Relationship between brassinosteroids and genes controlling stomatal production in the Arabidopsis hypocotyl

Abstract

Stomata are excellent model systems for examining the mechanisms that regulate cell fate determination and pattern formation. It has recently been demonstrated that brassinosteroids control stomatal development by regulating both the MAPK kinase kinase YODA and the basic helix-loop-helix transcriptional factor SPEECHLESS. Here, we show that these plant regulators positively regulate stomatal formation in the hypocotyl and also accelerate their development. Hormone tests, reporter gene studies and mutant analyses revealed that brassinosteroids act upstream of the transcriptional factors CAPRICE and GLABRA2. These plant regulators control an earlier stage of stomatal production than those regulated by the membrane receptor TOO MANY MOUTHS. This work highlights differences in the genetic control of stomatal development between cotyledons or leaves and hypocotyls.

What Causes Opposing Actions of Brassinosteroids on Stomatal Development?

“…Loss of CHAL increased meristemoids in tmm hypocotyl (Abrash and Bergmann, 2010), in the same way as BL (Fuentes et al, 2012), most likely because of the repression of both YDA and MKK4 by BIN2 in this double mutant. Some of these meristemoids developed into stomata in tmm chal (Abrash and Bergmann, 2010), indicating that CHAL is required for a full repression of meristemoid progression in the tmm background.…”

“…Indeed, BL increases stomatal production, while brassinazole and triadimefon, two inhibitors of BR biosynthesis, reduce the number of stomata (Fuentes et al, 2012;Gudesblat et al, 2012a). Mutant backgrounds responded to these treatments as expected, with bri1-1 and bri1-4 displaying absolute insensitivity to BL, while det2-1 increased stomatal production in response to this plant regulator (Fuentes et al, 2012). Interestingly, the gain-of-function mutants bes1-D and bzr1-D had normal numbers of stomata in their hypocotyls (Gudesblat et al, 2012a).…”

“…Plants that either lacked BRs (cpd, det2-1) or had reduced sensitivity to BRs (bri1-1, bri1-4, bri1-116, and dominant bin2-1) developed a very low number of stomata in the hypocotyl, and those with enhanced BR responses (plants overexpressing either DWF4 or BRI1, bin2-3 bil1 bil2, and bin2-3) displayed the opposite phenotype, that is, a strong increase in stomatal production (Fuentes et al, 2012;Gudesblat et al, 2012a). Indeed, BL increases stomatal production, while brassinazole and triadimefon, two inhibitors of BR biosynthesis, reduce the number of stomata (Fuentes et al, 2012;Gudesblat et al, 2012a).…”

“…The tmm mutant hypocotyl lacked stomata, but it exhibited arrested meristemoids (Bhave et al, 2009). Interestingly, BL not only failed to reverse the lack of stomata in the tmm-1 hypocotyl (Fuentes et al, 2012;Gudesblat et al, 2012a) but also increased the production of meristemoids (Fuentes et al, 2012). In light of these results, Fuentes et al (2012) proposed that BRs promote the initiation of the stomatal pathway, and TMM is required in later stages of stomatal development for the progression of meristemoids toward stomata.…”

“…In light of these results, Fuentes et al (2012) proposed that BRs promote the initiation of the stomatal pathway, and TMM is required in later stages of stomatal development for the progression of meristemoids toward stomata. Consistent with these results, bri1-1, bri1-4, and det2-1 mutants and wild-type plants treated with the inhibitor of BR biosynthesis triadimefon did not display arrested meristemoids (Fuentes et al, 2012).…”