GSK3 function in floral organs and cell expansion

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Molecular and genetic analysis has confirmed roles for Arabidopsis GSK3s in the development of flowers and reproductive organs. AtSK11 and AtSK12 show specific strong expression in early floral meristems, which later becomes restricted to sepal primordia, petals, carpels and the pollen-containing regions of the anthers [45]. Within the carpels, AtSK11 and AtSK12 expression concentrates on adaxial sides (nearest the central axis) of the carpels and in ovule primordia, particularly in the integuments and megaspore mother cell [45]. A quantitative RT-PCR study of all ten Arabidopsis GSK3s revealed that a third GSK3, AtSK31, was also expressed relatively highly in floral organs [46]. Moreover, the AtSK31 protein localizes to the nuclei of developing tissues, particularly in floral organs, gametophytes and embryos [47].

Consistent with the expression data, antisense reduction in either AtSK11 or AtSK12 transcript levels results in disrupted cell division in the floral meristem, in flowers with increased numbers of sepals and petals, and in abnormal carpel development [45]. Interestingly, overexpression of different AtSK32 isoforms in wild-type Arabidopsis causes varying effects [48]. Overexpression of either wild-type AtSK32 or a kinase-dead mutant (K167A) resulted in no detectable phenotype [48]. However, overexpression of a mutant specifically unable to phosphorylate primed GSK3 substrates (R178A; Figure 1) resulted in plants with short hypocotyls and reduced cell elongation in floral organs. Accordingly, AtSK32 (K167A)-overexpressing plants showed a marked downregulation of the genes encoding several cell wall-modifying enzymes involved in cell elongation [48]. This suggests that GSK3-mediated cell elongation responses may require the action of primed GSK3 substrates. It is likely that in addition to floral cell expansion, GSK3s may have a more general role in cell elongation in the plant given that BRs are instrumental in controlling cell elongation and dominant bin2/ucu1 mutants show cell elongation defects in leaves [19]. Given that GSK3 targets BZR1 and BES1 do not require a priming phosphorylation [21,30], it seems that new targets of AtSK32 await discovery.