The RALF1-FERONIA complex interacts with and activates TOR signaling in response to low nutrients

Target of rapamycin(TOR)kinase is an evolutionarily conserved major regulator of nutrient metabolism and organismal growth in eukaryotes.In plants,nutrients are remobilized and reallocated between shoots and roots under low-nutrient conditions,and nitrogen and nitrogen-related nutrients(e.g.,amino acids)are key upstream signals leading to TOR activation in shoots under low-nutrient conditions.However,how these forms of nitrogen can be sensed to activate TOR in plants is still poorly understood.Here we report that the Arabidopsis receptor kinase FERON IA(FER)interacts with the TOR pathway to regulate nutrient(nitrogen and amino acid)signaling under low-nutrient conditions and exerts similar metabolic effects in response to nitrogen deficiency.We found that FER and its partner,RPM1-induced protein kinase(RIPK),interact with the TOR/RAPTOR complex to positively modulate TOR signaling activity.During this process,the receptor complex FER/RIPK phosphorylates the TOR complex component RAPTOR1B.The RALF1 peptide,a ligand of the FER/RIPK receptor complex,increases TOR activation in the young leaf by enhancing FER-TOR interactions,leading to promotion of true leaf growth in Arabidopsis under lownutrient conditions.Furthermore,we showed that specific amino acids(e.g.,Gin,Asp,and Gly)promote true leaf growth under nitrogen-deficient conditions via the FER-TOR axis.Collectively,our study reveals a mechanism by which the RALF1-FER pathway activates TOR in the plant adaptive response to low nutrients and suggests that plants prioritize nutritional stress response over RALF1-mediated inhibition of cell growth under low-nutrient conditions.

A molecular link between autophagy and circadian rhythm in plants

Extremely high or low autophagy levels disrupt plant survival under nutrient starvation.Recently,autophagy has been reported to display rhythms in animals.However,the mechanism of circadian regulation of autophagy is still unclear.Here,we observed that autophagy has a robust rhythm and that various autophagy-related genes(ATGs)are rhythmically expressed in Arabidopsis.Chromatin immunoprecipitation(Ch IP)and dual-luciferase(LUC)analyses showed that the core oscillator gene TIMING OF CAB EXPRESSION 1(TOC1)directly binds to the promoters of ATG(ATG1 a,ATG2,and ATG8 d)and negatively regulates autophagy activities under nutritional stress.Furthermore,autophagy defects might affect endogenous rhythms by reducing the rhythm amplitude of TOC1 and shortening the rhythm period of CIRCADIAN CLOCK-ASSOCIATED 1(CCA1).Autophagy is essential for the circadian clock pattern in seedling development and plant sensitivity to nutritional deficiencies.Taken together,our studies reveal a plant strategy in which the TOC1-ATG axis involved in autophagy-rhythm crosstalk to fine-tune the intensity of autophagy.

TMK4 receptor kinase negatively modulates ABA signaling by phosphorylating ABI2 and enhancing its activity

In plants, clade A type 2 C protein phosphatases(PP2 CAs) have emerged as major players in abscisic acid(ABA)-regulated stress responses by inhibiting protein kinase activity. However, how different internal and external environmental signals modulate the activity of PP2 CAs are not well known. The transmembrane kinase(TMK) protein4(TMK4), one member of a previously identified receptor kinase subfamily on the plasma membrane that plays vital roles in plant cell growth,directly interacts with PP2 CAs member(ABAInsensitive 2, ABI2). tmk4 mutant is hypersensitive to ABA in both ABA-inhibited seed germination and primary root growth, indicating that TMK4 is a negative regulator in ABA signaling pathway.Further analyses indicate that TMK4 phosphorylates ABI2 at three conserved Ser residues,thus enhancing the activity of ABI2. The phosphorylation-mimic ABI2~(S139DS140DS266D)can complement butnon-phosphorylated form ABI2~(S139AS140AS266) Acannot complement ABA hypersensitive phenotype of the loss-of-function mutant abi1-2 abi2-2. This study provides a previously unidentified mechanism for positively regulating ABI2 by a plasma membrane protein kinase.

Preparation and luminescent properties of CaF_2:Ln^(3+)(Ln:Er, Er/Yb)/Nafion composite films

In this work, CaF_2:Ln^(3+)(Ln:Er,Er/Yb)/Nafion composite films were prepared using Nafion as modifications and matrices by dripping method. The composite films were characterized by Fourier transform infrared spectroscopy(FT-IR), X-ray diffraction(XRD) and scanning electron microscopy(SEM). Composite films are transparent and CaF_2:Ln^(3+)(Ln:Er,Er/Yb) nanoparticles are well dispersed in Nafion films.The thicknesses of CaF_2:Er^(3+)/Nafion and CaF_2:Er^(3+),Yb^(3+)/Nafion composite film are about 77 and 73 μm,respectively. The nanoparticles in composite film possess cubic phase. CaF_2:Er^(3+),Yb^(3+)/Nafion composite film has stronger characteristic emission of Er^(3+) around 1530 nm with full width at half-maximum(FWHM) of 73 nm and longer luminescence lifetimes of 22.04 μs(25.03%) and 100.77 μs(74.97%).