Chloroplast photooxidation inhibits the expression of a set of nuclear genes |
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Authors: | Stephen P. Mayfield and William C. Taylor |
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Affiliation: | (1) Department of Genetics, University of California, 94720 Berkeley, CA, USA;(2) Present address: Department of Molecular Biology, Scrips Research Clinic, 10666 North Torrey Pines Road, La Jolla, Calif, USA |
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Abstract: | Summary Mutations or herbicides which inhibit the accumulation of carotenoid pigments in higher plants also result in the arrest of chloroplast development at a very early stage. The cause is extensive photooxidative damage within the chloroplast in the absence of protective carotenoids. Because the extent of photooxidation is dependent upon light intensity, normal chloroplast development can occur when carotenoid-deficient seedlings are grown in very dim light. Normal accumulation of chloroplastic and cytosolic mRNAs encoding chloroplast proteins proceeds only under permissive dim light conditions. Illumination with higher intensity light causes rapid chlorophyll photooxidation and the loss of two cytosolic mRNAs coding for proteins destined for the chloroplast, but does not affect another light-regulated cytosolic mRNA encoding a cytosolic protein. This experimental system may have uncovered a mechanism which coordinates the expression of genes in different cellular compartments.Abbreviations LHCP light-harvesting chlorophyll a/b protein - SSu small subunit - RuBP fibulose 1,5-bisphoshate - PEP phosphoenolpyruvate |
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Keywords: | Carotenoid-deficient mutants Herbicide bleaching Plastid differentiation |
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