Connection
between RNA processing and amino acid signalling in the FGM pathway in Saccharomyces
cerevisiae.
Ole Lagatie,
Inge Holsbeeks, Lisbeth Maurissen, Johan M. Thevelein
Lab. of Molecular Cell Biology, KULeuven, Kasteelpark Arenberg 31, Leuven,
3001, Belgium (ole.lagatie@bio.kuleuven.ac.be)
Yeast cells starved for nitrogen on a glucose-containing medium enter G0 and acquire several features characteristic for stationary phase, such as accumulation of reserve carbohydrates, induction of STRE-controlled genes, repression of ribosomal protein genes and enhanced stress resistance. Addition of amino acids to such cells causes growth resumption and rapid reversal of these phenotypes. We have previously shown that the General Amino acid Permease Gap1 acts as an amino acid sensor for the pathway responsible for this rapid cellular adaptation upon re-addition of nitrogen. C-terminal truncations of Gap1 were constructed that caused a constitutive activation of the pathway. Here we report that the latter phenotype is dependent on an additional mutation in the genome of the gap1Δ strain used. Furthermore this mutation also influences the phenotype of other Gap1 alleles. The mutated gene was identified by complementation with a genomic library. First results show that RPP1 is mutated in this strain and that it is very likely that the mutation in this gene is responsible for the observed phenotypes. RPP1 is an essential gene and the encoded protein is part of the RNase P and RNase MRP complex that are involved in respectively tRNA and rRNA processing. In the future we will analyse the role of this gene in Gap1 signalling.