Light is a key environmental cue that inhibits hypocotyl cell elongation through the blue and red/far-red light photoreceptors cryptochrome- and phytochrome-mediated pathways in Arabidopsis. In contrast, as a pivotal endogenous phytohormone auxin promotes hypocotyl elongation through the auxin receptors TIR1/AFBs-mediated degradation of AUX/IAA proteins (AUX/IAAs). However, the molecular mechanisms underlying the antagonistic interaction of light and auxin signaling remain unclear. Here, we report that light inhibits auxin signaling through stabilization of AUX/IAAs by blue and red light-dependent interactions of cryptochrome 1 (CRY1) and phytochrome B with AUX/IAAs, respectively. Blue light-triggered interactions of CRY1 with AUX/IAAs inhibit the associations of TIR1 with AUX/IAAs, leading to the repression of auxin-induced degradation of these proteins. Our results indicate that photoreceptors share AUX/IAAs with auxin receptors as the same direct downstream signaling components. We propose that antagonistic regulation of AUX/IAA protein stability by photoreceptors and auxin receptors allows plants to balance light and auxin signals to optimize their growth.

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Cryptochromes (CRYs) are blue light photoreceptors that mediate a variety of light responses in plants and animals, including photomorphogenesis, flowering, and circadian rhythms. The signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motifcontaining E3 ubiquitin ligase, and its enhancer SPA1. Brassinosteroid (BR) is a key phytohormone involved in the repression of photomorphogenesis, and here, we show that the signaling mechanism of Arabidopsis CRY1 involves the inhibition of BR signaling. CRY1 and CRY2 physically interact with BES1-INTERACTING MYC-LIKE1 (BIM1), a basic helix-loop-helix protein. BIM1, in turn, interacts with and enhances the activity of BRI1-EMS SUPPRESSOR1 (BES1), a master transcription factor in the BR signaling pathway. In addition, CRY1 and CRY2 interact specifically with dephosphorylated BES1, the physiologically active form of BES1 that is activated by BR in a blue light-dependent manner. The CRY1-BES1 interaction leads to both the inhibition of BES1 DNA binding activity and the repression of its target gene expression. Our study suggests that the blue light-dependent, BR-induced interaction of CRY1 with BES1 is a tightly regulated mechanism by which plants optimize photomorphogenesis according to the availability of external light and internal BR signals.

Background Growing evidence has shown that alterations in the gut microbiota composition were associated with a variety of neuropsychiatric conditions. However, whether such associations reflect causality remains unknown. We aimed to reveal the causal relationships among gut microbiota, metabolites, and neuropsychiatric disorders including Alzheimer’s disease (AD), major depressive disorder (MDD), and schizophrenia (SCZ). Methods A two-sample bi-directional Mendelian randomization analysis was performed by using genetic variants from genome-wide association studies as instrumental variables for gut microbiota, metabolites, AD, MDD, and SCZ, respectively. Results We found suggestive associations of host-genetic-driven increase in Blautia (OR, 0.88; 95%CI, 0.79–0.99; P = 0.028) and elevated γ-aminobutyric acid (GABA) (0.96; 0.92–1.00; P = 0.034), a downstream product of Blautia-dependent arginine metabolism, with a lower risk of AD. Genetically increased Enterobacteriaceae family and Enterobacteriales order were potentially associated with a higher risk of SCZ (1.09; 1.00–1.18; P = 0.048), while Gammaproteobacteria class (0.90; 0.83–0.98; P = 0.011) was related to a lower risk for SCZ. Gut production of serotonin was potentially associated with an increased risk of SCZ (1.07; 1.00–1.15; P = 0.047). Furthermore, genetically increased Bacilli class was related to a higher risk of MDD (1.07; 1.02–1.12; P = 0.010). In the other direction, neuropsychiatric disorders altered gut microbiota composition. Conclusions These data for the first time provide evidence of potential causal links between gut microbiome and AD, MDD, and SCZ. GABA and serotonin may play an important role in gut microbiota-host crosstalk in AD and SCZ, respectively. Further investigations in understanding the underlying mechanisms of associations between gut microbiota and AD, MDD, and SCZ are required.

Summary Arabidopsis CRY1 and phyB are the primary blue and red light photoreceptors mediating blue and red light inhibition of hypocotyl elongation, respectively. Auxin is a pivotal phytohormone involved in promoting hypocotyl elongation. CRY1 and phyB interact with and stabilize auxin/indole acetic acid proteins (Aux/IAAs) to inhibit auxin signaling. The present study investigated whether photoreceptors might interact directly with Auxin Response Factors (ARFs) to regulate auxin signaling. Protein–protein interaction studies demonstrated that CRY1 and phyB interact physically with ARF6 and ARF8 through their N‐terminal domains in a blue and red light‐dependent manner, respectively. Moreover, the N‐terminal DNA‐binding domain of ARF6 and ARF8 is involved in mediating their interactions with CRY1. Genetic studies showed that ARF6 and ARF8 act partially downstream from CRY1 and PHYB to regulate hypocotyl elongation under blue and red light, respectively. Chromatin immunoprecipitation‐PCR assays demonstrated that CRY1 and phyB mediate blue and red light repression of the DNA‐binding activity of ARF6 and ARF6‐target gene expression, respectively. Altogether, the results herein suggest that the direct repression of auxin‐responsive gene expression mediated by the interactions of CRY1 and phyB with ARFs constitutes a new layer of the regulatory mechanisms by which light inhibits auxin‐induced hypocotyl elongation.

As promising electrode materials in supercapacitors, metal–organic frameworks (MOFs) have attracted significant attention. However, the poor electrical conductivity and the almost exclusively microporous structure largely limited the possibility for MOFs to fabricate high-performance electrodes of supercapacitors. To overcome these obstacles, hierarchical porous Zr-MOFs (HP-UiO-66) has been successfully fabricated using bimetallic Zn/Zr MOFs as a precursor, subsequently wiping off Zr-MOFs. When used as electrode materials for supercapacitors, under a current density of 0.2 A g–1, the specific capacitance of the prepared HP-UiO-66 is 849 F g–1, which is 8.36 times higher than the 101.5 F g–1 of bare UiO-66. The clearly enhanced electrochemical performance of HP-UiO-66 was benefited from the advantages of the hierarchical porous structure, the higher specific surface area and pore volume, as well as the sufficient surface defects. Furthermore, an aqueous asymmetric supercapacitor based on the HP-UiO-66 and porous carbon could show an energy density of 32 W h kg–1 at a power density of 240 W kg–1. This strategy may offer a versatile idea of tailoring new type of MOFs and opens the possibility of MOFs using in the future high-energy storage device.

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.