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High‐performance biosensors play a crucial role in elucidating the intricate spatiotemporal regulatory roles and dynamics of membrane phospholipids. However, enhancing the sensitivity and imaging performance remains a significant challenge. Here, optogenetic‐based strategies are presented to optimize phospholipid biosensors. These strategies involves presequestering unbound biosensors in the cell nucleus and regulating their cytosolic levels with blue light to minimize background signal interference in phospholipid detection, particularly under conditions of high expression levels of biosensor. Furthermore, optically controlled phase separation and the SunTag system are employed to generate punctate probes for substrate detection, thereby amplifying biosensor signals and enhancing visualization of the detection process. These improved phospholipid biosensors hold great potential for enhancing the understanding of the spatiotemporal dynamics and regulatory roles of membrane lipids in live cells and the methodological insights in this study might be valuable for developing other high‐performance biosensors. [ABSTRACT FROM AUTHOR]

The metabolic syndrome has become one of the major public health challenges in the world, and adjusting glucose and lipid levels to their normal values is crucial for treating the metabolic syndrome. Olfactory receptors (ORs) expressed in extra‐nasal tissues participate in diverse biological processes, including the regulation of glucose and lipid metabolism. Ectopic ORs can regulate a variety of metabolic events including insulin secretion, glucagon secretion, fatty acid oxidation, lipogenesis and thermogenesis. Understanding the physiological function and deciphering the olfactory recognition code by suitable ligands make ectopic ORs potential targets for the treatment of the metabolic syndrome. In this review, we delineate the roles and mechanisms of ectopic ORs in the regulation of glucose and lipid metabolism, summarize the corresponding natural ligands, and discuss existing problems and the therapeutic potential of targeting ORs in the metabolic syndrome. [ABSTRACT FROM AUTHOR]

Two new coordination polymers, namely poly[[hexathiocyanatotetrakis{μ3‐2,4,6‐trimethyl‐1,3,5‐tris[(triazol‐1‐yl)methyl]benzene}tricadmium(II)] 3.5‐hydrate], {[Cd3(SCN)6(C18H21N9)4]·3.5H2O}n (1), and poly[[hexathiocyanatotetrakis{μ3‐2,4,6‐trimethyl‐1,3,5‐tris[(triazol‐1‐yl)methyl]benzene}trizinc(II)] 3.5‐hydrate], {[Zn3(SCN)6(C18H21N9)4]·3.5H2O}n (2), have been synthesized under hydrothermal conditions and characterized by elemental analysis, IR spectroscopy and single‐crystal X‐ray diffraction analysis. From the X‐ray analysis, it is noteworthy that polymers 1 and 2 are isostructural, with their three‐dimensional structures composed of three kinds of four‐connection metal ions and two kinds of three‐connection 2,4,6‐trimethyl‐1,3,5‐tris[(triazol‐1‐yl)methyl]benzene (TTTMB) ligand nodes. Each metal ion is six‐coordinated in a slightly distorted octahedral geometry. The antioxidant activity against DPPH (2,2‐diphenyl‐1‐picrylhydrazyl) and the antidiabetic activity against α‐amylase of the synthesized compounds were evaluated in vitro. The results of the DPPH free‐radical scavenging assay showed that polymers 1 and 2 exhibited strong antioxidant effects, with IC50 values of 3.81 and 2.56 mg ml−1, respectively. The IC50 value in the antidiabetic studies of polymer 1 was 3.94 mg ml−1, while polymer 2 exhibited no antidiabetic activity. Polymers 1 and 2 revealed different inhibitory activities on DPPH and α‐amylase, which indicated that the metal ions play important roles in the biological activity of coordination polymers. In addition, the solid‐state photoluminescence properties and thermal stability of 1 and 2 have been investigated. [ABSTRACT FROM AUTHOR]

The phytohormone auxin controls plant growth and development via TIR1‐dependent protein degradation of canonical AUX/IAA proteins, which normally repress the activity of auxin response transcription factors (ARFs). IAA33 is a non‐canonical AUX/IAA protein lacking a TIR1‐binding domain, and its role in auxin signaling and plant development is not well understood. Here, we show that IAA33 maintains root distal stem cell identity and negatively regulates auxin signaling by interacting with ARF10 and ARF16. IAA33 competes with the canonical AUX/IAA repressor IAA5 for binding to ARF10/16 to protect them from IAA5‐mediated inhibition. In contrast to auxin‐dependent degradation of canonical AUX/IAA proteins, auxin stabilizes IAA33 protein via MITOGEN‐ACTIVATED PROTEIN KINASE 14 (MPK14) and does not affect IAA33 gene expression. Taken together, this study provides insight into the molecular functions of non‐canonical AUX/IAA proteins in auxin signaling transduction. Synopsis: IAA33, a non‐canonical AUX/IAA without typical domains I and II, negatively regulates auxin response through the competition with IAA5, a canonical AUX/IAA, and thus releases the repression of ARF10/16. Furthermore, auxin stabilizes the IAA33 protein through interaction with MPK14 without influencing its transcription. IAA33 negatively regulates auxin responses and root stem cell identity.IAA33 regulates auxin signaling through competition with IAA5 for ARF10/16 binding.Auxin activates the phosphorylation activity of MPK14.Auxin induces IAA33 accumulation through phosphorylation by MPK14. [ABSTRACT FROM AUTHOR]