CDK1 couples proliferation with protein synthesis [Repository Tables R1-R4]

DOI

Cell proliferation exerts a high demand on protein synthesis, yet the mechanisms coupling the two processes are not fully understood. A kinase and phosphatase screen for activators of translation, based on the formation of stress granules in human cells, revealed cell cycle-associated kinases as major candidates. CDK1 was identified as a positive regulator of global translation, and cell synchronization experiments showed that this is an extra-mitotic function of CDK1. Different pathways including eIF2α, 4EBP1 and S6K1 signaling contribute to controlling global translation downstream of CDK1. Moreover, Ribo-Seq analysis uncovered that CDK1 exerts a particularly strong effect on the translation of 5’TOP mRNAs, which includes mRNAs encoding for ribosomal proteins and several translation factors. This effect requires the 5’TOP mRNA-binding protein LARP1, concurrent to our finding that LARP1 phosphorylation is strongly dependent on CDK1. Thus, CDK1 provides a direct means to couple cell proliferation with biosynthesis of the translation machinery and the rate of protein synthesis.

Identifier
DOI https://doi.org/10.11588/data/EFHOBZ
Related Identifier https://doi.org/10.1083/jcb.201906147
Metadata Access https://heidata.uni-heidelberg.de/oai?verb=GetRecord&metadataPrefix=oai_datacite&identifier=doi:10.11588/data/EFHOBZ
Provenance
Creator Haneke, Katharina; Stoecklin, Georg
Publisher heiDATA
Contributor Haneke, Katharina; Division of Biochemistry, Medical Faculty Mannheim; Stoecklin, Georg
Publication Year 2020
Funding Reference Deutsche Forschungsgemeinschaft SFB1036, 201348542 ; Deutsche Forschungsgemeinschaft TRR186, 278001972
Rights info:eu-repo/semantics/openAccess
OpenAccess true
Contact Haneke, Katharina (Division of Biochemistry, Mannheim Institute for Innate Immunoscience (MI3), Medical Faculty Mannheim, Heidelberg University, Germany)
Representation
Resource Type Dataset
Format text/tab-separated-values
Size 42061; 4257; 464593; 44384
Version 1.1
Discipline Life Sciences; Medicine