TRANSPARENT TESTA GLABRA1 regulates high-intensity blue light-induced phototropism by reducing CRYPTOCHROME1 levels

Abstract The asymmetrical distribution of auxin supports high intensity blue light (HBL)-mediated phototropism. Flavonoids, secondary metabolites induced by blue light and TRANSPARENT TESTA GLABRA1 (TTG1), alter auxin transport. However, the role of TTG1 in HBL-induced phototropism in Arabidopsis (A...

Full description

Saved in:
Bibliographic Details
Published inPlant physiology (Bethesda) Vol. 196; no. 2; pp. 1475 - 1488
Main Authors Wang, Yu-xi, Zhao, Qing-ping, Zhu, Jin-dong, Chu, Fang-yuan, Fu, Xiang-lin, Li, Xing-kun, Ding, Mei-chen, Liu, Yan-fei, Wu, Qi-qi, Xue, Lin-lin, Xin, Guang-yuan, Zhao, Xiang
Format Journal Article
LanguageEnglish
Published US Oxford University Press 01.10.2024
Online AccessGet full text

Cover

Loading…
More Information
Summary:Abstract The asymmetrical distribution of auxin supports high intensity blue light (HBL)-mediated phototropism. Flavonoids, secondary metabolites induced by blue light and TRANSPARENT TESTA GLABRA1 (TTG1), alter auxin transport. However, the role of TTG1 in HBL-induced phototropism in Arabidopsis (Arabidopsis thaliana) remains unclear. We found that TTG1 regulates HBL-mediated phototropism. HBL-induced degradation of CRYPTOCHROME 1 (CRY1) was repressed in ttg1-1, and depletion of CRY1 rescued the phototropic defects of the ttg1-1 mutant. Moreover, overexpression of CRY1 in a cry1 mutant background led to phototropic defects in response to HBL. These results indicated that CRY1 is involved in the regulation of TTG1-mediated phototropism in response to HBL. Further investigation showed that TTG1 physically interacts with CRY1 via its N-terminus and that the added TTG1 promotes the dimerization of CRY1. The interaction between TTG1 and CRY1 may promote HBL-mediated degradation of CRY1. TTG1 also physically interacted with blue light inhibitor of cryptochrome 1 (BIC1) and Light-Response Bric-a-Brack/Tramtrack/Broad 2 (LRB2), and these interactions either inhibited or promoted their interaction with CRY1. Exogenous gibberellins (GA) and auxins, two key plant hormones that crosstalk with CRY1, may confer the recovery of phototropic defects in the ttg1-1 mutant and CRY1-overexpressing plants. Our results revealed that TTG1 participates in the regulation of HBL-induced phototropism by modulating CRY1 levels, which are coordinated with GA or IAA signaling.Specific interactions among proteins involved in blue light signaling reduce blue light photoreceptor abundance, thereby regulating high-intensity blue light-mediated phototropism in Arabidopsis.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0032-0889
1532-2548
1532-2548
DOI:10.1093/plphys/kiae322