ArticleTuberculosis (Edinburgh, Scotland)2009
Mycobacterium tuberculosis ftsZ expression and minimal promoter activity.
Article in Tuberculosis (Edinburgh, Scotland), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Novel Populations ofMicroorganisms · 2024Article
- Aureolic Acid Group of Agents as Potential Antituberculosis Drugs.Antibiotics (Basel, Switzerland) · 2020Article
- The conserved actinobacterial transcriptional regulator FtsR controls expression of ftsZ and further target genes and influences growth and cell division in Corynebacterium glutamicum.BMC microbiology · 2019Article
- Bacterial Cell Division: Nonmodels Poised to Take the Spotlight.Annual review of microbiology · 2017Review
- Investigating essential gene function in Mycobacterium tuberculosis using an efficient CRISPR interference system.Nucleic acids research · 2016Article
- Cloning and characterization of filamentous temperature-sensitive protein Z from Xanthomonas oryzae pv. Oryzae.SpringerPlus · 2016Article
- Replacement of Mycobacterium smegmatis dnaA gene by Mycobacterium tuberculosis homolog results in temperature sensitivity.Tuberculosis (Edinburgh, Scotland) · 2011Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Optimal levels of ftsZ gene product are shown to be required for initiation of the cell division process in Mycobacterium tuberculosis. Here, we report that the ftsZ gene expression is sharply down-regulated during starvation and hypoxia, conditions that are believed to result in growth arrest, but is restored upon dilution of cultures into fresh oxygen-rich media. Primer extension analysis identified four transcriptional start sites, designated as P1, P2, P3 and P4 at nucleotide positions -43, -101, -263, and -787, respectively, in the immediate upstream flanking region of the ftsZ initiation codon. Promoter deletion and homologous recombination experiments revealed that ftsZ expression from the 101-bp region is sufficient for M. tuberculosis viability. All promoter strains had reduced FtsZ levels compared to wild-type, although the loss of P4 severely compromised FtsZ levels during both the active and stationary phases. We propose that ftsZ expression from all promoters is required for optimal intracellular FtsZ levels and that the activities of P4 and possibly other promoters are down-regulated during growth-arrest conditions.
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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.