Control of messenger RNA stability in Saccharomyces cerevisiae
The effect of glucose on ribosomal protein mRNA stability was examined. The addition of glucose, to a final concentration as low as 0.01%, resulted in a dramatic, transient increase in ribosomal protein mRNA stability. It has been demonstrated that protein kinase A (PKA) activity plays an important role in the up-regulation of ribosomal protein gene transcription in response to glucose addition. PKA pathway is required for the transient stabilisation of ribosomal protein mRNA following glucose addition, mRNA half-lives were determined in a PKA mutant strain. The data indicated that this glucose effect is not dependent upon a functional Ras-cAMP-PKA signalling pathway. Previously it was shown that the glucose-induced upshift in ribosomal protein gene transcription could be triggered by the addition of exogenous cAMP. However, that dibutyryl cAMP did not act efficiently as a second messenger in the signalling pathway mediating the glucose effect, or that cAMP signalling is not required for the transient stabilisation of ribosomal protein mRNAs. The involvement of specific glucose signalling factors was also examined. The glucose sensors, Snf3p and Rgt2p, were not required for the stabilisation of the ribosomal protein mRNAs. It was noted however, that phosphorylation of glucose by any one of the three yeast hexose kinases (Hxk1p, Hxk2p or Glk1p) was required to mediate this effect.