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Transcriptome analysis experiments enable researchers to characterize transcriptional activity (coding and non-coding), focus on a subset of relevant target genes and transcripts, or profile thousands of genes at once to create a global picture of cell function. It can demonstrate gene functions and structures from the whole level and reveal specific biological processes, such as biological evolution, basic metabolism, disease occurrence, and drug targets. In addition to the extensive utilization of RNA sequencing (RNA-Seq) in clinical research, it is very sensitive for measuring low abundance genes.

RNA-Seq is a high-throughput technology that can simultaneously measure the expression patterns of thousands of genes and provide insight into biological processes' functional pathways and regulation. RNA-Seq is a powerful method for studying drug-induced changes in gene expression across the genome. As a result, the method can assess a drug's global transcriptional effects and significantly speed up the procedure of drug target identification.

RNA-Seq can be used to investigate the differences in genome-wide gene expression between resistant microorganism and the original strain, which may be followed by validation using other molecular techniques like quantitative reverse transcription polymerase chain reaction (RT-qPCR).

Most of the changes that are found in the transcriptomes of resistant mutants are the consequence, not the cause of resistance. Therefore, the acquisition of resistance should be determined by means of mutations (including gene amplification) using whole-genome sequencing of the mutant as well as the original strain. Once this is known, transcriptomics may help to track second-order effects as well as to analyze the effect of acquiring resistance on the bacterial physiology.

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One specific example of the application of transcriptomics to antimicrobial drugs is the observation that chromosomal beta-lactamase genes can be induced by treatment of bacteria with beta-lactam antibiotics (e.g. penicillin). Since beta-lactamases degrade beta-lactam antibiotics, this is a potential source of inducible drug resistance.

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