ArticleBMC complementary medicine and therapies2025
CRISPRi knockdown of mycobacterial tkt gene potentiates the anti-mycobacterial activity of phyto-compounds from selected medicinal plants.
Article in BMC complementary medicine and therapies, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMycobacterium tuberculosis (Mtb) infection is well known to be challenging to treat. Treatment effectiveness is restricted by the pathogen's inherent drug resistance. A deeper understanding of essential bacterial pathways that influence Mtb growth and survival can expediate the development of more effective therapies from various sources. Here, using mycobacterial tkt gene as a model target, we report on the use of CRISPR interference gene knockdown to potentiate the antimycobacterial activity of selected medicinal plant extracts.
methodsThe growth phenotypes were investigated on solid and liquid media. Broth micro-dilution assay was used to determine minimum inhibitory concentrations. Potential cytotoxicity of the extracts was investigated using Vero cell lines. LC-MS was used for phytochemical analysis. In silico docking was performed on transketolase (Rv1449c), NADH-dependent enoyl-[acyl-carrier-protein] reductase (Rv1484), catalase-peroxidase (Rv1908c).
resultsPhenotypic characterisation of the CRISPRi mutants showed that gradual tkt knockdown fully, led to growth disruption. Chemical-genetic interactions showed that tkt knockdown increased the antimycobacterial activity of acetone extracts from Peltophorum africanum and Croton gratissimus by twofold in CRISPRi hypomoprhs. Molecular docking data revealed that Phlorizin from C. gratissimus (-8.1 kcal/mol), Ficus sur tritepernoid (-9.6 kcal/mol) and P. africanum (6-hydroxydelphinidin 3-glucoside) (-8.9 kcal/mol) had the best binding affinities to the TKT active site pocket. Moreover, these compounds had better binding affinities to both NADH-dependent reductase and catalase-peroxidase than Isoniazid.
conclusionThe research demonstrated that the mycobacterial tkt gene is crucial for bacterial growth, and CRISPRi-mediated knockdown of this gene enhanced the anti-mycobacterial activity of phyto-compounds, which showed multiple binding affinities to established anti-Mtb targets.
Indexed as
Identifiers
What Socratic 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 Socratic graph.