Abstract
The mutation of a nuclear gene in peanut (Arachis hypogaea L.) plants results in a reduced light-dependent development of chloroplast fine structure, soluble protein, ribulose-1, 5-diP carboxylase, NADP-glyceraldehyde-3-P dehydrogenase, fructose-1, 6-diP aldolase, glycerate-3-P kinase, phosphoenolpyruvate carboxylase, malate dehydrogenase, and dark respiration during the 72-hour lag period of chlorophyll synthesis in dark-grown leaves exposed to continuous light. The mutation has pleiotropic affects. Kinetic analysis shows there is also a 72-hour lag period in the light-dependent development of NADP-glyceraldehyde-3-P dehydrogenase and fructose-1, 6-diP aldolase in the mutant leaves, whereas there is no lag in the development of NAD-malate dehydrogenase and dark respiration. There is minimal development of the chloroplast during the 72-hour mutationally induced lag period, but there is pronounced cytoplasmic and mitochondrial activity during this phase. There is a 24-hour lag period in the light-dependent enlargement of the mutant leaves. At the completion of leaf enlargement, chloroplast differentiation is initiated. The mutation does not result in any chloroplast deletions, it only affects the timing of the synthesis of these components.Elimination of the lag period in leaf enlargement and chloroplast development (potentiation) requires a preliminary 72- to 96-hour dark period before exposing the dark-grown leaves to continuous light. There is extensive development of the etioplasts during this dark period. These results establish that the nuclear gene mutation affects the early stages of plastid development and not the light-dependent synthesis of plastid components. The nuclear gene may code for the regulation of the synthesis of a component (nutrient) in the dark (or during the lag phase in the light) which is essential for the development of mesophyll cells and plastids. Although, the chloroplast is a semi-autonomous organelle, nuclear gene control of chloroplast differentiation may not be independent of cellular growth.