Evidence map›Paper›PMID 38834545›Full record

ArticleNature communications2024

Burkholderia pseudomallei BipD modulates host mitophagy to evade killing.

Dongqi Nan, Chenglong Rao, Zhiheng Tang, Wenbo Yang, Pan Wu, Jiangao Chen, Yupei Xia, Jingmin Yan, Wenzheng Liu, Ziyuan Zhang and 7 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

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

12 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Frontiers in cellular and infection microbiology · 2025
    Article
  12. Autophagy · 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

17 authors.

Dongqi Nan *Department of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.ORCID http://orcid.org/0009-0002-5907-8016
Chenglong Rao *Department of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Zhiheng Tang *Department of Microbiology and Infectious Disease Center, NHC Key Laboratory of Medical Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Wenbo Yang *Department of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Pan WuDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Jiangao ChenDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Yupei XiaDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Jingmin YanDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Wenzheng LiuDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Ziyuan ZhangDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Zhiqiang HuDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Hai ChenSanya People's Hospital, Sanya, China.
Yaling LiaoDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China.
Xuhu MaoDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China. maoxh2012@hotmail.com.ORCID http://orcid.org/0000-0001-6903-9593
Xiaoyun LiuDepartment of Microbiology and Infectious Disease Center, NHC Key Laboratory of Medical Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China. xiaoyun.liu@bjmu.edu.cn.ORCID http://orcid.org/0000-0001-7083-5263
Quanming ZouDepartment of Microbiology and Biochemical Pharmacy, College of Pharmacy and Laboratory Medicine, Army Medical University (Third Military Medical University), Chongqing, China. qmzou@tmmu.edu.cn.
Qian LiDepartment of Clinical Microbiology and Immunology, College of Pharmacy and Medical Laboratory, Army Medical University (Third Military Medical University), Chongqing, China. liqianjane@163.com.ORCID http://orcid.org/0000-0003-2698-7782

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32270190
6 · The paper itself

Abstract

Mitophagy is critical for mitochondrial quality control and function to clear damaged mitochondria. Here, we found that Burkholderia pseudomallei maneuvered host mitophagy for its intracellular survival through the type III secretion system needle tip protein BipD. We identified BipD, interacting with BTB-containing proteins KLHL9 and KLHL13 by binding to the Back and Kelch domains, recruited NEDD8 family RING E3 ligase CUL3 in response to B. pseudomallei infection. Although evidently not involved in regulation of infectious diseases, KLHL9/KLHL13/CUL3 E3 ligase complex was essential for BipD-dependent ubiquitination of mitochondria in mouse macrophages. Mechanistically, we discovered the inner mitochondrial membrane IMMT via host ubiquitome profiling as a substrate of KLHL9/KLHL13/CUL3 complex. Notably, K63-linked ubiquitination of IMMT K211 was required for initiating host mitophagy, thereby reducing mitochondrial ROS production. Here, we show a unique mechanism used by bacterial pathogens that hijacks host mitophagy for their survival.

Indexed as

Bacterial ProteinsBurkholderia pseudomalleiMacrophagesMitochondriaMitophagyAnimalsHEK293 CellsHost-Pathogen InteractionsHumansMelioidosisMiceMice, Inbred C57BLMitochondrial MembranesRAW 264.7 CellsReactive Oxygen SpeciesType III Secretion SystemsBacterial ProteinsReactive Oxygen SpeciesType III Secretion Systems

Identifiers

PMID38834545
PMCPMC11150414

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.