Photoexcited CRYPTOCHROME 1 Interacts Directly with G-Protein β Subunit AGB1 to Regulate the DNA-Binding Activity of HY5 and Photomorphogenesis in Arabidopsis

Abstract

Light and the heterotrimeric G-protein are known to antagonistically regulate photomorphogenesis in Arabidopsis. However, whether light and G-protein coordinate the regulation of photomorphogenesis is largely unknown. Here we show that the blue light photoreceptor cryptochrome 1 (CRY1) physically interacts with the G-protein β subunit, AGB1, in a blue light-dependent manner. We also show that AGB1 directly interacts with HY5, a basic leucine zipper transcriptional factor that acts as a critical positive regulator of photomorphogenesis, to inhibit its DNA-binding activity. Genetic studies suggest that CRY1 acts partially through AGB1, and AGB1 acts partially through HY5 to regulate photomorphogenesis. Moreover, we demonstrate that blue light-triggered interaction of CRY1 with AGB1 promotes the dissociation of HY5 from AGB1. Our results suggest that the CRY1 signaling mechanism involves positive regulation of the DNA-binding activity of HY5 mediated by the CRY1-AGB1 interaction, which inhibits the association of AGB1 with HY5. We propose that the antagonistic regulation of HY5 DNA-binding activity by CRY1 and AGB1 may allow plants to balance light and G-protein signaling and optimize photomorphogenesis.

Arabidopsis PEAPODs function with LIKE HETEROCHROMATIN PROTEIN1 to regulate lateral organ growth

“…In Arabidopsis , loss‐of‐function mutations in Gβ ( AGB1 ) lead to shorter hypocotyl, shorter petiole, and round lamina phenotypes caused by reduced cell division (Perfus‐Barbeoch et al 2004). Recent reports showed that AGB1 promotes hypocotyl elongation partially through directly inhibiting a B‐box (BBX)‐like zinc‐finger transcription factor (BBX21) (Xu et al 2017), and the shorter hypocotyl phenotype of agb1 can be partially suppressed by mutations in photoreceptors, cryptochrome 1 ( cry1 ) and phytochrome B ( phyB ) (Lian et al 2018; Xu et al 2018). Interestingly, AGB1 directly interacts with CRY1 or PHYB in a light‐dependent manner (Lian et al 2018; Xu et al 2018).…”

“…Recent reports showed that AGB1 promotes hypocotyl elongation partially through directly inhibiting a B‐box (BBX)‐like zinc‐finger transcription factor (BBX21) (Xu et al 2017), and the shorter hypocotyl phenotype of agb1 can be partially suppressed by mutations in photoreceptors, cryptochrome 1 ( cry1 ) and phytochrome B ( phyB ) (Lian et al 2018; Xu et al 2018). Interestingly, AGB1 directly interacts with CRY1 or PHYB in a light‐dependent manner (Lian et al 2018; Xu et al 2018). In addition, plant G‐proteins have been shown to negatively control the size of the shoot apical meristem (SAM) that is controlled by the CLAVATA signaling pathway (Bommert et al 2013; Ishida et al 2014).…”

The SNL‐HDA19 histone deacetylase complex antagonizes HY5 activity to repress photomorphogenesis in Arabidopsis

“…ChIP experiments were performed as described previously with minor modifications (Bowler et al ., 2004). The following antibodies were used: α‐HY5 (Lian et al ., 2018), α‐HDA19, α‐SNL1, and α‐H3 (07‐690; Millipore, Bedford, MA, USA), α‐H3Ac (06‐599; Millipore), α‐H3K9Ac (07‐352; Millipore). Briefly, 1–2 g of 6‐d‐old seedlings with various genetic backgrounds were harvested and fixed for 15 min in 1% (v/v) formaldehyde under vacuum.…”

Transcriptome and metabolomic analyses reveal regulatory networks and key genes controlling maize stomatal development in response to blue light

“…Transcription factor HY5 is a hierarchical regulator of transcription cascades in photomorphogenesis that acts on the downstream of many photoreceptors and serves as a signal bridge between light and metabolite [27]. First, HY5, as a target of COP1/SPA complex, is regulated by light and metabolites at the protein and transcription levels [28][29][30]. Second, HY5 bridges light and metabolites signals and promotes light morphogenesis at the transcription level by activating the gene transcription of metabolite signaling pathways [31].…”