<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE144nnn/GSE144250/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Other</omics_type><species>Saccharomyces cerevisiae</species><gds_type>Other</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144250</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>The Ccr4-Not complex monitors the translating ribosome for codon optimality</name><description>Control of messenger RNA (mRNA) decay rate is intimately connected to translation elongation, but the spatial coordination of these events is poorly understood. The Ccr4-Not complex initiates mRNA decay through deadenylation and activation of decapping. We used a combination of cryo–electron microscopy, ribosome profiling, and mRNA stability assays to examine the recruitment of Ccr4-Not to the ribosome via specific interaction of the Not5 subunit with the ribosomal E-site in Saccharomyces cerevisiae. This interaction occurred when the ribosome lacked accommodated A-site transfer RNA, indicative of low codon optimality. Loss of the interaction resulted in the inability of the mRNA degradation machinery to sense codon optimality. Our findings elucidate a physical link between the Ccr4-Not complex and the ribosome and provide mechanistic insight into the coupling of decoding efficiency with mRNA stability.</description><dates><publication>2020/04/16</publication></dates><accession>GSE144250</accession><cross_references><GSM>GSM4284447</GSM><GSM>GSM4284448</GSM><GSM>GSM4284449</GSM><GSM>GSM4284446</GSM><GPL>21656</GPL><SRA>SRP244728</SRA><GSE>144250</GSE><taxon>Saccharomyces cerevisiae</taxon><PMID>[32299921]</PMID></cross_references></HashMap>