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Plant Physiology 94:1237-1243 (1990)
© 1990 American Society of Plant Biologists

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Environmental and Stress Physiology

Hypoxic Stress-Induced Changes in Ribosomes of Maize Seedling Roots 1

Julia Bailey-Serres2 and Michael Freeling

Department of Plant Biology, University of California, Berkeley, California, 94720

The hypoxic stress response of Zea mays L. seedling roots involves regulation of gene expression at transcriptional and posttranscriptional levels. We investigated the effect of hypoxia on the translational machinery of seedling roots. The levels of monoribosomes and ribosomal subunits increased dramatically within 1 hour of stress. Prolonged hypoxia resulted in continued accumulation of nontranslating ribosomes, as well as increased levels of small polyribosomes. The return of seedlings to normal aerobic conditions resulted in recovery of normal polyribosome levels. Comparison of ribosomal proteins from control and hypoxic roots revealed differences in quantity and electrophoretic mobility. In vivo labeling of roots with [35S]methionine revealed variations in newly synthesized ribosomal proteins. In vivo labeling of roots with [32P]orthophosphate revealed a major reduction in the phosphorylation of a 31 kilodalton ribosomal protein in hypoxic stressed roots. In vitro phosphorylation of ribosomal proteins by endogenous kinases was used to probe for differences in ribosome structure and composition. The patterns of in vitro kinased phosphoproteins of ribosomes from control and hypoxic roots were not identical. Variation in phosphoproteins of polyribosomes from control and hypoxic roots, as well as among polyribosomes from hypoxic roots were observed. These results indicate that modification of the translational machinery occurs in response to hypoxic stress.


2 Present address: Department of Botany and Plant Sciences, University of California, Riverside, CA 92521.

1 Supported by postdoctoral research awards from National Institutes of Health (5-F32-GM11112-03) and U.S. Department of Agriculture (89-37264-4837) to J.B.-S. and a grant from National Institutes of Health grant (2-R01-GM21734-12) to M.F.




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