A few master regulatory genes, namely LEC1 (LEAFY COTYLEDON 1), LEC2 and FUS3 (FUSCA 3) have been shown to act as key transcriptional regulators of seed maturation, together with ABI3 (ABSCISIC ACID INSENSITIVE 3) (Figure 1) (for reviews, see Braybrook and Harada, 2008; Santos-Mendoza et al., 2008; Suzuki and McCarty, 2008). Accordingly, the corresponding mutants share overlapping and pleiotropic phenotypes, such as a reduced level of storage compounds, a lack of desiccation tolerance, or precocious germination. Interestingly, mutant cotyledons display various similarities with young leaves. Together, these phenotypes suggest that the regulators act by conferring embryonic competence to egg-derived cells. TANMEI (TAN), a protein with a WDR domain whose precise function is unknown, has overlapping roles with the proteins encoded by these genes during seed formation (Yamagishi et al., 2005). LEC2, FUS3 and ABI3 encode plant-specific transcription factors that possess a ‘B3’ DNA-binding domain, and LEC1 displays some similarities with a CAAT box-binding factor subunit. In recent years, genetic and molecular analyses have demonstrated that these regulatory proteins belong to a complex ‘AFL’ (for ABI3/FUS3/LEC2) network of local and redundant pathways that partially interact with other factors as well as with sugar and hormonal signalling (Figure 1) (e.g. GA, ABA and auxin; see Gazzarrini et al., 2004). Furthermore, the AFL complex directly triggers the expression of genes encoding SSPs and proteins embedded in the half unit-membrane surrounding oil bodies (Baud and Lepiniec, 2009). Other important regulators of SSP genes have been identified including, ABI4 [an APETALA 2 (AP2) family protein] or various bZIPs (e.g. ABI5 or ENHANCED EM LEVEL) acting in the same signalling pathway, but downstream of ABI3 (Alonso et al., 2009). Transcriptional activation of the fatty acid biosynthetic network appears to involve additional factors such as WRINKLED 1 (WRI1), a member of the AP2-ethylene response element binding factor family (Cernac and Benning, 2004). WRI1 specifies the regulatory action of LEC2, and possibly other master regulators, in this metabolic pathway (Figure 1). Interestingly, the AFL network can be repressed in seedlings through a variety of pathways, for example involving PICKLE, an ATP-dependent chromatin remodeller, several histone deacetylases, or the VP1/ABI3-LIKE (VAL)/HIGH-LEVEL EXPRESSION OF SUGAR-INDUCIBLE 2 (HSI2) family of transcription factors (Zhang and Ogas, 2009).
Figure 1. Schematic representation of the regulatory steps controlling Arabidopsis seed development. Model of the regulatory steps and elements currently known to be involved in the control of Arabidopsis seed development, as described in the text. The orange line indicates that the maturation programme can be bypassed in various mutants. Interestingly, various negative mechanisms have been identified that repress seed maturation and development programmes during seedling development and vegetative growth. ABA, Abscisic acid; GA, Gibberellic acid; PcG, Polycomb group; PCGP, Polycomb group protein; PRC2, Polycomb repressive complex 2; PKL, PICKLE; HDAC, histone deacetylase; HSI, HIGH-LEVEL EXPRESSION OF SUGAR-INDUCIBLE; VAL, VP1/ABI3-LIKE; LEC, LEAFY COTYLEDON; FUS3, FUSCA3; TAN,TANMEI; AGL15, AGAMOUS-like 15; ABI3, ABSCISIC ACID INSENSITIVE 3; SSP, Seed storage protein; WRI, WRINKLED 1; TAG, Triacylglycerol.
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