Small RNA Regulation of Virulence in Pathogenic Escherichia coli

Abstract

Enteric and extraintestinal pathotypes of Escherichia coli utilize a wide range of virulence factors to colonize niches within the human body. During infection, virulence factors such as adhesins, secretions systems, or toxins require precise regulation and coordination to ensure appropriate expression. Additionally, the bacteria navigate rapidly changing environments with fluctuations in pH, temperature, and nutrient levels. Enteric pathogens utilize sophisticated, interleaved systems of transcriptional and post-transcriptional regulation to sense and respond to these changes and modulate virulence gene expression. Regulatory small RNAs and RNA-binding proteins play critical roles in the post-transcriptional regulation of virulence. In this review we discuss how the mosaic genomes of Escherichia coli pathotypes utilize small RNA regulation to adapt to their niche and become successful human pathogens.

The phosphate-induced small RNA EsrL promotes E. coli virulence, biofilm formation, and intestinal colonization

“…sRNAs are regulatory, noncoding molecules in bacterial species, are typically 50 to 500 nucleotides in length, and are involved in various cell biological processes in bacteria ( 29 , 30 ). They are transcribed and processed from 3′UTRs, 5′UTRs, or coding regions of transcripts and modulate their targets through multiple mechanisms, such as ρ-dependent transcriptional termination or translational regulation ( 31 ). They are involved in environmental signal responses, in which they target genes by base pairing with mRNAs, thereby affecting their stability or efficiency of translation ( 32 ).…”

The stationary phase-specific sRNA FimR2 is a multifunctional regulator of bacterial motility, biofilm formation and virulence

“…Several Gram-negative pathogens employ type III secretion systems (T3SS) to deliver a wide range of effector proteins directly into the cytoplasm of their target cells ( 1 , 2 ) and type 1 pili (T1P) to adhere to and invade host cells ( 1 , 2 ). Bacterial virulence factors are under tight regulation via multiple mechanisms to minimize the use of precious resources in an unpredictable environment ( 3 ). CsrA is a translational regulator that governs the expression of T3SS effectors in bacterial pathogens.…”

“…Recently, trans -encoded small non-coding RNAs (sRNAs) have emerged as potent regulators of gene expression in various bacterial species ( 13 ). By partially base pairing with various target mRNAs and regulating their expression at the post-transcriptional level, these non-coding RNAs (ncRNAs) govern various aspects of bacterial physiology ( 14 ), with various roles described in bacterial virulence and biofilm formation ( 3 , 15 , 16 ). For instance, EHEC GlmY and GlmZ sRNAs promote the formation of A/E lesions through induction of the T3SS effector EspFu, and diminish the expression of other T3SS effectors ( 17 ).…”

The stationary phase-specific sRNAfimR2is a multifunctional regulator of bacterial motility, biofilm formation and virulence

“…Which virulence factors to use and when to employ them are two important aspects for microbial infections not only to ensure a successful attack, but also to minimize the loss of resources for the pathogen in an unpredictable and harsh environment (Sy and Tree, 2021). For these reasons, bacterial virulence factors are under tight regulation via multiple mechanisms acting in concordance and have been refined across long stretches of evolutionary history.…”

“…Recently, trans -encoded small non-coding RNAs (sRNAs) have emerged as potent regulators of gene expression in various bacterial species (Hör et al, 2020). By partially base pairing with various target mRNAs and regulating their expression at the post-transcriptional level, these non-coding RNAs (ncRNAs) govern various aspects of bacterial physiology (Nitzan et al, 2017), with various roles described in bacterial virulence and biofilm formation (Sy and Tree, 2021, Chambers and Sauer, 2013). For instance, EHEC GlmY and GlmZ sRNAs promote the formation of A/E lesions through induction of the T3SS effector EspFu, and diminish the expression of other T3SS effectors (Gruber et al, 2014).…”