From the earlier account of the association of variation in the expression of genes with germination and dormancy, a hypothetical model of these genes was developed. The model is based around the two hormones, ABA and GA. Levels of, and sensitivity to, these hormones may be influenced by the genotype and the environment. ABA is associated with maturation and dormancy, which in turn is associated with LEAs and other genes not directly controlling dormancy but have a role in, e.g. deposition of storage reserves or protecting the seed. Balancing ABA and GA are the proposed key genes involved in the switch between dormancy and germination of A. fatua seeds. In the centre is Vp1, which is a seed-specific gene linked with dormancy in A. fatua (Jones et al., 1997, 2000). Vp1 is induced by ABA and represses GA induced expression of germination genes such as AMY (Hoecker et al., 1995). Vp1 was also found to activate ABI5 and together they bind ABA-responsive elements (ABREs) in promotion of ABA induced genes (Suzuki et al., 2003). Vp1 interacts with the bZIP TRAB1 from rice (Hobo et al., 1999); so Vp1 protein may also interact with the bZIP TaABF (Johnson et al., 2002). TaABF is similar to ABI5 of which there are many types from the same gene family, apparently with an overlapping function and perhaps individually important in different tissues. The homologue Avena fatua ABF (AfABF) appears to be the best candidate for a seed-specific bZIP gene involved in A. fatua dormancy. TaABF is ABA induced and is a physiological substrate for PKABA1 (i.e. PKABA1 phos-phorylates TaABF) (Johnson et al., 2002). PKABA1 is ABA induced (Anderberg and Walker-Simmons, 1992) and overexpression represses GA-mediated expression of AMY (Gómez-Cadenas et al., 1999). ABI4 is hypothesized to balance ABA sensitivity via interaction with ABI5, ABI4 and ABI3 loci (Soderman et al., 2000). ABI1 and ABI2 mRNA and enzyme activity increase in response to ABA (Leung et al., 1997; Merlot et al., 2001). These genes are negative regulators of ABA signalling and it is speculated that ABI1/ABI2 act as phosphatases in a negative feedback regulatory loop, allowing the cell to monitor ABA levels (Merlot et al., 2001). Suzuki et al. (2003) presented a model of the feed forward regulation of ABA signalling mediated by Vp1. This shows that ABA induces Vp1 and ABI1/2, while Vp1 inhibits ABA induction of ABI1/ABI2. PP2Cs also phosphorylate and inactivate SNF1 protein kinases, SnRK1 (Sugden et al., 1999), which may be a link between the SnRK1 complex and ABI genes.
High levels of Lycopersicon esculentum SNF4 (LeSNF4) are associated with tomato seed dormancy and ABA, while a decrease in expression was observed during non-dormant seed germination or imbibition in GA (Bradford et al., 2003). It is hypoth esized that during maturation LeSNF4 (^-subunit of the SnRKl complex) binds to LeSNFl/SnRKl promoting accumulation of storage reserves. LeSNFl transcripts were present in mature, dry and imbibed seeds, but ABA, GA, dormancy or germination status did not affect abundance. SnRKl (with >80% amino acid identity to LeSNFl) is also present in wheat and was able to inhibit the AMY promoter in developing seeds (Laurie et al., 2003).
Germination genes in the model include GA20-oxidase. ABA suppresses transcription of this gene in sorghum and beech (Pérez-Flores et al., 2003; Calvo et al., 2004). Expression was also low in GA3 treated seeds (Calvo et al., 2004). Rht orthologues such as the DELLA protein SLNl from barley (Chandler et al., 2002) and RGL2 from Arabidopsis (Dill and Sun, 200l) may also be important in seeds. RGL2 is enhanced by other DELLAs (Lee et al., 2002) and protein degradation is induced by GA via Spindly-l (SLYl) (Tyler et al., 2004). ABA has no effect on GA enhanced SLNl degradation (Gubler et al., 2002). Also important in the GA response pathway is GA-regulated myeloblastosis (GAMYB), which is upregulated by GA (Gubler et al., l995) and binds to AMY and other promoters of genes encoding hydrolytic enzymes (Gubler et al., l999). SLNl is thought to repress GAMYB via PKABA1 (Zentella et al., 2002). The comatose (CTS) locus also regulates germination potential by enhancing after-ripening, and increasing sensitivity to GA and pre-chilling (Russell et al., 2000). CTS, an ATP binding cassette (ABC) transporter, does not increase in imbibed dormant seeds, but increases in non-dormant seeds and regulates transport of acyl-coenzyme As (acylCoAs) into the peroxisome (Footitt et al., 2002).
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