Macromolecular physiology of plastids XII. Tigrina mutants in barley: genetic, spectroscopic and structural characterization

Abstract

Several tigrina mutants of barley, namely tig‐b7, ‐b19, ‐b23, ‐b24, ‐f11, ‐m31, ‐n32, ‐33, and ‐o34 can accumulate chlorophyll(ide) a (abbr. Chl a) with an absorption maximum near 742 nm in addition to Chl a absorbing near 676 nm. The amount of 742 nm absorbing Chl a present in mutant leaves is dependent on the allele and the growth conditions. The accumulation of 742 nm absorbing Chl a is accompanied by formation of abnormal membrane organizations in the plastids. Etiolated leaves of seedlings homozygous for mutations in the regulatory genes tig‐b, tig‐d, tig‐n, tig‐33, or tig‐o accumulate protochlorophyll(ide) (Pchl) in amounts exceeding the wild type level. The final Pchl content is dependent on the particular mutant gene. Seedlings heterozygous for tig‐b and tig‐d mutations accumulate more Pchl than wild type seedlings. The increased Pchl contents are coupled with changed absorption properties of the etiolated leaves, the main absorption maximum in the red region being near 633 nm rather than near 650 nm. Abnormal membrane organizations are observed in etioplasts of the mutants tig‐b7, ‐b19, ‐h23, ‐b24, ‐n32, ‐33, and ‐o34, while the ultrastructure of etioplasts of tig‐d12 closely resembled that of the wild type. Membrane abnormalities in etioplasts are paralleled by altered carotenoid compositions in the mutants. Likewise, only those regulatory mutants with an aberrant carotenoid composition can accumulate 742 nm absorbing Chl a. © 1974 Mendelian Society of Lund