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Complementation, test crosses and F analyses have revealed that of 53 mutations influencing the epicuticular waxes on barley spikes and stems, (the uppermost internodes and leaf sheaths), one is dominantly and the other 52 recessively inherited alterations of the cer-n gene. The extent of the apparent wax loss or reduction is organ specific with the precise levels being susceptible to environmental factors. The ten analyzed mutants were divided into five types on the basis of their spike wax composition. Lipid classes derived from the acyl elongase system (alkanes, primary alcohols and esterified alkan-1-ols) and/or those arising via the β-keto acyl elongase system (β-diketones, hydroxy-β-diketones and esterified alkan-2-ols) can be affected. Furthermore, which and how many of the lipid classes synthesized by either system as well as the type of changes resulting are a property of the individual mutations. Whether cer-n represents a structural or regulatory locus for epicuticular wax biosynthesis is not clear, although the product of this gene must have a minimum of two functional sites. [ABSTRACT FROM AUTHOR]

Seventeen mutations resulting in an apparent loss of the epicuticular wax on barley spikes have been shown by complementation, test cross and F analyses to be dominantly inherited alterations of the Cer-yy gene. The chemical composition determined by the four alleles 966, 968, 975 and 984 differs from that determined by the wild type in that none of the β-ketoacyl derived lipids (β-diketones, hydroxy-β-diketones and esters containing alkan-2-ols) are synthesized while the composition of the other wax lipids (alkanes, primary alcohols, aldehydes, esters containing alkan-1-ols and free acids) is markedly altered toward that characteristic of leaf blade waxes. We suggest that the Cer-yy gene determines a regulatory component which upon mutation activates the gene(s) in the spike for the leaf blade acyl elongase system and at the same time represses the spike acyl and β-ketoacyl elongase systems. [ABSTRACT FROM AUTHOR]