Various plant growth regulators are also involved in the control of the endocycle. A brassinosteroid (BR) deficient mutant cpm17 displays short hypocotyl phenotypes in the dark and this is associated with reduced ploidy (Gen-dreau et al. 1998), suggesting that BR positively regulates the endocycle in the dark. In contrast, other BR signalling mutants such as de-etiolated2 (det2) and brassinosteroid-insensitive1 (bri1) that display a severe dwarf phenotype in the light have a normal ploidy level (Stacey and Sugimoto-Shirasu, unpublished results), suggesting that BR may act downstream of light signalling to modulate endoreduplication.
Gibberellin (GA) also appears to promote the endocycle since ga1 mutants, deficient in GA biosynthesis, show a strongly reduced ploidy phenotype in the dark (Gendreau et al. 1998). Consistent with this, the spindly (spy) mutation, which exhibits a constitutive GA response (Jacobsen et al. 1996), shows an increased ploidy phenotype in light-grown leaves. The spy mutation causes an over-branched trichome phenotype and this is enhanced in the try mutant background (Perraza et al. 1999), indicating that GA promotes an additional round of endocycle in a pathway independent from the TRY-mediated genetic pathway.
The involvement of ethylene in the endocycle control is demonstrated from studies on the constitutive triple response1 (ctr1) mutants that show constitutive ethylene-response phenotypes. When ctr1 mutants are grown in the dark, they develop short and thick hypocotyls, and microscopic analyses revealed that this is associated with increased ploidy, suggesting that ethylene acts as a positive regulator of the endocycle (Gendreau et al. 1999).
It is also likely that the endocycle is under the control of many other small signalling molecules. One potential modulator of these signals that has been recently identified is FRILL1 (FRL1) which encodes SMT2, a sterol metyl-transferase (Hase et al. 2005). Most cells in floral organs such as sepals and petals do not normally undergo endoreduplication in Arabidopsis, but in frl1 these cells endoreduplicate ectopically, leading to the development of serrated sepals and petals (Hase et al. 2000). Further studies revealed that the ploidy level is also increased in other tissues and that the composition of endogenous sterol is altered in frl1 (Hase et al. 2005). The application of BR and several other known sterols does not rescue the frl1 mutant phenotypes (Hase et al. 2005), suggesting that some novel sterol compound controls the switch from the mitotic cell cycle to the endocycle.
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