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Guard cells control hypocotyl elongation through HXK1, HY5, and PIF4.

Authors :
Kelly, Gilor
Brandsma, Danja
Egbaria, Aiman
Stein, Ofer
Doron-Faigenboim, Adi
Lugassi, Nitsan
Belausov, Eduard
Zemach, Hanita
Shaya, Felix
Carmi, Nir
Sade, Nir
Granot, David
Source :
Communications Biology; 6/21/2021, Vol. 4 Issue 1, p1-14, 14p
Publication Year :
2021

Abstract

The hypocotyls of germinating seedlings elongate in a search for light to enable autotrophic sugar production. Upon exposure to light, photoreceptors that are activated by blue and red light halt elongation by preventing the degradation of the hypocotyl-elongation inhibitor HY5 and by inhibiting the activity of the elongation-promoting transcription factors PIFs. The question of how sugar affects hypocotyl elongation and which cell types stimulate and stop that elongation remains unresolved. We found that overexpression of a sugar sensor, Arabidopsis hexokinase 1 (HXK1), in guard cells promotes hypocotyl elongation under white and blue light through PIF4. Furthermore, expression of PIF4 in guard cells is sufficient to promote hypocotyl elongation in the light, while expression of HY5 in guard cells is sufficient to inhibit the elongation of the hy5 mutant and the elongation stimulated by HXK1. HY5 exits the guard cells and inhibits hypocotyl elongation, but is degraded in the dark. We also show that the inhibition of hypocotyl elongation by guard cells' HY5 involves auto-activation of HY5 expression in other tissues. It appears that guard cells are capable of coordinating hypocotyl elongation and that sugar and HXK1 have the opposite effect of light on hypocotyl elongation, converging at PIF4. Kelly et al. show that Arabidopsis hexokinase1 (HXK1) expressed in guard-cells is sufficient to drive hypocotyl elongation through increasing the activity of PIF4 and auxin level, and competing with the effects of HY5. This study provides insights into how light and sucrose antagonistically coordinate the effort to achieve the height necessary for efficient photosynthetic, autotrophic sugar production. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
23993642
Volume :
4
Issue :
1
Database :
Complementary Index
Journal :
Communications Biology
Publication Type :
Academic Journal
Accession number :
151002417
Full Text :
https://doi.org/10.1038/s42003-021-02283-y