Evidence map›Paper›PMID 33306672›Full record

ArticlePloS one2020

Ancestry of the AUTS2 family-A novel group of polycomb-complex proteins involved in human neurological disease.

Robert A Sellers, David L Robertson, May Tassabehji

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. AUTS2 Syndrome: Molecular Mechanisms and Model Systems.Frontiers in molecular neuroscience · 2022
    Review
  8. Comparing a Novel Malformation Syndrome Caused by Pathogenic Variants inFrontiers in cell and developmental biology · 2021
    Review
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

3 authors at 2 institutions in 1 country.

Robert A SellersEvolution & Genomic Sciences, School of Biological Sciences, University of Manchester, Manchester, United Kingdom.
David L RobertsonMRC-University of Glasgow Centre for Virus Research, Garscube Campus, Glasgow, United Kingdom.
May TassabehjiEvolution & Genomic Sciences, School of Biological Sciences, University of Manchester, Manchester, United Kingdom.ORCID 0000-0002-6577-3640
University of Manchester · GBMRC University of Glasgow Centre for Virus Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism susceptibility candidate 2 (AUTS2) is a neurodevelopmental regulator associated with an autosomal dominant intellectual disability syndrome, AUTS2 syndrome, and is implicated as an important gene in human-specific evolution. AUTS2 exists as part of a tripartite gene family, the AUTS2 family, which includes two relatively undefined proteins, Fibrosin (FBRS) and Fibrosin-like protein 1 (FBRSL1). Evolutionary ancestors of AUTS2 have not been formally identified outside of the Animalia clade. A Drosophila melanogaster protein, Tay bridge, with a role in neurodevelopment, has been shown to display limited similarity to the C-terminal of AUTS2, suggesting that evolutionary ancestors of the AUTS2 family may exist within other Protostome lineages. Here we present an evolutionary analysis of the AUTS2 family, which highlights ancestral homologs of AUTS2 in multiple Protostome species, implicates AUTS2 as the closest human relative to the progenitor of the AUTS2 family, and demonstrates that Tay bridge is a divergent ortholog of the ancestral AUTS2 progenitor gene. We also define regions of high relative sequence identity, with potential functional significance, shared by the extended AUTS2 protein family. Using structural predictions coupled with sequence conservation and human variant data from 15,708 individuals, a putative domain structure for AUTS2 was produced that can be used to aid interpretation of the consequences of nucleotide variation on protein structure and function in human disease. To assess the role of AUTS2 in human-specific evolution, we recalculated allele frequencies at previously identified human derived sites using large population genome data, and show a high prevalence of ancestral alleles, suggesting that AUTS2 may not be a rapidly evolving gene, as previously thought.

Indexed as

Evolution, MolecularAnimalsCytoskeletal ProteinsDrosophila melanogasterGenomeHumansLymphokinesNuclear ProteinsPhylogenyPolycomb-Group ProteinsSequence Homology, Nucleic AcidTranscription FactorsAUTS2 protein, humanCytoskeletal ProteinsfibrosinLymphokinesNuclear ProteinsPolycomb-Group ProteinsTranscription Factors

Identifiers

PMID33306672
PMCPMC7732068
OpenAlexW2984996015

What Socratic 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 Socratic graph.