Temperature regulation of seed dormancy and germination in Arabidopsis thaliana

The environmental regulation of seed dormancy and germination by temperature is an important process which allows the environmental conditions experienced by plants in the following generation to be controlled. Coping with temperature effects during seed maturation is essential for the consistent production of high quality seeds, but currently temperature signalling pathways in seeds are poorly understood. Previous work has shown that temperature during seed maturation regulates the levels of dormancy which are induced in the seed, although a mechanism for this pathway is currently unknown. Low temperature during imbibition promotes germination and although this is known to involve alterations to GA metabolism, again a mechanism is missing. Therefore, the aim of this study was to identify components of the mechanisms which regulate the temperature control of dormancy and germination in the model plant Arabidopsis thaliana.
Cool and warm seed maturation temperatures induce high and low levels of dormancy respectively in Arabidopsis. These changes to dormancy levels are coupled with altered ABA and GA levels and gene expression controlling hormone synthesis and breakdown. Changes in maturation temperature do not appear to be linked to altered seed coat morphology or embryo development.
During testing of cold-response mutants for dormancy phenotypes the expression of CBFs, a group of transcription factors which were characterised through the study of cold acclimation, was found to be necessary for dormancy. CBF RNAi and mutant seeds display reduced dormancy when matured at low temperature. However, the expression of CBFs is not promoted by exposure to low temperature in seeds, suggesting that this is not an important mechanism for the temperature control of dormancy.
More strikingly, the E3 ligase HOS1 is absolutely required for high dormancy levels in response to low maturation temperature. hos1 mutants show a complete loss of dormancy when matured at any temperature and this phenotype is maternally inherited. The germination of hos1 seeds in the presence of PAC or ABA does not differ from wild-type, thus suggesting that sensitivity to GA and ABA is not altered in these seeds. However, levels of GA are increased in hos1 mutant seeds, which could be important for the reduced dormancy phenotype. The expression of TT genes, which are responsible for the accumulation of anthocyanidins in the seed coat, is downregulated in hos1 mutants and so could be involved in the regulation of dormancy by HOS1. Therefore; HOS1 defines a novel essential maternal pathway that regulates dormancy levels which involves the regulation of GA metabolism.
A forward genetic screen identified a number of cold stratification insensitive (cosi) mutants. A thorough characterisation of these mutants revealed interesting phenotypes, but phenotypic variation and a lack of robust segregation data meant that the cosi mutants were not mapped.