A Regulatory Circuit between AGL103 and TCPs Balances Growth and Stress Tolerance in Arabidopsis thaliana.

Enhancing cold tolerance through HubZIP6-mediated CBF activation and salicylic acid signaling in pitaya

Cold stress severely limits the yield and quality of fruit crops, yet its regulatory mechanisms in pitaya remain poorly understood. Here, we identified a cold-inducible bZIP transcription factor, HubZIP6, that plays a central role in enhancing cold tolerance in pitaya. HubZIP6 is a nuclear-localized protein with transcriptional activation activity, and its overexpression in Arabidopsis and tomato significantly improved cold tolerance, as reflected by higher survival rates, reduced ion leakage, and lower reactive oxygen species accumulation. Mechanistically, HubZIP6 directly binds to ACGT motifs in the promoters of HuCBF1 and HuCBF3, thereby activating their expression under cold stress. In addition, HubZIP6 physically interacts with the salicylic acid-binding protein HuSABP2, which synergistically enhances the transcriptional activation of HuCBF genes. Notably, HubZIP6 also directly activates HuSABP2, forming a regulatory loop that connects CBF transcriptional control with salicylic acid signaling. Consistently, overexpression of HuSABP2 further enhances cold tolerance in transgenic plants. Collectively, these findings demonstrate that cold tolerance is enhanced through HubZIP6-mediated integration of CBF activation and salicylic acid signaling, providing a promising genetic target for improving stress resilience in fruit crops.

Transcription factor MYB102 regulates plant growth and tolerance to multiple abiotic stresses in Arabidopsis thaliana

PHYTOCHROME-INTERACTING FACTOR 3 represses plant salt tolerance through MADS-box transcription factor AGAMOUS-LIKE 21.

It is demonstrated that PIF3 negatively regulates plant salt tolerance in Arabidopsis, and salt stress significantly enhances the interaction between PIF3 and light-activated PHYTOCHROME B (PHYB), leading to accelerated degradation of PIF3 in light, thus alleviating its negative regulation on plant salt tolerance.

CPL1/FRY2 Regulates ABA Biosynthesis and Modulates SA/JA-Mediated Defence in Arabidopsis.

The RNA polymerase II C-terminal domain (CTD) phosphatase CPL1/FRY2 is a multifunctional regulator involved in diverse stress responses, yet its role in orchestrating hormone-mediated immunity remains poorly understood. Here, we demonstrate that CPL1 regulates ABA biosynthesis and modulates SA/JA-associated defence responses in Arabidopsis thaliana. Loss of CPL1 function compromises resistance to the hemibiotrophic bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (Pst DC3000), coinciding with suppressed SA signalling and ectopic activation of JA-, ethylene-, and abscisic acid (ABA)-responsive genes. Hormone profiling revealed that upon Pst DC3000 infection, cpl1 mutants specifically accumulated ABA, but not SA, JA, or ethylene. Epistasis analyses showed that this ABA accumulation stems from the derepression of the seed-specific transcription factor FUSCA3 (FUS3) in vegetative tissues, which in turn drives expression of the ABA biosynthetic gene NCED3. Chromatin immunoprecipitation analyses further revealed that FUS3 silencing in wild-type plants is maintained by repressive epigenetic marks, including low histone acetylation and high H3K9me2/3 levels, modifications that are disrupted in cpl1 mutants. Consequently, CPL1 promotes resistance to biotrophic/hemibiotrophic pathogens by epigenetically silencing FUS3 to prevent pathogen-induced ABA biosynthesis, thereby modulating SA/JA-associated defence responses. Our findings position CPL1 as a key integrator of epigenetic regulation, hormone crosstalk, and pathogen-specific immune tuning.

The transcription factor ZmMYB3R targets CYCB1;2 to modulate maize drought tolerance.

The R1R2R3-MYB (3R-MYB) transcription factor subfamily is associated with stress tolerance; however, the underlying mechanisms in crops remain poorly understood. This study investigates the function of maize MYB3R in regulating seedling drought tolerance. We characterised MYB3R overexpression lines and CRISPR-Cas9 loss-of-function mutants in maize and rice using physiological assays and transcriptome profiling. DNA affinity purification sequencing (DAP-seq) and molecular interaction assays were employed to identify direct downstream targets. MYB3R overexpression enhanced drought tolerance by promoting root development, stomatal closure and antioxidant defence, whereas mutants displayed hypersensitivity. MYB3R binds the mitosis-specific activator (MSA) motif to directly transactivate the B-type cyclin gene CYCB1;2, and cycb1;2 mutants phenocopied the myb3r drought defects. These findings establish that the MYB3R-CYCB1;2 module positively regulates maize drought tolerance by coordinating developmental and physiological adaptations. This pathway provides a valuable molecular target for breeding drought-resilient crops.

A transposon-derived transcription factor senses ionic stress through phase separation to govern plant autophagy.

Salt stress severely impairs plant growth through two distinct cellular insults: osmotic stress caused by water limitation and ionic toxicity resulting from excessive Na+ accumulation. Although plant osmosensors have been identified, the mechanisms underlying ionic stress perception remain elusive. Salt stress also activates autophagy, a conserved degradation pathway that removes damaged organelles and protein aggregates to promote stress tolerance. In animals, master regulators such as transcription factor EB (TFEB) coordinate this response by activating autophagy genes across the pathway, but no analogous regulator has been identified in plants. Here, we show that MUSTANG4 (MUG4), a transcription factor derived from Mutator-like element (MULE) transposons, functions as an ionic stress sensor and the primary transcriptional driver of salt-induced autophagy in Arabidopsis. MUG4 responds to elevated monovalent cation concentrations, but not chloride anions or osmotic stress, thereby distinguishing ionic from osmotic stress. Ionic stress compacts the intrinsically disordered region (IDR) of MUG4 and drives liquid-liquid phase separation of the full-length protein, as demonstrated by Förster resonance energy transfer-fluorescence lifetime imaging, in vitro assays, and coarse-grained molecular dynamics simulations. Genome-wide in vivo CUT&Tag sequencing and RNA sequencing reveal that MUG4 directly and coordinately activates autophagy genes spanning multiple functional stages of the pathway. IDR deletion abolishes phase separation, reduces autophagy gene activation and autophagic flux, and prevents the truncated protein from rescuing the salt-sensitive phenotype of mug4 mutants. These findings identify a dedicated plant ionic stress sensor and establish a mechanistic link between exapted transposable elements, phase separation, and transcriptional stress responses, thereby integrating ionic stress perception with autophagy activation.