Evidence map›Paper›PMID 41039221›Full record

ArticleBMC microbiology2025

Repression of mab_1999 impairs growth and alters cellular morphology of Mycobacterium abscessus.

Azizah Fitriana Nurul Ilmi, Pornchai Kaewsapsak, Suwatchareeporn Rotcheewaphan

Abstract read
In one paragraph

Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

3 authors.

Azizah Fitriana Nurul IlmiMedical Sciences Program, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Pornchai KaewsapsakDepartment of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Suwatchareeporn RotcheewaphanCenter of Excellence in Systems Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand. suwatchareeporn.r@chula.ac.th.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCell division is essential for bacterial survival and represents a promising target for the development of novel antibiotics, particularly in mycobacteria. The role of the division protein FtsL in Mycobacterium abscessus remains poorly understood. This study investigated the effects of MAB_1999, a predicted homolog of FtsL, on the growth and cell division of M. abscessus.

methodTo investigate the function of mab_1999, a knockdown mutant was generated via CRISPR interference (CRISPRi). The phenotypic impact of mab_1999 suppression was evaluated, with a focus on its effects on M. abscessus growth, cellular morphology, and antibiotic susceptibility.

resultsThe putative homolog of FtsL in M. abscessus (MAB_1999) shares 54% amino acid sequence identity with FtsL from M. smegmatis (MSMEG_4234). CRISPRi-mediated repression of mab_1999 expression resulted in cell elongation and growth defects, although complete growth arrest was not observed. Furthermore, reduced mab_1999 expression increased the susceptibility of M. abscessus to β-lactam antibiotics, including ceftriaxone and imipenem.

conclusionsOur findings suggest that mab_1999 is involved in cell division and cell wall integrity in M. abscessus. However, further investigation is necessary to confirm its identity as FtsL and to fully elucidate its role in the cell division process and cell wall synthesis.

Indexed as

Bacterial ProteinsMycobacterium abscessusAnti-Bacterial AgentsCell DivisionCRISPR-Cas SystemsGene Expression Regulation, BacterialGene Knockdown TechniquesMicrobial Sensitivity TestsMycobacterium smegmatisAnti-Bacterial AgentsBacterial ProteinsCell divisionCRISPRiFtsLMycobacterium abscessus

Identifiers

PMID41039221
PMCPMC12492608

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.