Zhiyi Yu

Stomata are pores at the leaf surface that facilitate CO ₂ entry for photosynthesis while controlling transpirational water loss. Stomatal movements are governed by reversible changes in turgor and cell volume, driven by the transport of osmotic solute across the membrane of guard cells surrounding the pore. Membrane transport depends on the activities of transporters and ion channels present at the membrane and also on their abundance, determined by vesicle traffic. Although much is known about how pumps and ion channels in the membrane are regulated, this is not the case for vesicle trafficking and certainly not in relation to CO ₂ . Here, we report on experiments following the traffic of the K ⁺ channel KAT1 that is important for K ⁺ uptake during stomatal opening. We found that elevated CO ₂ triggers changes in channel mobility within the plane of the plasma membrane and its internalization therefrom. CO ₂ ‐sensitive KAT1 traffic depends on SYP121, a vesicle‐trafficking (SNARE) protein previously associated with water stress and abscisic acid (ABA) that also binds the K ⁺ channel to promote its activation. The CO ₂ ‐sensitive pathway parallels vesicle traffic evoked by ABA, but it also shows important differences, with KAT1–SYP121 binding sensitive to CO ₂ . We show that stomatal response to changes in CO ₂ levels is slowed in the syp121 null mutant, affecting shoot growth and whole‐plant water‐use efficiency. Thus, we uncover a new target for CO ₂ regulation in vesicle traffic and a novel perspective on plant responses to climate change.

Stomata of plant leaves open to enable CO ₂ entry for photosynthesis and close when CO ₂ in the leaf is elevated. CO ₂ is thought to promote stomatal closure in part by activating the SLAC1 anion channel at the guard cell plasma membrane. Carbonic anhydrases (CAs) contribute to this activation, but their contribution as distinct from CO ₂ -H ₂ CO ₃ catalysis remains controversial. Here we show that the β-carbonic anhydrase CA4 binds selectively with the guard-cell anion channel SLAC1 to enhance channel current. The interaction is CO ₂ -dependent, but binding is mediated by amino acids distal from the CO ₂ -binding site of CA4 and is separable from carbonic-anhydrase activity. CA4 mutants impaired in channel binding eliminate the CO ₂ -sensitivity of SLAC1 in vivo and slow stomatal kinetics with a commensurate loss in water use efficiency. The findings demonstrate that CA4 contributes directly to the CO ₂ -response mechanics regulating SLAC1 at near-ambient CO ₂ in guard cells and to stomatal kinetics in the plant.

The aberrant changes of fussion/fission-related proteins can trigger mitochondrial dynamics imbalance, which cause mitochondrial dysfunctions and result insulin resistance (IR). However, the relationship between the inner mitochondrial membrane fusion protein optic atrophy 1 (Opa1) and hepatic IR as well as the specific molecular mechanisms of signal transduction has not been fully elucidated. In this study, we explore whether abnormalities in the Opa1 cause hepatic IR and whether berberine (BBR) can prevent hepatic IR through the SIRT1/Opa1 signalling pathway. High-fat diet (HFD)-fed mice and db/db mice are used as animal models to study hepatic IR in vivo. IR, morphological changes, and mitochondrial injury of the liver are examined to explore the effects of BBR. SIRT1/Opa1 protein expression is determined to confirm whether the signalling pathway is damaged in the model animals and is involved in BBR treatment-mediated mitigation of hepatic IR. A palmitate (PA)-induced hepatocyte IR model is established in HepG2 cells in vitro. Opa1 silencing and SIRT1 overexpression are induced to verify whether Opa1 deficiency causes hepatocyte IR and whether SIRT1 improves this dysfunction. BBR treatment and SIRT1 silencing are employed to confirm that BBR can prevent hepatic IR by activating the SIRT1/Opa1 signalling pathway. Western blot analysis and JC-1 fluorescent staining results show that Opa1 deficiency causes an imbalance in mitochondrial fusion/fission and impairs insulin signalling in HepG2 cells. SIRT1 and BBR overexpression ameliorates PA-induced IR, increases Opa1, and improves mitochondrial function. SIRT1 silencing partly reverses the effects of BBR on HepG2 cells. SIRT1 and Opa1 expressions are downregulated in the animal models. BBR attenuates hepatic IR and enhances SIRT1/Opa1 signalling in db/db mice. In summary, Opa1 silencing-mediated mitochondrial fusion/fission imbalance could lead to hepatocyte IR. BBR may improve hepatic IR by regulating the SIRT1/Opa1 signalling pathway, and thus, it may be used to treat type-2 diabetes.

To find potent fungicides, 35 analogs of diphenyl ketones were synthesized and evaluated for their antifungal activity. These compounds possessed a furyl–carbonyl–phenyl skeleton. Bioassay results showed that the synthesized compounds were effective in promoting the antifungal activity of diphenyl ketones. Compound 3 showed the best activity against the four tested fungi (100%, 100%, 100% and 96.4%) and could be used as potent fungicide for further research.