Abstract
Three mutations, opaque-2 (o2), opaque-7 (o7) and floury-2 (fl2), each of which causes a depression in zein synthesis were studied. The processing efficiencies of the rough endoplasmic reticulum membranes in vitro, the levels of RNA transcription using cloned zein probes, and the genomic organization of the zein sequences as possible sites for the genetic defects were examined. The steps in prezein translation and processing occurring on the protein body membranes are not accountable for the lowered zein content in any of the mutations. The o2 mutation that typically shows a paucity of 22.5-kdalton zein polypeptides had a concomitant reduction in a particular subgroup of mRNAs coding for this size class. Southern analyses suggest that the o2 mutation is not the result of a large deletion of tandem-linked zein genes.