willi SyndromeRNA, MessengerRNA, Small NucleolarSelection, GeneticRNA, MessengerRNA, Small Nucleolar

Identifiers

PMID24945811
PMCPMC4063771
OpenAlexW2078769764

What OpenQuestion holds

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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.