Abstract
Dpl, a cytoplasmically inherited plastid defect of Nicotiana tabacum L., has been further characterized by pigment and ribulose diphosphate carboxylase (RuDPCase) assays and electron microscopy. RuDPCase activity was reduced in defective plastids to 20–67% of that in normal chloroplasts. The chlorophyll content was reduced to 5% or less of that in normal chloroplasts. Leaf areas with only defective plastids were very light green for several days after the leaf began to expand but eventually turned white. This loss of chlorophyll was correlated with a reduction in internal plastid lamellae, but there was much less reduction in RuDPCase activity. The presence of cells with both mutant and normal plastids indicate that the plastid and not some other cytoplasmic factor was the site of the controlling unit.
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Scientific Paper No. 3812, College of Agriculture, Washington State University, Pullman, Projects 1916 and 1920. Supported in part by funds provided for medical and biological research by Washington State Initiative Measure 171.
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Shumway, L.K., Kleinhofs, A. Aspects of the biochemistry and ultrastructure of a cytoplasmically inherited plastid defect (Dp1) of tobacco. Biochem Genet 8, 271–280 (1973). https://doi.org/10.1007/BF00486180
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DOI: https://doi.org/10.1007/BF00486180