Mutations affecting flowering time
Much of the early work to identify mutants affected in flowering time was based on screening for late-flowering mutants (Redei, 1962; Koornneef et al., 1991; Koornneef et al., 1998a) . In these populations the co, gigantea (gi) and luminidependens (ld) mutants were the first to be identified (Redei, 1962) . One of the reasons that these early screens identified only mutations that delay flowering was that the progenitor accessions (Ler; Col ; Wassilewskija (Ws)) were all early flowering under the screening conditions used. More recently screening was also carried out using later flowering accessions leading to the identification of early-flowering mutants (Michaels and Amasino, 1999) , also early-flowering accessions screened under non-inductive conditions yielded different early flowering mutants (Noh and Amasino, 2003) .
The construction of double mutants carrying two mutations that delay flowering enabled the positions of genes into genetic pathways (Figure 1.1). If double mutants flowered at a similar time to single mutants, then the affected genes were placed in the same genetic pathway. Conversely if mutations showed an additive effect upon flowering time, so that a double mutant flowered later than either single mutant, then the mutations were proposed to affect different pathways (Koornneef et al., 1991; Coupland, 1995a).
The genetic analysis was supported by physiological data. So for example, mutations positioned in one pathway (later called the autonomous pathway) based on genetic criteria all confirmed a response to vernalisation, and those placed in a second pathway (later called the photoperiod pathway) did not confer a vernalisation response but were day length insensitive. This combination of physiological and genetic analysis identified the four main pathways responsible for flowering-time control in Arabidopsis.
Early flowering mutants identified genes required to repress flowering (Sung et al., 2003) . These mutants include early flowering 3 and 4 (elf3; elf4); terminal flower 1 (tfl1); early flowering in short days (efs); early in short days 4 (esd4); flc and mads affecting flowering1/flowering locus m (maf1/flm) (Zagotta et al., 1996; Liljegren et al., 1999; Michaels and Amasino, 1999; Sheldon et al., 1999; Soppe et al., 1999; Hicks et al., 2001; Ratcliffe et al., 2001; Scortecci et al., 2001; Doyle et al., 2002; Reeves et al., 2002) . Some of these genes were highly pleiotrophic and later proved to have general effects in chromatin remodelling, including terminal flower 2 (tfl2); embryonic flower 1 and 2 (emf1; emf2) and fertilisation-independent endosperm (fie) (Sung et al., 1992; Larsson et al., 1998; Ohad et al., 1999; Aubert et al., 2001; Yoshida et al., 2001).
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