PKA isoforms coordinate mRNA fate during nutrient starvation

Vanesa Tudisca, Clare Simpson, Lydia Castelli, Jennifer Lui, Nathaniel Hoyle, Silvia Moreno, Mark Ashe, Paula Portela

    Research output: Contribution to journalArticlepeer-review

    Abstract

    A variety of stress conditions induce mRNA and protein aggregation into mRNA silencing foci, but the signalling pathways mediating these responses are still elusive. Previously we demonstrated that PKA catalytic isoforms Tpk2 and Tpk3 localise with processing and stress bodies in Saccharomyces cerevisiae. Here, we show that Tpk2 and Tpk3 are associated with translation initiation factors Pab1 and Rps3 in exponentially growing cells. Glucose starvation promotes the loss of interaction between Tpk and initiation factors followed by their accumulation into processing bodies. Analysis of mutants of the individual PKA isoform genes has revealed that the TPK3 or TPK2 deletion affects the capacity of the cells to form granules and arrest translation properly in response to glucose starvation or stationary phase. Moreover, we demonstrate that PKA controls Rpg1 and eIF4G1 protein abundance, possibly controlling cap-dependent translation. Taken together,our data suggest that the PKA pathway coordinates multiple stages in the fate of mRNAs in association with nutritional environment and growth status of the cell. © 2012.
    Original languageEnglish
    Pages (from-to)5221-5232
    Number of pages11
    JournalJournal of Cell Science
    Volume125
    Issue number21
    DOIs
    Publication statusPublished - 2012

    Keywords

    • PKA
    • Saccharomyces cerevisiae
    • Translation

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