BLUS1 functions as a phototropin substrate and primary regulator of stomatal control

 

Phosphorylation of BLUS1 kinase by phototropins is a primary step in stomatal opening

by Takemiya A.Sugiyama N.Fujimoto H.Tsutsumi T.Yamauchi S.Hiyama A.Tada Y.Christie J. M.Shimazaki K.-i. (2013)

in Nature Communications 4 – doi:10.1038/ncomms3094  –

Medline – http://www.nature.com/ncomms/2013/130628/ncomms3094/full/ncomms3094.html – 

https://www.nature.com/articles/ncomms3094

Abstract

Opening of stomata in the plant facilitates photosynthetic CO2 fixation and transpiration. Blue-light perception by phototropins (phot1, phot2) activates the plasma membrane H+-ATPase, causing stomata to open.

Here we describe a regulator that connects these components, a Ser/Thr protein kinase, BLUS1 (BLUE LIGHT SIGNALING1), which mediates a primary step for phototropin signalling in guard cells.

blus1 mutants identified by infrared thermography result in a loss of blue light-dependent stomatal opening. BLUS1 encodes a protein kinase that is directly phosphorylated by phot1 in vitro and in vivo at Ser-348 within its C-terminus. Both phosphorylation of Ser-348 and BLUS1 kinase activity are essential for activation of the H+-ATPase.

blus1 mutants show lower stomatal conductance and CO2 assimilation than wild-type plants under decreased ambient CO2.

Together, our analyses demonstrate that BLUS1 functions as a phototropin substrate and primary regulator of stomatal control to enhance photosynthetic CO2assimilation under natural light conditions.

AHA1 plays a major role in blue light-dependent stomatal opening

 

 

Plasma membrane H+-ATPase1 (AHA1) plays a major role in Arabidopsis thaliana for stomatal opening in response to blue light

by Yamauchi S., Takemiya A., Sakamoto T., Shimazaki K.-i. (2016)

in Plant physiology · June 2016 –

https://www.researchgate.net/publication/303797064_Plasma_membrane_H-ATPase1_AHA1_plays_a_major_role_in_Arabidopsis_thaliana_for_stomatal_opening_in_response_to_blue_light 

Abstract
Stomata open in response to a weak blue light under strong red light illumination. A blue light signal is perceived by phototropins and transmitted to the plasma membrane H+-ATPase that drivesstomatal opening.
To identify the components in this pathway, we screened for mutants impaired in blue light-dependent stomatal opening. We analyzed one such mutant, provisionally named blus2 (blue light signaling2), and found that stomatal opening in leaves was impaired by 65%, although the magnitude of red light-induced opening was not affected.
Blue light-dependent stomatal opening in the epidermis and H+ pumping in guard cell protoplasts were inhibited by 70% in blus2. Whole genome re-sequencing identified a mutation in the AHA1 gene of the mutant at Gly-602. T-DNA insertion mutants of AHA1 exhibited a similar phenotype to blus2; this phenotype was complemented by the AHA1 gene.
We renamed blus2 as aha1-10. T-DNA insertion mutants of AHA2 and AHA5 did not show any impairment in stomatal response, although the transcript levels of AHA2 and AHA5 were higher than those of AHA1 in wild-type guard cells.
Stomata in ost2, a constitutively active AHA1 mutant, did not respond to blue light. A decreased amount of H+-ATPase in aha1-10 accounted for the reduced stomatal blue light responses and the decrease was likely caused by proteolysis of misfolded AHA1.
From these results, we conclude that AHA1 plays a major role in blue light-dependent stomatal opening in Arabidopsis and that the mutation made the AHA1 protein unstable in guard cells.