The nuclear-cytoplasmic distribution of
tRNA depends on the balance between
tRNA nuclear export/re-export and retrograde
tRNA nuclear import in Saccharomyces cerevisiae. The distribution of
tRNA is sensitive to nutrient availability as cells deprived of various nutrients exhibit
tRNA nuclear accumulation.
Starvation induces numerous events that result in translational repression and P-body formation. This study investigated the possible coordination of these responses with
tRNA nuclear-cytoplasmic distribution. Dhh1 and Pat1 function in parallel to promote translation repression and P-body formation in response to
starvation. Loss of both, Dhh1 and Pat1, results in a failure to repress translation and to induce P-body formation in response to
glucose starvation. This study reports that nutrient deprived dhh1 pat1 cells also fail to accumulate
tRNA within nuclei. Conversely, inhibition of translation initiation and induction of P-body formation by overproduction of Dhh1 or Pat1 cause
tRNA nuclear accumulation in nutrient-replete conditions. Also, loss of the
mRNA decapping activator, Lsm1, causes
tRNA nuclear accumulation. However, the coordination between P-body formation, translation repression, and
tRNA distribution is limited to the early part of the P-body formation/translation repression pathway as loss of
mRNA decapping or 5' to 3' degradation does not influence
tRNA nuclear-cytoplasmic dynamics. The data provide the first link between P-body formation/translation initiation and
tRNA nuclear-cytoplasmic dynamics. The current model is that Dhh1 and Pat1 function in parallel to promote
starvation-induced
tRNA nuclear accumulation.