Evidence map›Paper›PMID 40597320›Full record

ArticleBMC biology2025

Mutations of the complex I PSST target gene confers acaricide resistance and a fitness cost in Panonychus citri.

Deng Pan, Menghao Xia, Chuanzhen Li, Xunyan Liu, Lewis Archdeacon, Andrias O O'Reilly, Guorui Yuan, Jinjun Wang, Wei Dou

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

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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

2 citing papers in PubMed.

  1. Article
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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

9 authors.

Deng PanKey Laboratory of Entomology and Pest Control Engineering, College of Plant Protection, Southwest University, Chongqing, 400715, China.
Menghao XiaKey Laboratory of Entomology and Pest Control Engineering, College of Plant Protection, Southwest University, Chongqing, 400715, China.
Chuanzhen LiKey Laboratory of Entomology and Pest Control Engineering, College of Plant Protection, Southwest University, Chongqing, 400715, China.
Xunyan LiuKey Laboratory of Entomology and Pest Control Engineering, College of Plant Protection, Southwest University, Chongqing, 400715, China.
Lewis ArchdeaconSchool of Biological and Environmental Sciences, Liverpool John Moores University, Liverpool, UK.
Andrias O O'ReillySchool of Biological and Environmental Sciences, Liverpool John Moores University, Liverpool, UK.
Guorui YuanKey Laboratory of Entomology and Pest Control Engineering, College of Plant Protection, Southwest University, Chongqing, 400715, China.
Jinjun WangKey Laboratory of Entomology and Pest Control Engineering, College of Plant Protection, Southwest University, Chongqing, 400715, China. wangjinjun@swu.edu.cn.
Wei DouKey Laboratory of Entomology and Pest Control Engineering, College of Plant Protection, Southwest University, Chongqing, 400715, China. douwei80@swu.edu.cn.

Funding

Fundamental Research Funds for the Central Universities SWU-XDPY22001Medical Research Council grant MR/W002159/1
6 · The paper itself

Abstract

backgroundPesticide resistance is a serious problem that threatens crop industries. Major resistance towards pyridaben, an acaricidal inhibitor of mitochondrial electron transport complex I (METI-Is), has been reported in tetranychids following its extensive use worldwide. Understanding mechanisms of pyridaben resistance is crucial for sustainable resistance management.

resultsThe inheritance of pyridaben resistance was incompletely recessive and controlled by multiple genes in P. citri, which was determined by reciprocal crosses and backcross experiments. Bulked segregant analysis was performed to identify gene loci underlying pyridaben resistance. Subsequently, the two PSST-subunit mutations H107R and the previously undiscovered V103I mutation were positively correlated with pyridaben resistance in different populations or strains by single mite genotyping. The bioassay further showed that H107R contributed to moderate resistance, while V103I in combination with H107R was responsible for a very high level of resistance in homozygous P. citri strains. These contributions to pyridaben resistance were also verified in transgenic Drosophila through the introduction of the wildtype, single- or double-mutated P. citri PSST subunit. In addition, life-table analysis and behavioral measures were conducted to assess the fitness cost associated with resistance development. Accompanied by reduced ATP levels and complex I activity, a fitness cost was observed as reduced fecundity and lower mobility due to PSST mutations.

conclusionsOur findings provide direct evidence that PSST mutations conferred the evolution of pyridaben resistance but simultaneously led to a fitness cost due to functional defects in complex I. These data provide theoretical insights into sustainable resistance management in agricultural production.

Indexed as

AcaricidesArthropod ProteinsDrug ResistanceElectron Transport Complex IGenetic FitnessMutationPyridazinesTetranychidaeAnimalsAcaricidesArthropod ProteinsElectron Transport Complex IpyridabenPyridazinesBulked segregation analysisCitrus red miteFitness costInheritanceTarget-site mutation

Identifiers

PMID40597320
PMCPMC12220261

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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.