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Molecular Biology and Gene Regulation

Chloramphenicol Stimulates the Accumulation of Light-Harvesting Chlorophyll a/b Protein II by Affecting Posttranscriptional Events in the Chlorina CD3 Mutant Wheat ¹

Department of Plant Pathology, University of Kentucky, Lexington, Kentucky 04546, Department of Botany, North Dakota State University, Fargo, North Dakota 58105, Northern Regional Research Center, Agricultural Research Services, United States Department of Agriculture, Peoria, Illinois 61604

The levels of total chlorophyll (Chl), total carotenoids, light-harvesting Chl a/b apoprotein of photosystem II (LHCPII), and light-harvesting Chl a/b apoprotein (LHCP) mRNA were examined in the CD3 chlorina mutant wheat (Triticum aestivum, L.) after 18 hours greening at either a low (3 micromoles of photons per square meter per second) or moderate (200 micromoles of photons per square meter per second) irradiance. The Chl b and LHCPII deficient mutant wheat accumulated significantly greater levels of Chl and LHCPII when greened under low irradiance than when greened under a moderate irradiance level. The level of LHCP mRNA, as measured by dot-blot and Northern hybridization analyses to a cDNA probe, increased in response to the irradiance level in the wheat. Applications of chloramphenicol (CAP) to the mutant wheat increased total Chl, Chl b, and LHCPII accumulations at both irradiance levels. Even though the CAP-treated CD3 mutant wheat accumulated similar levels of plastid pigments as those of CAP-treated wild type, the LHCPII amounts were much higher in the wild type than in the CD3 mutant of wheat. CAP treatment did not significantly increase the LHCP mRNA level in either wheat. Applications of either benzyladenine or CAP to the mutant, greened under the moderate irradiance level for 72 hours, increased all plastid pigment levels except for -carotene. The benzyladenine plus CAP combination treatment had little effect on the LHCPII levels in the wild-type wheat. The combination treatment increased the LHCPII accumulation in the CD3 mutant of wheat by about twice that of the untreated mutant. Excess LHC pigment accumulation was promoted in each wheat line. We conclude that the regulation of LHCPII in the CD3 mutant of wheat is controlled by a posttranscriptional event. Furthermore, the accumulation of LHC bound pigments is not coupled with the accumulation of LHCPII in wheat thylakoid membranes.