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Regulation of mRNA Export by Nutritional Status in Fission Yeast
William A. Whalena, Jin Ho Yoona, Rulong Shenb, and Ravi Dharaa Basic Sciences Laboratory, National Cancer Institute, Bethesda, Maryland 20892
b ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702
Corresponding author: Ravi Dhar, National Institutes of Health, Bldg. 41, Rm. B506, Bethesda, MD 20892., dharr{at}dce41.nci.nih.gov (E-mail)
Communicating editor: P. G. YOUNG
nup184 null mutant is viable and also is synthetically lethal with rae1-167. In a rae1+ background, both the nup184-1 and
nup184 mutations confer sensitivity to growth in nutrient-rich medium (YES) that is accompanied by nuclear poly(A)+ RNA accumulation. Removal of the cAMP-dependent protein kinase, Pka1p, relieved the growth and mRNA export defects of nup184 mutants when grown in nutrient-rich medium. The activation of Pka1p is necessary, but not sufficient, to cause the severe poly(A)+ RNA export defects when nup184 mutant cells are incubated in YES, suggesting nutritional status can also regulate poly(A)+ RNA export. Our results suggest that the regulation of poly(A)+ RNA export by Pka1p kinase appears to be indirect, via a translation-dependent step, but post-translationally in response to YES.
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