Evidence map›Paper›PMID 25982742›Full record

ArticleMolecular genetics and genomics : MGG2015

The phylogeny and evolutionary history of the Lesion Simulating Disease (LSD) gene family in Viridiplantae.

Caroline Cabreira, Alexandro Cagliari, Lauro Bücker-Neto, Márcia Margis-Pinheiro, Loreta B de Freitas, Maria Helena Bodanese-Zanettini

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In one paragraph

Article in Molecular genetics and genomics : MGG, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

3 citing papers in PubMed, 15 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

6 authors at 2 institutions in 1 country.

Caroline CabreiraDepartamento de Genética, Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), PO Box 15053, Porto Alegre, RS, CEP 91501-970, Brazil.
Alexandro CagliariUniversidade Estadual do Rio Grande do Sul (UERGS), Santa Cruz do Sul, RS, Brazil.
Lauro Bücker-NetoDepartamento de Genética, Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), PO Box 15053, Porto Alegre, RS, CEP 91501-970, Brazil.
Márcia Margis-PinheiroDepartamento de Genética, Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), PO Box 15053, Porto Alegre, RS, CEP 91501-970, Brazil.
Loreta B de FreitasDepartamento de Genética, Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), PO Box 15053, Porto Alegre, RS, CEP 91501-970, Brazil.
Maria Helena Bodanese-ZanettiniDepartamento de Genética, Programa de Pós-Graduação em Genética e Biologia Molecular, Universidade Federal do Rio Grande do Sul (UFRGS), PO Box 15053, Porto Alegre, RS, CEP 91501-970, Brazil. maria.zanettini@ufrgs.br.
Universidade Federal do Rio Grande do Sul · BRUniversidade Estadual do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Lesion Simulating Disease (LSD) genes encode a family of zinc finger proteins that play a role in programmed cell death (PCD) and other biological processes, such as plant growth and photosynthesis. In the present study, we report the reconstruction of the evolutionary history of the LSD gene family in Viridiplantae. Phylogenetic analysis revealed that the monocot and eudicot genes were distributed along the phylogeny, indicating that the expansion of the family occurred prior to the diversification between these clades. Sequences encoding proteins that present one, two, or three LSD domains formed separate groups. The secondary structure of these different LSD proteins presented a similar composition, with the β-sheets being their main component. The evolution by gene duplication was identified only to the genes that contain three LSD domains, which generated proteins with equal structure. Moreover, genes encoding proteins with one or two LSD domains evolved as single-copy genes and did not result from loss or gain in LSD domains. These results were corroborated by synteny analysis among regions containing paralogous/orthologous genes in Glycine max and Populus trichocarpa. The Ka/Ks ratio between paralogous/orthologous genes revealed that a subfunctionalization process possibly could be occurring with the LSD genes, explaining the involvement of LSD members in different biological processes, in addition to the negative regulation of PCD. This study presents important novelty in the evolutionary history of the LSD family and provides a basis for future research on individual LSD genes and their involvement in important pathway networks in plants.

Indexed as

Evolution, MolecularGenes, PlantPhylogenyAmino Acid SequenceChromosome MappingMolecular Sequence DataPlant DiseasesPlant ProteinsProtein Structure, SecondarySequence Homology, Amino AcidViridiplantaePlant ProteinsGene duplicationLesion Simulating Disease (LSD)LSD family phylogenyProtein secondary structureSyntenyZinc finger LSD domain

Identifiers

PMID25982742
OpenAlexW1492464031

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.