br MADS box proteins in plants a
MADS box proteins in plants, a flourishing family In contrast to animals, homeotic genes in plants do not code for homeodomain-containing proteins, but rather, in almost all cases, for MADS domain proteins. The sequencing of the genome of Arabidopsis thaliana revealed more than 100 putative MADS box proteins, which belong to type I and type II classes (Fig. 1)Riechmann et al., 2000, De Bodt et al., 2003. Type II class of MADS box proteins contains, in addition to their animal and fungal counterparts, a distinct coiled-coil domain (K box) Alvarez-Buylla et al., 2000, Riechmann et al., 2000. With so many MADS box proteins in plants, it is likely that some of them may have redundant functions. Indeed, obtention of mutant phenotypes sometimes requires mutations in two or even three genes. The best-studied plant MADS box genes are those determining floral organ identity in Arabidopsis and Antirrhinum, where many flower homeotic mutants have been described and found to be caused by mutations in MADS box genes Sommer et al., 1990, Coen, 1992, Weigel and Meyerowitz, 1994. However, the role that MADS box proteins play is not restricted to flower development. This multigene family contains members that are expressed in parts of the plant other than flowers, and MADS box genes are also present in nonflowering plants (gymnosperms, ferns and mosses). They have been shown to play key roles in plant development regulating the transition from vegetative to reproductive growth, determining the identity of the floral meristem, ovules and root development (reviewed in Riechmann and Meyerowitz, 1997, Theissen et al., 2000). Floral organ identity in TWS119 synthesis seems to be controlled by three conserved genetic functions that act in a combinatorial manner (Coen and Meyerowitz, 1991). The ABC model, which describes the role of these functions in floral development, proposes that sepal identity is controlled by the A-function, petals by the A- and B-functions, stamens by B- and C-functions and carpels by the C-function. The Arabidopsis class A genes are APETALA1 (AP1) and APETALA2 (AP2), the class B genes are APETALA3 (AP3) and PISTILLATA (PI) and the only class C gene is AGAMOUS (AG). Apart from AP2, these genes are all members of the MADS box family Coen and Meyerowitz, 1991, Schwarz-Sommer et al., 1992, Theissen et al., 2000. In addition, the SEP genes, SEPALLATA1, SEPALLATA2 and SEPALLATA3, represent another class of homeotic genes, termed class E genes which together with the class B and C genes is required for the specification of organ identity in the petals (A+B+E), stamens (B+C+E) and carpels (C+E) Pelaz et al., 2000, Theissen, 2001, Theissen and Saedler, 2001. One possible mechanism by which AP1, AP3 and PI (which specify petals) and AP3, PI and AG (which specify stamens) could act combinatorially to dictate a developmental program is through heteromeric complex formation. AP1, AP3, PI and AG are all capable of interacting with each other, but only AP1 homodimers, AG homodimers and AP3–PI heterodimers are capable of binding to CArG sequences (Riechmann et al., 1996). More recently, it was demonstrated that protein complexes PI–AP3–AP1 and PI–AP3–SEP3 are sufficient to activate the AP3 promoter, which contains three CArG boxes (Honma and Goto, 2001). As both AP1 and SEP3 form homodimers, dimers probably provide the activation domain, and then tetramers increase the DNA binding affinity. Moreover, ectopic expression of PI–AP3–SEP3 and PI–AP3–AP1 is sufficient to transform leaves into petaloid organs and that of PI–AP3–SEP–AG is sufficient to convert leaves into stamenoid organs. Taken together, these results led Theissen and Saedler to propose the “quartet model” which directly links floral organ identity to the action of four different tetrameric transcription factor complexes composed of MADS box proteins (Fig. 8). According to the model, two dimers of each tetramer recognize two different DNA sites (CArG boxes) on the same strand of DNA which are both in close proximity by DNA bending (Theissen and Saedler, 2001).