Wheat is susceptible to atmospheric ozone (O) pollution, thus the increasing O is a serious threat to wheat production. γ-aminobutyric acid (GABA) is found to play key roles in the tolerance of plants to stress. However, few studies elaborated the function of GABA in response of wheat to O. Here, we incorporated metabolome and transcriptome data to provide a more comprehensive insight on the role of GABA in enhancing the O-tolerance of wheat. In our study, there were 31, 23, and 32 differentially accumulated flavonoids in the carbon-filtered air with GABA, elevated O with or without GABA treatments compared to the carbon-filtered air treatment, respectively. Elevated O triggered the accumulation of dihydroflavone, flavonols, and flavanols. Exogenous GABA enhanced dihydroflavone and dihydroflavonol, and also altered the expression of genes encoding some key enzymes in the flavonoid synthesis pathway. Additionally, GABA stimulated proline accumulation and antioxidant enzyme activities under elevated O, resulting in the less accumulation of HO and malondialdehyde. Consequently, GABA alleviated the grain yield loss from 19.6% to 9.6% induced by elevated O. Our study provided comprehensive insight into the role of GABA in the alleviating the detrimental effects of elevated O on wheat, and a new avenue to mitigate O damage to the productivity of crops.
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http://dx.doi.org/10.1016/j.jhazmat.2023.133202 | DOI Listing |
MicroPubl Biol
December 2024
Faculty of Environment and Information Studies, Keio University, Kanagawa, Japan.
In , axial elongation beyond the tailbud stage requires gamma-aminobutyric acid (GABA). However, the role of GABA synthesized during early development in this process remains unclear. In this study, by treating embryos with allylglycine (AG), an inhibitor of GABA synthesis, we observed a significant reduction in axial elongation.
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November 2024
Faculty of Human Sciences, Sophia University, Chiyoda-ku, Tokyo, Japan.
Introduction: The (EMB) theory, a major causal hypothesis of autism (ASD: autism spectrum disorder), attributes excess androgens during early development as one of the causes. While studies have generally followed the EMB theory in females at birth, the co-occurrence of ASD in males at birth has been observed in conditions that are assumed to be associated with reduced androgen action during early development, including Klinefelter syndrome (KS) and sexual minorities. ASD is also associated with atypical sensory sensitivity, synesthesia, and savant syndrome.
View Article and Find Full Text PDFMol Neurodegener
January 2025
Center for Cognition and Sociality, Life Science Institute (LSI), Institute for Basic Science (IBS), Daejeon, Republic of Korea.
Background: Alzheimer's Disease (AD) is a neurodegenerative disease with drastically altered astrocytic metabolism. Astrocytic GABA and HO are associated with memory impairment in AD and synthesized through the Monoamine Oxidase B (MAOB)-mediated multi-step degradation of putrescine. However, the enzymes downstream to MAOB in this pathway remain unidentified.
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January 2025
Department of Neurology, the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 1, Minde Road, 330006 Nanchang, Jiangxi, China. Electronic address:
Wogonin, an O-methylated flavonoid extracted from Scutellaria baicalensis, has demonstrated profound neuroprotective effects in a range of central nervous system (CNS) diseases. This review elucidates the pharmacological mechanisms underlying the protective effects of wogonin in CNS diseases, including ischemic stroke, hemorrhagic stroke, traumatic brain injury, epilepsy, anxiety, neurodegenerative diseases, and CNS infections. Wogonin modulates key signaling pathways, such as the MAPK, NF-κB, and ROS pathways, contributing to its anti-inflammatory, antioxidant, and antiapoptotic properties.
View Article and Find Full Text PDFNeurology
February 2025
Division of Clinical and Metabolic Genetics, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Ontario, Canada.
Pathogenic variants in cause congenital muscular dystrophy through hypoglycosylation of alpha-dystroglycan (OMIM #615350). The established phenotypic spectrum of GMPPB-related disorders includes recurrent rhabdomyolysis, limb-girdle muscular dystrophy, neuromuscular transmission abnormalities, and congenital muscular dystrophy with variable brain and eye anomalies. We report a 9-month-old male infant with congenital muscular dystrophy, infantile spasms, and compound heterozygous pathogenic variants (c.
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