Evidence map›Paper›PMID 42771160›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2027

Experimental Evolution of Drug Resistance for Antibiotic Target Discovery in Chlamydia trachomatis.

Aakriti Singh, Barbara S Sixt

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Article in Methods in molecular biology (Clifton, N.J.), 2027. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

2 authors.

Aakriti SinghDepartment of Molecular Biology, Umeå University, Umeå, Sweden.
Barbara S SixtDepartment of Molecular Biology, Umeå University, Umeå, Sweden. barbara.sixt@umu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recent application of experimental and computational drug discovery workflows has identified hundreds of new molecules that display potent, and in some cases highly selective, activity against bacteria of the genus Chlamydia. The full value of these novel antichlamydial molecules, however, depends critically on our ability to determine their molecular targets and modes of action. A particularly powerful and widely applied strategy for identifying candidate targets involves selecting for bacterial mutants that have acquired resistance to a compound's inhibitory activity, followed by determining the mutations responsible for this resistance. Such mutations often pinpoint the compound's direct target or reveal cellular pathways that modulate target engagement. Here, we present a detailed, step-by-step protocol for applying this approach to the clinically important, human-pathogenic species Chlamydia trachomatis. The workflow includes: (1) determining compound potency by quantitative dose-response analysis, (2) generating a resistant C. trachomatis mutant through serial passaging under progressively increasing selective pressure, (3) confirming the resistance phenotype, and (4) isolating bacterial genomic DNA for whole-genome sequencing to identify resistance-associated mutations and facilitate downstream target discovery.

Indexed as

Anti-Bacterial AgentsChlamydia trachomatisDrug DiscoveryDrug Resistance, BacterialChlamydia InfectionsGenome, BacterialHumansMicrobial Sensitivity TestsMutationWhole Genome SequencingAnti-Bacterial AgentsAntibiotic discoveryAntibiotic potencyAntibiotic resistanceChlamydia trachomatisDNA isolationIC50Resistance-causing mutationsResistant mutantsSmall moleculesWhole-genome sequencing

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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.