ArticleScientific reports2017
An Amidase_3 domain-containing N-acetylmuramyl-L-alanine amidase is required for mycobacterial cell division.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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.
Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- A Division-Associated Envelope Protein, MAB_2363, Drives Intrinsic Resistance and Virulence inMicroorganisms · 2026Article
- The Ubiquitination ofBiology · 2025Article
- The combinatorial deletion of mycobacterial dd-carboxypeptidases is readily tolerated in Mycobacterium smegmatis.Access microbiology · 2025Article
- Mycobacterial FtsEX-RipC interaction is required for normal growth and cell morphology in rifampicin and low ionic strength conditions.Microbiology spectrum · 2024Article
- MtrA modulates Mycobacterium tuberculosis cell division in host microenvironments to mediate intrinsic resistance and drug tolerance.Cell reports · 2023Article
- Effect of NaCl stress on exoproteome profiles ofFrontiers in microbiology · 2023Article
- Amidation of glutamate residues in mycobacterial peptidoglycan is essential for cell wall cross-linking.Frontiers in cellular and infection microbiology · 2023Article
- Peptidoglycan compositional analysis of Mycobacterium smegmatis using high-resolution LC-MS.Scientific reports · 2022Article
- Article
- Genome-Wide Essentiality Analysis ofmBio · 2021Article
- Characterisation of a putative M23-domain containing protein in Mycobacterium tuberculosis.PloS one · 2021Article
- Functional Characterization of theCells · 2020Article
- Article
- ¡vIVA la DivIVA!Journal of bacteriology · 2019Review
- SweC and SweD are essential co-factors of the FtsEX-CwlO cell wall hydrolase complex in Bacillus subtilis.PLoS genetics · 2019Article
- Mycobacterium smegmatis HtrA Blocks the Toxic Activity of a Putative Cell Wall Amidase.Cell reports · 2019Article
- The Dream of a Mycobacterium.Microbiology spectrum · 2019Review
- Resuscitation-Promoting Factors Are Required for Mycobacterium smegmatis Biofilm Formation.Applied and environmental microbiology · 2018Article
- The structure of the S-layer of Clostridium difficile.Journal of cell communication and signaling · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Mycobacteria possess a multi-layered cell wall that requires extensive remodelling during cell division. We investigated the role of an amidase_3 domain-containing N-acetylmuramyl-L-alanine amidase, a peptidoglycan remodelling enzyme implicated in cell division. We demonstrated that deletion of MSMEG_6281 (Ami1) in Mycobacterium smegmatis resulted in the formation of cellular chains, illustrative of cells that were unable to complete division. Suprisingly, viability in the Δami1 mutant was maintained through atypical lateral branching, the products of which proceeded to form viable daughter cells. We showed that these lateral buds resulted from mislocalization of DivIVA, a major determinant in facilitating polar elongation in mycobacterial cells. Failure of Δami1 mutant cells to separate also led to dysregulation of FtsZ ring bundling. Loss of Ami1 resulted in defects in septal peptidoglycan turnover with release of excess cell wall material from the septum or newly born cell poles. We noted signficant accumulation of 3-3 crosslinked muropeptides in the Δami1 mutant. We further demonstrated that deletion of ami1 leads to increased cell wall permeability and enhanced susceptiblity to cell wall targeting antibiotics. Collectively, these data provide novel insight on cell division in actinobacteria and highlights a new class of potential drug targets for mycobacterial diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.