Photooxidative destruction of chloroplasts and its consequences for cytosolic enzyme levels and plant development.

Mustard (Sinapis alba L.) seedlings were grown in the presence of herbicides (Difunon, Norflurazon) which inhibit carotenoid synthesis without affecting development, in darkness or in continuous far-red light. In strong white light (12,000 lx) the cotyledons of the herbicide-treated seedlings did not contain normal chloroplasts, but only small chlorophyll-free rudiments whose internal structure had almost disappeared. The plastid marker enzyme NADP-dependent glyceraldehyde-3-phosphate dehydrogenase was almost lacking. Plastid ribosomes and ribosomal RNAs were no longer detectable nor could synthesis of mature plastidal ribosomal RNAs be detected. Cytosolic ribosomes and rRNAs were not affected. Plastid DNA was apparently still intact as shown by restriction analysis. The appearance of marker enzymes of glyoxisomes, mitochondria and cytosol was not impaired while the level of marker enzymes of peroxisomes was drastically lowered. Accumulation of anthocyanin in mustard cotyledons was normal after a short, transient delay. Levels of representative enzymes of flavonoid biogenesis (phenylalanine ammonia-lyase, chalcone synthase) were somewhat increased rather than inhibited in the cotyledons of herbicide-treated, white-light-grown seedlings. The growth rate of hypocotyl and cotyledons was inhibited to the same extent in the herbicide-treated, white-light-grown seedling, although light inhibits growth of hypocotyls and promotes growth of cotyledons. Analysis of the data shows that photomorphogenesis of a herbicide-treated, white-light-grown seedling is normal, and is thus independent of plastid gene expression However, a 'factor' which coacts multiplicatively with phytochrome in determining the growth rate of the organs seems to originate from the plastids. Biogenesis of anthocyanin and synthesis of major enzymes of the flavonoid pathway are not affected adversely by a photooxidative elimination of plastid gene expression.