Cu-II-directed self-assembly of fullerenols to ameliorate copper stress in maize seedlings.

Widespread use of copper-based agrochemical may cause copper excessive accumulation in agricultural soil to seriously threaten crop production. Recently, fullerenols are playing important roles in helping crops build resistance to abiotic stresses by giving ingenious and successful resolutions. However, there is a lack of knowledge on their beneficial effects in crops under stresses induced by heavy metals. Herein, the visual observation of Cu2+-mediated assembly of fullerenols via electrostatic and coordination actions was carried out in vitro, showing that water-soluble nanocomplexes and water-insoluble cross-linking nanohybrids were selectively fabricated by precisely adjusting feeding ratios of fullerenols and CuSO4. Furthermore, maize simultaneous exposure of fullerenols and CuSO4 solutions was tested to investigate the comparative effects of seed germination and seedling growth relative to exposure of CuSO4 alone. Under moderate Cu2+ stresses (40 and 80 µM), fullerenols significantly mitigated the detrimental effects of seedlings, including phenotype, root and shoot elongation, biomass accumulation, antioxidant capacity, and Cu2+ uptake and copper transporter-related gene expressions in roots. Under 160 µM of Cu2+ as a stressor, fullerenols also accelerated germination of Cu2+-stressed seeds eventually up to the level of the control. Summarily, fullerenols can enhance tolerance of Cu2+-stressed maize mainly due to direct detoxification through fullerenol-Cu2+ interactions restraining the Cu2+ intake into roots and reducing free Cu2+ content in vivo, as well as fullerenol-maize interactions to enhance resistance by maintaining balance of reactive oxygen species and optimizing the excretion and transport of Cu2+. This will unveil valuable insights into the beneficial roles of fullerenols and its mechanism mode in alleviating heavy metal stress on crop plants.

Calcineurin B-like protein ZmCBL8-1 promotes salt stress resistance in Arabidopsis.

MAIN CONCLUSION: ZmCBL8-1 enhances salt stress tolerance in maize by improving the antioxidant system to neutralize ROS homeostasis and inducing Na+/H+ antiporter gene expressions of leaves. Calcineurin B-like proteins (CBLs) as plant-specific calcium sensors have been explored for their roles in the regulation of abiotic stress tolerance. Further, the functional variations in ZmCBL8, encoding a component of the salt overly sensitive pathway, conferred the salt stress tolerance in maize. ZmCBL8-1 is a transcript of ZmCBL8 found in maize, but its function in the salt stress response is still unclear. The present study aimed to characterize the protein ZmCBL8-1 that was determined to be composed of 194 amino acids (aa) with three conserved EF hands responsible for binding Ca2+. However, a 20-aa fragment was found to be missing from its C-terminus relative to another transcript of ZmCBL8. Results indicated that it harbored a dual-lipid modification motif MGCXXS at its N-terminus and was located on the cell membrane. The accumulation of ZmCBL8-1 transcripts was high in the roots but relatively lower in the leaves of maize under normal condition. In contrast, its expression was significantly decreased in the roots, while increased in the leaves under NaCl treatment. The overexpression of ZmCBL8-1 resulted in higher salt stress resistance of transgenic Arabidopsis in a Ca2+-dependent manner relative to that of the wild type (WT). In ZmCBL8-1-overexpressing plants exposed to NaCl, the contents of malondialdehyde and hydrogen peroxide were decreased in comparison with those in the WT, and the expression of key genes involved in the antioxidant defense system and Na+/H+ antiporter were upregulated. These results suggested that ZmCBL8-1 played a positive role in the response of leaves to salt stress by inducing the expression of Na+/H+ antiporter genes and enhancing the antioxidant system to neutralize the accumulation of reactive oxygen species. These observations further indicate that ZmCBL8-1 confers salt stress tolerance, suggesting that transcriptional regulation of the ZmCBL8 gene is important for salt tolerance.

Therapeutic effects of honokiol on motor impairment in hemiparkinsonian mice are associated with reversing neurodegeneration and targeting PPARγ regulation.

Parkinson's disease (PD) is a profound neurodegenerative disorder with gradual loss of dopamine nigrostriatal neurons linked to serious behavioral symptoms. While the current treatment strategies present limitations on halting the progression of PD, this study aimed to investigate the therapeutic potential of honokiol, as a partial peroxisome proliferator-activated receptor-gamma (PPARγ) mimic, on the proceeding behavioral and biochemical alterations in hemiparkinsonian mice. Results showed that unilateral striatal 6-hydroxydopamine (6-OHDA)-lesioned mice exhibited motor impairment, reflecting the contralateral rotation induced by apomorphine at 1-3 weeks post-lesion. Subchronic honokiol administration for 1-2 weeks, beginning 7 days after 6-OHDA-lesion, dose-dependently ameliorated motor dysfunction in hemiparkinsonian mice. Recovery of motor function was correlated with reversal of nigrostriatal dopaminergic neuronal loss, accompanied by higher tyrosine hydroxylase (TH) density, dopamine transporter (DAT) expression and vesicular monoamine transporter-2 (VMAT2) levels. Furthermore, honokiol attenuated oxidative stress and reactive astrocyte induction via decreasing NADPH-oxidase and glial fibrillary acidic protein (GFAP) expressions in 6-OHDA-lesioned striatum. The reversal effects of honokiol on behavioral impairment and striatal PPARγ expression were impeded by PPARγ antagonist GW9662. Notably, subchronic honokiol treatment extended the lifespan of these hemiparkinsonian mice. The present findings demonstrate the therapeutic activities of honokiol in ameliorating motor impairment and progressive dopaminergic damage that could be associated with regulating PPARγ signaling. Therefore, honokiol may potentially exert as a novel therapeutic candidate through PPARγ activation for management of motor symptoms and progressive neurodegeneration in PD.