PETAL LOSS and ROXY1 interact to limit growth within and between sepals but to promote petal initiation in <i>Arabidopsis thaliana</i>

The activity of genes controlling organ development may be associated with the redox state of subregions within the meristem. Glutaredoxins react to the level of oxidative potential and can reduce cysteine dithiols, in some cases to activate specific transcription factors. In Arabidopsis, loss of function of the glutaredoxin ROXY1 or the trihelix transcription factor PETAL LOSS (PTL) each results in reduced numbers of petals. Here, genetic studies have revealed that loss of petals in ptl mutant plants depends on ROXY1 function. The two genes also act together to restrain stamen-identifying C function from entering the outer whorls. On the other hand, they suppress growth between sepals and in sepal margins, with ROXY1 action partially redundant to that of PTL. Genetic interactions with aux1 mutations indicate that auxin activity is reduced in the petal whorl of roxy1 mutants as in ptl mutants. However, it is apparently increased in the sepal whorl of triple mutants associated with the ectopic outgrowth of sepal margins, and of finger-like extensions of inter-sepal zones that in 20% of cases are topped with bunches of ectopic sepals. These interactions may be indirect, although PTL and ROXY1 proteins can interact directly when co-expressed in a transient assay. Changes of conserved cysteines within PTL to similar amino acids that cannot be oxidized did not block its function. It may be in some cases that under reducing conditions ROXY1 binds PTL and activates it by reducing specific conserved cysteines, thus resulting in growth suppression.