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J. Bacteriol., 12 1995, 6761-6765, Vol 177, No. 23
DD Markwardt, JM Garrett, S Eberhardy and W Heideman
Cells carrying mutations that activate the Ras/cyclic AMP (Ras/cAMP)
pathway fail to accumulate in G1 as unbudded cells and lose viability in
response to nitrogen starvation. This observation has led to the idea that
cells carrying this type of mutation are sensitive to nitrogen starvation
because they are unable to appropriately arrest in G1. In this study, we
tested predictions made by this model. We found that cells with activating
Ras/cAMP pathway mutations do not continue to divide after nitrogen
starvation, show a normal decrease in steady state levels of START-specific
transcripts, and are not rescued by removal of cAMP during nitrogen
starvation. These findings are inconsistent with the idea that activation
of the Ras/cAMP pathway prevents growth arrest in cells starved for
nitrogen. Our finding that cells with an active Ras/cAMP pathway have
dramatically reduced amino acid stores suggests an alternative model. We
propose that cells at high cAMP levels are unable to store sufficient
nutrients to allow return to the G1 phase of the cell cycle when they are
suddenly deprived of nitrogen. It is this inability to return to G1, rather
than a failure to arrest, which leaves cells at different points in the
cell cycle following nitrogen starvation.
Copyright © 1995, American Society for Microbiology
Activation of the Ras/cyclic AMP pathway in the yeast Saccharomyces cerevisiae does not prevent G1 arrest in response to nitrogen starvation
School of Pharmacy, University of Wisconsin, Madison 53706, USA.
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