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Summary: Cold stress is a major abiotic stress that threatens maize (Zea mays L.) production worldwide. Understanding the molecular mechanisms underlying cold tolerance is crucial for breeding resilient maize varieties. Tonoplast intrinsic proteins (TIPs) are a subfamily of aquaporins in plants. Here, we report that TIP family proteins are involved in maize cold tolerance. The expression of most TIP genes was responsive to cold stress. Overexpressing TIP2;1, TIP3;2 or TIP4;3 reduced the cold tolerance of maize seedlings, while loss‐of‐function mutants of TIP4;3 exhibited enhanced cold tolerance. Candidate gene‐based association analysis revealed that a 328‐bp transposon insertion in the promoter region of TIP4;3 was strongly associated with maize cold tolerance. This transposon insertion conferred cold tolerance by repressing TIP4;3 expression through increased methylation of its promoter region. Moreover, TIP4;3 was found to suppress stomatal closure and facilitate reactive oxygen species (ROS) accumulation under cold stress, thereby inhibiting the expression of cold‐responsive genes, including DEHYDRATION‐RESPONSIVE ELEMENT BINDING FACTOR 1 (DREB1) genes and a subset of peroxidase genes, ultimately attenuating maize cold tolerance. This study thus elucidates the mechanism underlying TIP‐mediated cold tolerance and identifies a favourable TIP4;3 allele as a potential genetic resource for breeding cold‐tolerant maize varieties. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a pressing concern in neurodegenerative research. To address the challenges in AD drug development, especially those targeting Aβ, this study uses deep learning and a pharmacological approach to elucidate the potential of pyrroloquinoline quinone (PQQ) as a neuroprotective agent for AD. Using deep learning for a comprehensive molecular dataset, blood–brain barrier (BBB) permeability is predicted and the anti‐inflammatory and antioxidative properties of compounds are evaluated. PQQ, identified in the Mediterranean‐DASH intervention for a diet that delays neurodegeneration, shows notable BBB permeability and low toxicity. In vivo tests conducted on an Aβ₁₋₄₂‐induced AD mouse model verify the effectiveness of PQQ in reducing cognitive deficits. PQQ modulates genes vital for synapse and anti‐neuronal death, reduces reactive oxygen species production, and influences the SIRT1 and CREB pathways, suggesting key molecular mechanisms underlying its neuroprotective effects. This study can serve as a basis for future studies on integrating deep learning with pharmacological research and drug discovery. [ABSTRACT FROM AUTHOR]

Cold stress is a major abiotic stress that adversely affects plant growth and crop productivity. The C‐REPEAT BINDING FACTOR/DRE BINDING FACTOR 1 (CBF/DREB1) transcriptional regulatory cascade plays a key role in regulating cold acclimation and freezing tolerance in Arabidopsis (Arabidopsis thaliana). Here, we show that max (more axillary growth) mutants deficient in strigolactone biosynthesis and signaling display hypersensitivity to freezing stress. Exogenous application of GR245DS, a strigolactone analog, enhances freezing tolerance in wild‐type plants and strigolactone‐deficient mutants and promotes the cold‐induced expression of CBF genes. Biochemical analysis showed that the transcription factor WRKY41 serves as a substrate for the F‐box E3 ligase MAX2. WRKY41 directly binds to the W‐box in the promoters of CBF genes and represses their expression, negatively regulating cold acclimation and freezing tolerance. MAX2 ubiquitinates WRKY41, thus marking it for cold‐induced degradation and thereby alleviating the repression of CBF expression. In addition, SL‐mediated degradation of SMXLs also contributes to enhanced plant freezing tolerance by promoting anthocyanin biosynthesis. Taken together, our study reveals the molecular mechanism underlying strigolactones promote the cold stress response in Arabidopsis. Synopsis: Plants respond to extreme cold stress by synthesizing strigolactones; however, how this class of plant hormones promotes freezing tolerance is still poorly understood. Here, cold‐induced strigolactones are shown to promote plant survival in sub‐zero temperatures by enhancing expression of freezing tolerance regulators DREB1/CBF.Strigolactones positively regulate plant freezing tolerance via a CBF‐dependent pathway.The E3 ligase MAX2 interacts with and ubiquitinates the transcription factor WRKY41, mediating its cold‐induced degradation.WRKY41 represses the cold‐induced expression of CBFs by directly binding to their promoters.SLs‐mediated degradation of SMXLs also contributes to enhanced freezing tolerance by accumulating anthocyanin. [ABSTRACT FROM AUTHOR]