Evidence map›Paper›PMID 38618721›Full record

ArticleThe ISME journal2024

Lactic acid bacteria modulate the CncC pathway to enhance resistance to β-cypermethrin in the oriental fruit fly.

Tian Zeng, Qianyan Fu, Fangyi Luo, Jian Dai, Rong Fu, Yixiang Qi, Xiaojuan Deng, Yongyue Lu, Yijuan Xu

Open access · goldAbstract read
In one paragraph

Article in The ISME journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
18.9field-weighted citation impact, top 1% 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

9 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Insects · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Two detoxification enzyme genes,Frontiers in physiology · 2024
    Article
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 at 2 institutions in 1 country.

Tian ZengGuangdong Laboratory for Lingnan Modern Agriculture, Department of Entomology, South China Agricultural University, Guangzhou 510642, China.
Qianyan FuGuangdong Laboratory for Lingnan Modern Agriculture, Department of Entomology, South China Agricultural University, Guangzhou 510642, China.
Fangyi LuoGuangdong Provincial Sericulture & Mulberry Engineering Research Center, Guangdong Prov Key Lab of AgroAnimal Genomics & Molecular Breeding, College of Animal Science, South China Agricultural University, Guangzhou 510642, China.
Jian DaiGuangdong Laboratory for Lingnan Modern Agriculture, Department of Entomology, South China Agricultural University, Guangzhou 510642, China.
Rong FuGuangdong Laboratory for Lingnan Modern Agriculture, Department of Entomology, South China Agricultural University, Guangzhou 510642, China.
Yixiang QiGuangdong Laboratory for Lingnan Modern Agriculture, Department of Entomology, South China Agricultural University, Guangzhou 510642, China.
Xiaojuan DengGuangdong Provincial Sericulture & Mulberry Engineering Research Center, Guangdong Prov Key Lab of AgroAnimal Genomics & Molecular Breeding, College of Animal Science, South China Agricultural University, Guangzhou 510642, China.
Yongyue LuGuangdong Laboratory for Lingnan Modern Agriculture, Department of Entomology, South China Agricultural University, Guangzhou 510642, China.
Yijuan XuGuangdong Laboratory for Lingnan Modern Agriculture, Department of Entomology, South China Agricultural University, Guangzhou 510642, China.
Key Laboratory of Guangdong Province · CNSouth China Agricultural University · CN

Funding

Laboratory of Lingnan Modern Agriculture Project NZ2021022National Key R&D Program of China 2021YFC2600404
6 · The paper itself

Abstract

The gut microbiota of insects has been shown to regulate host detoxification enzymes. However, the potential regulatory mechanisms involved remain unknown. Here, we report that gut bacteria increase insecticide resistance by activating the cap "n" collar isoform-C (CncC) pathway through enzymatically generated reactive oxygen species (ROS) in Bactrocera dorsalis. We demonstrated that Enterococcus casseliflavus and Lactococcus lactis, two lactic acid-producing bacteria, increase the resistance of B. dorsalis to β-cypermethrin by regulating cytochrome P450 (P450) enzymes and α-glutathione S-transferase (GST) activities. These gut symbionts also induced the expression of CncC and muscle aponeurosis fibromatosis. BdCncC knockdown led to a decrease in resistance caused by gut bacteria. Ingestion of the ROS scavenger vitamin C in resistant strain affected the expression of BdCncC/BdKeap1/BdMafK, resulting in reduced P450 and GST activity. Furthermore, feeding with E. casseliflavus or L. lactis showed that BdNOX5 increased ROS production, and BdNOX5 knockdown affected the expression of the BdCncC/BdMafK pathway and detoxification genes. Moreover, lactic acid feeding activated the ROS-associated regulation of P450 and GST activity. Collectively, our findings indicate that symbiotic gut bacteria modulate intestinal detoxification pathways by affecting physiological biochemistry, thus providing new insights into the involvement of insect gut microbes in the development of insecticide resistance.

Indexed as

Gastrointestinal MicrobiomeInsecticide ResistancePyrethrinsReactive Oxygen SpeciesTephritidaeAnimalsCytochrome P-450 Enzyme SystemEnterococcusGlutathione TransferaseInsecticidesInsect ProteinsLactobacillalesLactococcus lactiscypermethrinCytochrome P-450 Enzyme SystemGlutathione TransferaseInsecticidesInsect ProteinsPyrethrinsReactive Oxygen SpeciesBactrocera dorsaliscytochrome P450detoxificationintestinal immunitysymbiotic bacteria

Identifiers

PMID38618721
PMCPMC11069359
OpenAlexW4394815218

What OpenQuestion 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 OpenQuestion graph.