Binding of the hepatitis C virus IRES to the 40S ribosomal subunit induces a pronounced conformational change and closes the mRNA binding cleft at about 20 A resolution.
The study reveals the structural mechanism by which HCV IRES positions mRNA in the ribosomal decoding center by inducing conformational changes in the 40S subunit.
Initiation of protein synthesis in eukaryotes requires recruitment of the 40S ribosomal subunit to the messenger RNA (mRNA). In most cases, this depends on recognition of a modified nucleotide cap on the 5' end of the mRNA. However, an alternate pathway uses a structured RNA element in the 5' untranslated region of the messenger or viral RNA called an internal ribosomal entry site (IRES). Here, we present a cryo-electron microscopy map of the hepatitis C virus (HCV) IRES bound to the 40S ribosomal subunit at about 20 A resolution. IRES binding induces a pronounced conformational change in the 40S subunit and closes the mRNA binding cleft, suggesting a mechanism for IRES-mediated positioning of mRNA in the ribosomal decoding center.
Spahn et al. (Fri,) conducted a other in Hepatitis C Virus. Hepatitis C Virus IRES RNA was evaluated on Conformational change in the 40S ribosomal subunit. Binding of the hepatitis C virus IRES to the 40S ribosomal subunit induces a pronounced conformational change and closes the mRNA binding cleft at about 20 A resolution.
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