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The non-coding RNA rprA can increase the resistance to ampicillin in Escherichia coli

Azita Sahni1, Mohammadreza Hajjari2, Jamshid Raheb3

  • 1Nour Danesh Institute of Higher Education, Department of Biology, Isfahan, Iran.

Microbial Pathogenesis
|February 26, 2019
PubMed
Abstract

Insights

The non-coding RNA rprA influences ampicillin resistance in Escherichia coli. Upregulating rprA enhances resistance, while downregulating it increases susceptibility, highlighting rprA

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Antibiotic resistance is a growing global health threat.
  • Non-coding RNAs play crucial roles in bacterial gene regulation.
  • The specific role of rprA in ampicillin resistance in E. coli was previously unknown.

Purpose of the Study:

  • To investigate the effect of rprA expression on ampicillin resistance in Escherichia coli.
  • To analyze the impact of rprA upregulation and downregulation on bacterial response to ampicillin.

Main Methods:

  • Bacterial DNA extraction and amplification via PCR.
  • Construction and transformation of recombinant plasmids (pET28a/rprA-sense and -antisense).
  • Analysis of rprA expression using semi-quantitative RT-PCR and assessment of ampicillin resistance via broth dilution method.

Main Results:

  • Significant differences in turbidity were observed between upregulated and control bacteria (p < 0.0001).
  • Significant differences were also found between downregulated and control bacteria (p < 0.0001).
  • Upregulation of rprA correlated with increased ampicillin resistance, while downregulation led to increased susceptibility.

Conclusions:

  • rprA expression plays a significant role in modulating ampicillin resistance in E. coli.
  • Upregulation of rprA confers ampicillin resistance, whereas its downregulation increases susceptibility.
  • These findings suggest rprA as a potential target for combating ampicillin resistance in E. coli.
Keywords:
Ampicillin resistanceEscherichia coliSmall non-coding RNArprA

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