RESUMEN
Consistent with its location on the ribosome, reporter assays demonstrate a role for Rps26 in recognition of the Kozak sequence. Consequently, Rps26-deficient ribosomes display preference for mRNAs encoding components of the high salt and high pH stress response pathways and accumulate in yeast exposed to high salt or pH. Here we use this information to reprogram the cellular response to high salt by introducing point mutations in the Kozak sequence of key regulators for the cell wall MAP-kinase, filamentation, or DNA repair pathways. This stimulates their translation upon genetic, or salt-induced Rps26 depletion from ribosomes. Stress resistance assays show activation of the targeted pathways in an Rps26- and salt-dependent manner. Genomic alterations in diverse yeast populations indicate that analogous tuning occurs during adaptation to ecological niches. Thus, evolution shapes translational control across the genome by taking advantage of the accumulation of diverse ribosome populations.