MdWRKY71 promotes the susceptibility of apple to Glomerella leaf spot by controlling salicylic acid degradation.

Glomerella leaf spot (GLS), a fungal disease caused by Colletotrichum fructicola, severely affects apple (Malus domestica) quality and yield. In this study, we found that the transcription factor MdWRKY71 was significantly induced by C. fructicola infection in the GLS-susceptible apple cultivar Royal Gala. The overexpression of MdWRKY71 in apple leaves resulted in increased susceptibility to C. fructicola, whereas RNA interference of MdWRKY71 in leaves showed the opposite phenotypes. These findings suggest that MdWRKY71 functions as a susceptibility factor for the apple-C. fructicola interaction. Furthermore, MdWRKY71 directly bound to the promoter of the salicylic acid (SA) degradation gene Downy Mildew Resistant 6 (DMR6)-Like Oxygenase 1 (DLO1) and promoted its expression, resulting in a reduced SA level. The sensitivity of 35S:MdWRKY71 leaves to C. fructicola can be effectively alleviated by knocking down MdDLO1 expression, confirming the critical role of MdWRKY71-mediated SA degradation via regulating MdDLO1 expression in GLS susceptibility. In summary, we identified a GLS susceptibility factor, MdWRKY71, that targets the apple SA degradation pathway to promote fungal infection.

CERK1 compromises Fusarium solani resistance by reducing jasmonate level and undergoes a negative feedback regulation via the MMK2-WRKY71 module in apple.

Fusarium spp., a necrotrophic soil-borne pathogen, causes root rot disease on many crops. CERK1, as a typical pattern recognition receptor, has been widely studied. However, the function of CERK1 during plant-Fusarium interaction has not been well described. We determined that MdCERK1 is a susceptibility gene in the apple-Fusarium solani (Fs) interaction, and jasmonic acid (JA) plays a crucial role in this process. MdCERK1 directly targets and phosphorylates the lipoxygenase MdLOX2.1, an enzyme initiating the JA biosynthesis, at positions Ser326 and Thr327. These phosphorylations inhibit its translocation from the cytosol to the chloroplasts, leading to a compromised JA biosynthesis. Fs upregulates MdCERK1 expression during infection. In turn, when the JA level is low, the apple MdWRKY71, a transcriptional repressor of MdCERK1, is markedly upregulated and phosphorylated at Thr99 and Thr102 residues by the MAP kinase MdMMK2. The phosphorylation of MdWRKY71 enhances its transcription inhibition on MdCERK1. Taken together, MdCERK1 plays a novel role in limiting JA biosynthesis. There seems to be an arms race between apple and Fs, in which Fs activates MdCERK1 expression to reduce the JA level, while apple senses the low JA level and activates the MdMMK2-MdWRKY71 module to elevate JA level by inhibiting MdCERK1 expression.

Simultaneous Detection and Decontamination of Dichromate Ions: The Fluorescence Response and Photocatalysis of Thiadiazole-Modified Zr-Metal-Organic Frameworks.

The simultaneous analysis and removal of highly toxic hexavalent chromium (Cr (VI)) in contaminated water via an easy method remain a serious task. Based on the guidance of bibliometric analysis, a thiadiazole ligand-modified zirconium metal-organic framework (Zr-MOF) heralds a new and simple approach to Cr (VI) treatment. The concentration can be determined by fluorescence quenching with a low detection limit of 1.4 µM and a high quenching constant of 6.88 × 103 M-1. For the sensing mechanism, the fluorescence intensity of the Zr-MOF decreased rapidly due to the competition of Cr (VI) with the Zr-MOF for absorption excitation energy and the induction of Zr-MOF aggregation. The analysis system also displayed satisfactory stability and applicability. Apart from sensing application, Zr-MOF can convert Cr (VI) to Cr (III), and the reduction rate constant was 0.004 min-1 under irradiation. Therefore, the bifunctional Zr-MOF provided a potential application method for controlling the pollution caused by Cr (VI) in wastewater.

2D MOF-enhanced SPR sensing platform: Facile and ultrasensitive detection of Sulfamethazine via supramolecular probe.

Sulfamethazine (SMZ) is widely present in the environment and can cause severe allergic reactions and cancer in humans. Accurate and facile monitoring of SMZ is crucial for maintaining environmental safety, ecological balance, and human health. In this work, a real-time and label-free surface plasmon resonance (SPR) sensor was devised using a two-dimensional metal-organic framework with superior photoelectric performance as an SPR sensitizer. The supramolecular probe was incorporated at the sensing interface, allowing for the specific capture of SMZ from other analogous antibiotics through host-guest recognition. The intrinsic mechanism of the specific interaction of the supramolecular probe-SMZ was elucidated through the SPR selectivity test in combination with analysis by density functional theory, including p-π conjugation, size effect, electrostatic interaction, π-π stacking, and hydrophobic interaction. This method facilitates a facile and ultrasensitive detection of SMZ with a limit of detection of 75.54 pM. The accurate detection of SMZ in six environmental samples demonstrates the potential practical application of the sensor. Leveraging the specific recognition of supramolecular probes, this direct and simple approach offers a novel pathway for the development of novel SPR biosensors with outstanding sensitivity.

Overexpression of the FERONIA receptor kinase MdMRLK2 confers apple drought tolerance by regulating energy metabolism and free amino acids production.

Drought is a major abiotic stress limiting the growth and production of apple trees worldwide. The receptor-like kinase FERONIA is involved in plant growth, development and stress responses; however, the function of FERONIA in apple under drought stress remains unclear. Here, the FERONIA receptor kinase gene MdMRLK2 from apple (Malus domestica) was shown to encode a plasma membrane-localized transmembrane protein and was significantly induced by abscisic acid and drought treatments. 35S::MdMRLK2 apple plants showed less photosystem damage and higher photosynthetic rates compared with wild-type (WT) plants, after withholding water for 7 days. 35S::MdMRLK2 apple plants also had enhanced energy levels, activated caspase activity and more free amino acids, than the WT, under drought conditions. By performing yeast two-hybrid screening, glyceraldehyde-3-phosphate dehydrogenase and MdCYS4, a member of cystatin, were identified as MdMRLK2 interaction partners. Moreover, under drought conditions, the 35S::MdMRLK2 apple plants were characterized by higher abscisic acid (ABA) content. Overall, these findings demonstrated that MdMRLK2 regulates apple drought tolerance, probably via regulating levels of energetic matters, free amino acids and ABA.

The apple FERONIA receptor-like kinase MdMRLK2 negatively regulates Valsa canker resistance by suppressing defence responses and hypersensitive reaction.

Valsa canker, caused by the fungus Valsa mali, is one of the most destructive diseases of apple trees in China and other East Asian countries. The plant receptor-like kinase FERONIA is involved in plant cell growth, development, and immunity. However, little is known about the function of FERONIA in apple defence against V. mali. In this study, we found that MdMRLK2 was highly induced by V. mali in twigs of V. mali-susceptible Malus mellana but not in those of the resistant species Malus yunnaensis. 35S:MdMRLK2 apple plants showed compromised resistance relative to wild-type (WT) plants. Further analyses indicated that 35S:MdMRLK2 apple plants had enhanced abscisic acid (ABA) levels and reduced salicylic acid (SA) levels relative to the WT on V. mali infection. MdMRLK2 overexpression also suppressed polyphenol accumulation and inhibited the activities of phenylalanine ammonia-lyase (PAL), ß-1,3-glucanase (GLU), and chitinase (CHT) during V. mali infection. Moreover, MdMRLK2 interacted with MdHIR1, a hypersensitive-induced response protein, and suppressed the MdHIR1-mediated hypersensitive reaction (HR), probably by impairing MdHIR1 self-interaction. Collectively, these findings demonstrate that overexpression of MdMRLK2 compromises Valsa canker resistance, probably by (a) altering ABA and SA levels, (b) suppressing polyphenol accumulation, (c) inhibiting PAL, GLU, and CHT activities, and (d) blocking MdHIR1-mediated HR by disrupting MdHIR1 self-interaction.