Evidence map›Paper›PMID 22583633›Full record

ArticleBMC evolutionary biology2012

Molecular evolution of pentatricopeptide repeat genes reveals truncation in species lacking an editing target and structural domains under distinct selective pressures.

Michael L Hayes, Karolyn Giang, R Michael Mulligan

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In one paragraph

Article in BMC evolutionary biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

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23citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

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

  1. Pooled it
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  5. Identification and expression analysis of the grape pentatricopeptide repeat (PPR) gene family in abiotic stress.Physiology and molecular biology of plants : an international journal of functional plant biology · 2022
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  15. The Pentatricopeptide Repeat Gene Family inMolecules (Basel, Switzerland) · 2018
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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Michael L HayesDevelopmental & Cell Biology, University of California, Irvine, CA 92697, USA.
Karolyn Giang
R Michael Mulligan

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPentatricopeptide repeat (PPR) proteins are required for numerous RNA processing events in plant organelles including C-to-U editing, splicing, stabilization, and cleavage. Fifteen PPR proteins are known to be required for RNA editing at 21 sites in Arabidopsis chloroplasts, and belong to the PLS class of PPR proteins. In this study, we investigate the co-evolution of four PPR genes (CRR4, CRR21, CLB19, and OTP82) and their six editing targets in Brassicaceae species. PPR genes are composed of approximately 10 to 20 tandem repeats and each repeat has two α-helical regions, helix A and helix B, that are separated by short coil regions. Each repeat and structural feature was examined to determine the selective pressures on these regions.

resultsAll of the PPR genes examined are under strong negative selection. Multiple independent losses of editing site targets are observed for both CRR21 and OTP82. In several species lacking the known editing target for CRR21, PPR genes are truncated near the 17th PPR repeat. The coding sequences of the truncated CRR21 genes are maintained under strong negative selection; however, the 3' UTR sequences beyond the truncation site have substantially diverged. Phylogenetic analyses of four PPR genes show that sequences corresponding to helix A are high compared to helix B sequences. Differential evolutionary selection of helix A versus helix B is observed in both plant and mammalian PPR genes.

conclusionPPR genes and their cognate editing sites are mutually constrained in evolution. Editing sites are frequently lost by replacement of an edited C with a genomic T. After the loss of an editing site, the PPR genes are observed with three outcomes: first, few changes are detected in some cases; second, the PPR gene is present as a pseudogene; and third, the PPR gene is present but truncated in the C-terminal region. The retention of truncated forms of CRR21 that are maintained under strong negative selection even in the absence of an editing site target suggests that unrecognized function(s) might exist for this PPR protein. PPR gene sequences that encode helix A are under strong selection, and could be involved in RNA substrate recognition.

Indexed as

Evolution, MolecularRNA EditingSelection, GeneticAmino Acid SequenceArabidopsisArabidopsis ProteinsChloroplastsDNA, PlantModels, MolecularMolecular Sequence DataPhylogenyTandem Repeat SequencesArabidopsis ProteinsDNA, Plantpentatricopeptide repeat protein, Arabidopsis

Identifiers

PMID22583633
PMCPMC3441922

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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.