Abstract
A spontaneous mutation arising in Festuca pratensis has the effect of stabilizing the pigmentproteolipid complexes of thylakoid membranes so that leaf tissue does not turn yellow during senescence. Inheritance of the non-yellowing character was analysed in crosses between the wild-type cultivar Rossa and a mutant line Bf 993. Electrophoretic variants of cytoplasmic phosphoglucoisomerase coded by alleles of the nuclear gene Pgi-2 were used to identify hybrids during intercrossing. About 96% of the F1 progeny were heterozygous and all were phenotypically yellowing. In the F2 generation yellow ∶ green segregated in a ratio of 2.14∶1, not significantly different from 3∶1. In the backcross between F1 and Bf 993 the ratio was 1∶1 yellow ∶ green. There was no indication of linkage to Pgi-2. Senescence of detached Bf 993 and Rossa leaves was compared with that of the F1 hybrid. The hybrid behaved in an essentially identical fashion to the wildtype parent, and in marked contrast to the mutant, in all aspects of the senescence syndrome investigated, including loss of chlorophyll, carotenoids and the light-harvesting chlorophyll-protein of thylakoid membranes, and elevation of the particulate protein ∶ chlorophyll ratio in the terminal stages. It is concluded that there exists in Festuca pratensis a nuclear gene, designated Sid (senescence-induced degradation) which regulates turnover of hydrophobic components of photosynthetic membranes in ageing leaf tissue and which occurs in at least two allelic forms, y (yellow) dominant over g (green).