Evidence map›Paper›PMID 17916234›Full record

ArticleBMC evolutionary biology2007

Family expansion and gene rearrangements contributed to the functional specialization of PRDM genes in vertebrates.

Irene Fumasoni, Natalia Meani, Davide Rambaldi, Gaia Scafetta, Myriam Alcalay, Francesca D Ciccarelli

Abstract read
In one paragraph

Article in BMC evolutionary biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

84 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Same rule, different genes:Science advances · 2024
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  16. PRDM16 expression and function in mammalian cochlear development.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
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  19. Review
  20. Review

24 more citing papers are in PubMed but not listed here.

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

6 authors.

Irene FumasoniDepartment of Experimental Oncology, European Institute of Oncology, IFOM-IEO Campus, Via Adamello 16, 20139 Milan, Italy. irene.fumasoni@ifom-ieo-campus.it
Natalia Meani
Davide Rambaldi
Gaia Scafetta
Myriam Alcalay
Francesca D Ciccarelli

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgressive diversification of paralogs after gene expansion is essential to increase their functional specialization. However, mode and tempo of this divergence remain mostly unclear. Here we report the comparative analysis of PRDM genes, a family of putative transcriptional regulators involved in human tumorigenesis.

resultsOur analysis assessed that the PRDM genes originated in metazoans, expanded in vertebrates and further duplicated in primates. We experimentally showed that fast-evolving paralogs are poorly expressed, and that the most recent duplicates, such as primate-specific PRDM7, acquire tissue-specificity. PRDM7 underwent major structural rearrangements that decreased the number of encoded Zn-Fingers and modified gene splicing. Through internal duplication and activation of a non-canonical splice site (GC-AG), PRDM7 can acquire a novel intron. We also detected an alternative isoform that can retain the intron in the mature transcript and that is predominantly expressed in human melanocytes.

conclusionOur findings show that (a) molecular evolution of paralogs correlates with their expression pattern; (b) gene diversification is obtained through massive genomic rearrangements; and (c) splicing modification contributes to the functional specialization of novel genes.

Indexed as

Gene RearrangementMultigene FamilyAmino Acid SequenceAnimalsDNA PrimersEvolution, MolecularGene DuplicationGene Expression RegulationHumansPhylogenyRepressor ProteinsReverse Transcriptase Polymerase Chain ReactionSequence AlignmentSpecies SpecificityTranscription FactorsVertebratesDNA PrimersRepressor ProteinsTranscription Factors

Identifiers

PMID17916234
PMCPMC2082429

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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.