Key result
sRNA Spot42 represses sdhC mRNA translation by recruiting Hfq to compete with 30S ribosomal subunits.
Why the study?
The canonical model of sRNA regulation posits that sRNAs directly compete with initiating ribosomes while Hfq plays only an indirect role, but this mechanism was not fully understood for certain mRNAs.
This study identifies a novel noncanonical mechanism of translation initiation repression where the RNA chaperone Hfq directly represses the target mRNA, with the sRNA acting only as a recruitment factor.
Novel Hfq recruitment mechanism defined in bacteria; extends prokaryotic regulation models but leaves open cardiovascular relevance.
The RNA chaperone Hfq is mostly known to help small regulatory RNAs (sRNAs) interact with target mRNAs to block initiating ribosomes. In this model, whereas the sRNA is directly competing with initiating 30S ribosomal subunits, Hfq plays only an indirect role, allowing optimal sRNA-mRNA pairing. Here we report that Hfq is recruited by a sRNA, Spot42, to bind to a precise AU-rich region in the vicinity of the translation initiation region (TIR) of sdhC mRNA and competes directly with 30S ribosomal subunits. We show that the sRNA Spot42 binds sdhC too far upstream of the TIR to directly repress translation initiation in vitro and in vivo. Contrary to the canonical model of sRNA regulation, this suggests a new mechanism where Hfq is directly involved in the translational repression of the target mRNA and where the sRNA acts only as a recruitment factor.
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Desnoyers et al. (2012) studied this question. sRNA Spot42 and Hfq was evaluated on Translational repression of sdhC mRNA. The sRNA Spot42 recruits the RNA chaperone Hfq to bind near the translation initiation region of sdhC mRNA, directly competing with 30S ribosomal subunits to repress translation.
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