
Dosage suppression of the Kluyveromyces lactis zymocin by Saccharomyces cerevisiae ISR1 and UGP1
Author(s) -
Mehlgarten Constance,
Zink Sabrina,
Rutter Jared,
Schaffrath Raffael
Publication year - 2007
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2007.00216.x
Subject(s) - kluyveromyces lactis , biology , saccharomyces cerevisiae , cyclin dependent kinase , mutant , cyclin dependent kinase 1 , kinase , kluyveromyces , biochemistry , genetics , microbiology and biotechnology , cell cycle , cell , yeast , gene
The Kluyveromyces lactis zymocin complex kills Saccharomyces cerevisiae cells in a process that involves tRNA cleavage by its tRNAse γ‐toxin subunit. In contrast to the γ‐toxin mode of action, the early steps of the zymocin response are less well characterized. Here, we present high‐dosage suppressors of zymocin that encode a putative Pkc1‐related kinase ( ISR1 ) and UDP‐glucose pyrophosphorylase (UGPase) ( UGP1 ). Anti‐UGPase Western blots and GAL10 – ISR1 overexpression suggest that zymocin suppression correlates with overproduction of UGPase or Isr1. As judged from protection against exo‐zymocin and unaltered sensitivity to endogenous γ‐toxin, high‐copy ISR1 and UGP1 operate in early, nontarget steps of the zymocin pathway. Consistent with a recent report on in vitro phosphorylation of Isr1 and UGPase by the CDK Pho85, high‐copy ISR1 and UGP1 suppression of zymocin is abolished in a pho85 null mutant lacking CDK activity of Pho85. Moreover, suppression requires UGPase enzyme activity, and ISR1 overexpression also protects against CFW, a chitin‐interfering poison. Our data agree with roles for UGPase in cell wall biosynthetic processes and for Isr1 in Pkc1‐related cell wall integrity. In sum, high‐copy ISR1 and UGP1 cells affect early steps of the zymocin response and potentially prevent the lethal K. lactis killer complex from establishing cell surface recognition and/or contact.