Although C2H2 zinc finger transcription factors are important in plant growth, development, and stress resistance, their specific roles in fruit ripening have been less explored. Here, we demonstrate that the C2H2 zinc finger transcription factor 5 (SlZAT5) regulates fruit ripening in tomato (Solanum lycopersicum L.). Overexpression of SlZAT5 delayed ripening, while its knockout accelerated it, confirming its role as a negative regulator. SlZAT5 functions as a transcriptional repressor by directly inhibiting ripening-related genes, including SlACS4, SlPL8, and SlGRAS38, thereby delaying ripening. Furthermore, SlZAT5 interacts with the type 2C protein phosphatase SlPP2C2, which regulates the repressor activity of SlZAT5 by dephosphorylating SlZAT5 at Ser-65. This interaction is crucial in modulating ethylene production, thereby influencing the ripening process. These findings reveal a regulatory function of SlZAT5 in tomato fruit development, offering insights into the SlZAT5-SlPP2C2 module and potential targets for genetic modification to improve fruit quality and extend fruit shelf life.

As crucial signal transducers, G-proteins and G-protein-coupled receptors (GPCRs) have attracted increasing attention in the field of signal transduction. Research on G-proteins and GPCRs has mainly focused on animals, while research on plants is relatively rare. The mode of action of G-proteins is quite different from that in animals. The G-protein α (Gα) subunit is the most essential member of the G-protein signal cycle in animals and plants. The G-protein is activated when Gα releases GDP and binds to GTP, and the relationships with the GPCR and the downstream signal are also achieved by Gα coupling. It is important to study the role of Gα in the signaling pathway to explore the regulatory mechanism of G-proteins. The existence of a self-activated Gα in plants makes it unnecessary for the canonical GPCR to activate the G-protein by exchanging GDP with GTP. However, putative GPCRs have been found and proven to play important roles in G-protein signal transduction. The unique mode of action of G-proteins and the function of putative GPCRs in plants suggest that the same definition used in animal research cannot be used to study uncanonical GPCRs in plants. This review focuses on the different functions of the Gα and the mode of action between plants and animals as well as the functions of the uncanonical GPCR. This review employs a new perspective to define uncanonical GPCRs in plants and emphasizes the role of uncanonical GPCRs and Gα subunits in plant stress resistance and agricultural production.

Gray mold caused by the fungal pathogen Botrytis cinerea is a major disease of vegetable and fruit crops. This study elucidates mechanism that fine-tunes B. cinerea resistance mediated by the transcription factor SlMYC2 in tomato (Solanum lycopersicum), characterized by a dynamic balance between “active braking” and “brake release.” The Lateral Organ Boundaries Domain (LBD) transcription factor family members SlLBD40 and SlLBD42 repress transcription and form homodimers or heterodimers, with heterodimers demonstrating higher activity. SlLBD40 and SlLBD42 are transcriptionally upregulated by SlMYC2, but SlLBD40 and SlLBD42 attenuate SlMYC2-orchestrated defenses against B. cinerea, thereby safeguarding the plant from immune over-activation. Moreover, the BTB/POZ-MATH (BPM) protein family member SlBPM4 targets and degrades SlLBD40 and SlLBD42, releasing the defense response and enhancing B. cinerea resistance. Genetic analyses demonstrated that SlLBD40 and SlLBD42 are epistatic to SlBPM4. Additionally, SlLBD40 and SlLBD42 play dual roles in fruit development and B. cinerea defense, and SlBPM4 functions as a protective factor under pathogen attack. Our study uncovered a MYC2-LBD40/42-CRL3BPM4 module in tomato that allocates growth and defense resources by finely regulating gene expression and balancing immune response activation levels. This module also provides potential targets for optimizing the balance between plant growth and defense through gene-editing technologies.

Plants exhibit remarkable regenerative abilities under stress conditions like injury, herbivory, and damage from harsh weather, particularly through adventitious root formation. They have sophisticated molecular mechanisms to recognize and respond to wounding. Jasmonic acid (JA), a wound hormone, triggers auxin synthesis to stimulate root regeneration. Melatonin (MT), structurally similar to auxin, also significantly influences root induction, but its specific mechanism is unclear. Phytomelatonin's signal transduction is discovered in wound‐induced root formation, identifying SlPMTR1/2 as phytomelatonin receptors, transmitting signals to SHOOT BORNE ROOTLESS 1 (SlSBRL1), a key regulator of wound‐induced root regeneration, via the G protein α subunit 1 (SlGPA1). Additionally, SlPMTR1/2 is activated by JA, and targeted by SlMYC2. Overall, the specific mechanisms of phytomelatonin on wound‐induced root regeneration is uncovered and revealed a crosstalk between phytomelatonin and JA, offering new insights into plant repair mechanisms.

Light serves as an energy source for cell division and expansion during fruit development. Cell expansion significantly influences fruit size and is closely linked to endoreduplication, a unique cell cycle variation characterized by DNA replication without cytokinesis. Paradoxically, under conditions of ample photosynthates, light signaling suppresses cell expansion. The intricate regulation of endoreduplication in response to light signaling during fruit development has remained an intriguing question. Here, our study revealed that Tubby-like F-box protein 8 (SlTLFP8) orchestrated endoreduplication to facilitate fruit cell expansion. As an Skp1-Cullin-F-box (SCF)-type E3 ligase, SlTLFP8 promoted the ubiquitination and subsequent degradation of CYCLIN-DEPENDENT KINASE B2 (SlCDKB2), thereby elevating DNA ploidy. The light signaling component PHYTOCHROME-INTERACTING FACTOR 1a (SlPIF1a), identified as a pivotal negative regulator in the plant’s light response, was found to directly interact with the promoter of the SlTLFP8 gene, thereby stimulating its transcriptional activation. Indeed, SlPIF1a contributed to a faster expansion rate of tomato fruit during nighttime. Altogether, our results elucidate the connection between light signals and fruit size regulation through endoreduplication.

Aluminum (Al) stress, a prevalent constraint in acidic soils, inhibits plant growth by inhibiting root elongation through restricted cell expansion. The molecular mechanisms of Al-induced root inhibition, however, are not fully understood. This study aimed to elucidate the role of Small Auxin-up RNAs (SlSAURs), which function downstream of the key Al stress-responsive transcription factor SENSITIVE TO PROTON RHIZOTOXICITY 1 (SlSTOP1) and its enhancer STOP1-INTERACTING ZINC-FINGER PROTEIN 1 (SlSZP1), in modulating root elongation under Al stress in tomato (Solanum lycopersicum). Our findings demonstrated that tomato lines with knocked out SlSAURs exhibited shorter root lengths when subjected to Al stress. Further investigation into the underlying mechanisms revealed that SlSAURs interact with Type 2C Protein Phosphatases (SlPP2Cs), specifically D-clade Type 2C Protein Phosphatases (SlPP2C.Ds). This interaction was pivotal as it suppresses the phosphatase activity, leading to the degradation of SlPP2C.D's inhibitory effect on plasma membrane H⁺-ATPase. Consequently, this promoted cell expansion and root elongation under Al stress. These findings increase our understanding of the molecular mechanisms by which Al ions modulate root elongation. The discovery of the SlSAUR-SlPP2C.D interaction and its impact on H⁺-ATPase activity also provides a perspective on the adaptive strategies employed by plants to cope with Al toxicity, which may lead to the development of tomato cultivars with enhanced Al stress tolerance, thereby improving crop productivity in acidic soils.