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Distinct modes of non-canonical initiation regulate selective host versus viral mRNA translation during poxvirus-induced shutoff

ABSTRACT: Distinct modes of non-canonical initiation regulate selective host versus viral mRNA translation during poxvirus-induced shutoff

PROVIDER: PRJNA1166334 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30826313_1.fastq.gz	Fastqsanger.gz
	SRR30826313_2.fastq.gz	Fastqsanger.gz
	SRR30826314_1.fastq.gz	Fastqsanger.gz
	SRR30826314_2.fastq.gz	Fastqsanger.gz
	SRR30826315_1.fastq.gz	Fastqsanger.gz

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Distinct modes of non-canonical initiation regulate selective host versus viral mRNA translation during poxvirus-induced shutoff

Project description:Many viruses potently inhibit host protein synthesis while employing unconventional strategies to sustain their own translation, but how and why certain cellular mRNAs continue to be translated remains unclear. Here, we show that during shutoff by Vaccinia Virus (VacV) several host mRNAs increase in polysome occupancy but few, topped by JUN, result in increased protein abundance. Translation of viral mRNAs depended on the small ribosomal protein, Receptor for Activated C Kinase 1 (RACK1) and the eukaryotic Initiation Factor, eIF3. Cryo-electron microscopy (cryo-EM) further showed that eIF3 bound to virus-modified RACK1-containing 40S subunits that exhibit altered head rotation during infection. By contrast, RACK1 and eIF3 were dispensable for JUN translation. Moreover, structurally distinct 5’ untranslated regions (5’UTRs) in viral versus JUN mRNAs conferred differential eIF3 dependencies. Altogether, we reveal how distinct modes of non-canonical initiation support the production of both host and viral proteins that facilitate poxvirus replication despite infection-induced shutoff.

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Project description:Growing evidence suggests that ribosomes selectively regulate translation of specific mRNA subsets. Here, quantitative proteomics and cryo-electron microscopy demonstrated that poxvirus infection does not alter ribosomal subunit protein (RP) composition but skews 40S rotation states and displaces the 40S head domain. Genetic knockout screens employing metabolic assays and a dual-reporter virus further identified two RPs that selectively regulate non-canonical translation of late poxvirus mRNAs which contain unusual 5 polyA-leaders: RACK1 and RPLP2. RACK1 is a component of the altered 40S head domain while RPLP2 is a subunit of the P-stalk, wherein RPLP0 anchors two heterodimers of RPLP1 and RPLP2 to the large 60S subunit. RPLP0 was required for global translation, yet RPLP1 was dispensable while RPLP2 was specifically required for non-canonical poxvirus protein synthesis. Combined, we demonstrate that poxviruses structurally customize ribosomes and become reliant upon traditionally non-essential RPs from both ribosomal subunits for efficient initiation on their late mRNAs.

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