The yeast LSM1/PAT1 complex essential for decapping
deadenylated mRNA is required for virus mRNA translation.
Amine Noueiry (1), Juana Diez (2), Shaun Falk (1), Paul Ahlquist
(1)
(1) IMV, U. of Wisconsin, Madison, 1525 Linden drive, Madison, WI 53706,
USA;
(2) Universidad Pompeu Fabra, Barcelona, Spain
The transition from mRNA translation to decapping and subsequent
degradation is a critical but poorly understood step in post-transcriptional regulation of gene expression. In this study, we used
the ability of the positive-strand RNA virus brome mosaic virus (BMV) to
replicate in yeast to understand viral RNA replication, cellular mRNA
decapping, and the interaction of these pathways with cellular mRNA
translation. Upon entering the host cell, viral genomes must first be
translated and then selectively recruited out of translation for
replication. We previously showed that a mutation in the yeast
LSM1 gene inhibits BMV RNA replication by inhibiting viral RNA
recruitment to the replication complex. Our recent results extend these
findings and show that both BMV RNA recruitment and translation are
closely connected to the cellular decapping pathway. We show that
LSM1 and other genes specifically required for deadenylated mRNA
decapping, including LSM6, LSM7, and PAT1, were all
selectively required for BMV RNA translation. In addition, we show that
the yeast genes UPF1-3, required for decapping aberrant mRNA, and
VPS16, and EDC1-2, required for decapping aberrant and
deadenylated mRNA, were not essential for BMV RNA translation.
Collectively, these results indicate that the LSM1/PAT1 complex
functions in decapping and translation of at least some mRNAs, and that
viral RNA replication is linked to the cellular pathway that transfers
mRNAs from translation to degradation.
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