Evidence map›Paper›PMID 42030160›Full record

ArticleCell reports2026

The mycobacterial ATP burst is a lysis artifact and serves as an assay for drug-induced cell wall damage.

Claire V Mulholland, Bei Shi Lee, Alexander Chong, Jinhua Cui, Kevin Pethe, Michael Berney

Abstract read
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. A new Persister Enrichment Model inbioRxiv : the preprint server for biology · 2026
    Article
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Claire V MulhollandDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Bei Shi LeeLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; Department of Public and Global Health, EBPI, University of Zurich, Zurich, Switzerland.
Alexander ChongDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Jinhua CuiDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Kevin PetheLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; Singapore Centre for Environmental Life Sciences Engineering, Nanyang Technological University, Singapore, Singapore; National Center for Infectious Diseases (NCID), Singapore, Singapore.
Michael BerneyDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Department of Public and Global Health, EBPI, University of Zurich, Zurich, Switzerland. Electronic address: michael.berney@einsteinmed.edu.

Funding

Eradicating persistent M. tuberculosis by synthetic lethality of terminal respiratory oxidasesR01AI139465 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI BERNEY, MICHAEL · 2019 to 2023
$3.2M
Identification of new inhibitors of essential functions in M. tuberculosis by high-throughput metabolic profilingR01AI173328 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Michael Berney · 2023 to 2026
$2.6M
The PDIM paradox of M. tuberculosisR01AI175972 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI Michael Berney · 2023 to 2026
$2.0M
Coenzyme F420, helping mycobacteria find a niche in humansR21AI159348 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI BERNEY, MICHAEL · 2022 to 2023
$451k
NIAID NIH HHS R01 AI139465NIAID NIH HHS R01 AI173328NIAID NIH HHS R01 AI175972NIAID NIH HHS R21 AI159348
6 · The paper itself

Abstract

Antibiotics targeting the mycobacterial cell wall are a cornerstone of tuberculosis treatment, yet how these drugs facilitate bacterial killing remains incompletely understood. Studies using the BacTiter-Glo luminescence assay have reported increased mycobacterial ATP levels following treatment with cell wall inhibitors such as isoniazid, a phenomenon referred to as an "ATP burst." This is proposed to contribute to drug-induced killing. Here, we show the ATP burst is not a biological response but rather an experimental artifact resulting from enhanced cell lysis induced by cell-wall-targeting drugs. Mechanical lysis by bead beating abolishes the ATP burst, enabling more reliable assessment of ATP levels. We demonstrate the utility of this approach as a functional readout for identifying compounds that disrupt the mycobacterial cell wall and for screening synergistic or antagonistic interactions with cell wall inhibitors. These findings clarify the mechanistic basis of the ATP burst and provide a practical tool for antimycobacterial drug discovery.

Indexed as

Adenosine TriphosphateAntitubercular AgentsArtifactsCell WallMycobacterium tuberculosisIsoniazidAdenosine TriphosphateAntitubercular AgentsIsoniazidATPATP burstBacTiter-Globioenergetics inhibitorscell wallCP: Microbiologydrug screeningisoniazidlysismycobacteriaMycobacterium tuberculosis

Identifiers

PMID42030160
PMCPMC13270088

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.