Seeds ensure the survival of most land plant species and the conservation of their unique genetic resources. Seed longevity is a quantitative trait that depends on environmental conditions during formation, harvest and storage of seeds and on structures, macromolecules and chemical compounds that protect the embryo. Seed longevity is consequently a complex genetic trait to dissect. Its study requires the identification of factors that result in an improvement or in a reduction of seed longevity. Wild-type seeds of the model plant Arabidopsis remain viable for several years, which makes the study of longevity a time consuming process. An approach to overcome this problem makes use of the seed developmental mutants abi3-5 and lec1-3, that cause rapid seed deterioration. These mutants provide a sensitized genetic background in which the effects of genes influencing longevity can be faster evaluated. The Arabidopsis natural variation for longevity was exploited by crossing several Arabidopsis accessions with abi3-5 and lec1-3 mutants and subsequent selection of lines with improved longevity in the progeny. As a result, various introgression lines carrying natural modifiers alleles were identified. The three natural modifier lines with the strongest effects were selected. One had an introgression of the Seis am Schlern accession in abi3-5 background and two had different introgressions of the Shahdara accession in lec1-3 background. These lines were backcrossed with abi3-5 or lec1-3 to reduce the contribution of wild-type accession�s genome and to map the modifiers. The seed proteome profiles of modifier and mutant lines were studied in relation to longevity. This analysis revealed that the two modifiers from Shahdara could activate the expression of most seed storage proteins in a LEC1-independent way. In addition, four abi3-5 suppressor mutants derived from a mutagenesis screen were studied. In these lines the level of oxidative damage was correlated with seed longevity. The strongest suppressor, suppressor of abi3-5 (sua), reverted all of the abi3-5 mutant phenotypes. Fine mapping and map based cloning revealed that SUA encodes an RNA binding protein. Interestingly, sua only suppressed the abi3-5 allele but did not affect other abi3 alleles. Immunological analysis revealed that abi3-5 seeds contain a truncated abi3 protein which is restored to nearly full length ABI3 protein in the sua abi3-5 double mutant. Analysis of transcripts revealed that the sua mutation causes the splicing of a cryptic intron in ABI3 and the accumulation of a splice variant that repairs the abi3-5 mutation and results in a shorter but functional version of the ABI3 protein. The SUA gene is not directly implicated in seed longevity, but participates in mRNA metabolism processes
