Regulation of flowering time in Arabidopsis



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Flowering pathway

Gibberellin pathway



The Gibberellin transduction pathway


Interaction between GAs, GAI and SOC1


The GA transduction pathway is the only one inducing SOC1 in short days:

Moon et al. (2003) studied the interaction between the GA and the vernalization pathways in the regulation of flowering time. SOC1 expression was measured in two backgrounds fully responsive to vernalization (ga1-3 FRI FLC and GA1 FRI FLC). In long days (LD), vernalization accelerates flowering, and up-regulates SOC1 expression. However, in short days (SD), the FRI FLC plants still respond to vernalization but SOC1 expression does not increase in the ga1-3 FRI FLC plants.

In the ga1-3 FRI FLC plants, SOC1 expression is restored by GA treatment (Moon et al., 2003). This would indicate that GAs (instead of the whole GA transduction pathway) are sufficient to restore SOC1 expression. However, this is not the case, and the GAI function is also required (See below).

Plants over-expressing SOC1 in the ga1-3 background flower early in both short days and long days, but the effect is much stronger in short days (Blazquez et al., 2002).

The soc1-101d mutants constitutively over-express SOC1. They flower very early in SD and do not respond to GA treatment. The ga1-3 soc1-101d double mutants also flower early in SD. So, high levels of SOC1 can compensate (although not completely) for the effects of the ga1-3 mutation in SD. This confirms that the GA transduction pathway regulates SOC1 expression in SD (Moon et al., 2003).

SOC1 and miR159 are independent within the GA pathway:

An increase in the miR159 transcript levels does not affect SOC1 expression (Achard et al., 2004).

GAI is necessary for GA-induced up-regulation of SOC1 expression:

SOC1 expression is down-regulated in the gai-t6 mutants, and not affected by GA treatment. This means that the GAI function is necessary for the up-regulation of SOC1 by the GAs (Achard et al., 2004).

However, in the triple mutants ga1-3 gai-t6 rga-24, the SOC1 transcript levels are even higher than in the WT, either with or without GA treatment (Achard et al., 2004).

There is a paradox in these results, as the lack of either GAI or GA1 functions causes a down-regulation of SOC1 expression, but the lack of RGA, GAI and GA1 functions together results in a high expression of SOC1. According to Achard et al. (2004), this means that the rga and gai mutations suppress the effect of ga1-3 on SOC1 expression. But what would be the mechanism?