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1.
Microbiol Spectr ; 12(2): e0309023, 2024 Feb 06.
Artigo em Inglês | MEDLINE | ID: mdl-38189328

RESUMO

Sugarcane is a critical sugar and bioenergy crop in China. However, numerous factors, including root rot disease, hamper its yield. Root rot disease is a severe agricultural issue, reducing yield and threatening sustainable crop production. The current study aimed to explore the fungal community structure, identify and characterize the primary pathogen for sugarcane root rot in Guangzhou, China. Eighty-nine samples of sugarcane root, stalk, rhizosphere soil, and irrigation water were collected from five sites in Guangzhou, China. Subsequently, 276 fungal strains were isolated to identify the primary pathogens. The five most common genera identified were Penicillium, Fusarium, Gongronella, Trichoderma, and Cladosporium. Fusarium was more prevalent in the infected soil samples than in healthy ones. Pathogenic assays of the strains revealed that the strain GX4-46 caused 80% of the disease. The strain was confirmed as Fusarium commune through phylogenetic and genome sequence analysis. Rhizosphere soil samples from different regional crops were collected to better understand the fungal community structure and the primary pathogen. We observed a significant presence of Fusarium in irrigation water, indicating that the root rot disease could originate from the irrigation water and then spread as a soil-borne disease. This research is pioneering and one of the most comprehensive investigations on the occurrence and prevalence of sugarcane root rot disease. This study will serve as a reference for expanding the sugarcane industry and a foundation for further exploration and control of root rot.IMPORTANCESugarcane, a significant economic crop, faces challenges due to root rot pathogens that accumulate each year in plants and soil through ratoon planting. This disrupts soil microbial balance and greatly impedes sugarcane industry growth. Symptoms range from wilting and yellowing leaves to stunted growth and reduced seedling tillers. The rhizosphere microbiota plays an important role in plant development and soil health. Little is known about root rot fungal community structure, especially in sugarcane. Here, we focused on exploring the main causative pathogen of root rot in the area alongside a detailed survey of the rhizosphere soil of different severity sugarcane cultivars and rotation crops of the region. To validate the findings, we also investigated the irrigation water of the area. Our study revealed Fusarium commune as the causative pathogen of root rot in the area, primarily originating from water and later as soil-borne. Using Trichoderma can control the disease effectively.


Assuntos
Fusarium , Micobioma , Saccharum , Trichoderma , Raízes de Plantas/microbiologia , Filogenia , Trichoderma/genética , Solo/química , Produtos Agrícolas , Surtos de Doenças , Água
2.
Neurochem Int ; 59(6): 739-48, 2011 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-21864608

RESUMO

It is well established that stimulating delta-opioid receptor (DOR) with its specific agonists elicits neuroprotection against hypoxia/ischemia. Mitochondrial dysfunction plays a key role in hypoxic neuronal injury, but the effects of DOR activation on mitochondrial dysfunction in neurons are poorly elucidated. In this investigation, we studied the effects of [D-Ala2, D-Leu5] enkephalin (DADLE), a potent DOR agonist, on acute mitochondrial dysfunction and ensuing cell damage induced by sodium azide in primary rat cortical neuronal cultures, and explored possible mechanisms underlying. Here, we show that DADLE reverses NaN(3)-induced acute mitochondrial dysfunction by selectively activating DOR, mainly including mitochondrial membrane depolarization, mitochondrial Ca(2+) overload and reactive oxygen species generation. DOR stimulation also inhibits cytochrome c release and caspase-3 activation, and attenuates neuronal death caused by acute NaN(3) insults. Furthermore, DOR activation with DADLE protects neurons from acute NaN(3) insults mainly through PKC-ERK pathway, and mitochondrial ERK activation is especially required for DOR neuroprotection against acute mitochondrial dysfunction.


Assuntos
Citoproteção/fisiologia , Doenças Mitocondriais/tratamento farmacológico , Doenças Mitocondriais/enzimologia , Doenças Mitocondriais/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/fisiologia , Receptores Opioides delta/agonistas , Doença Aguda , Analgésicos Opioides/farmacologia , Animais , Citoproteção/efeitos dos fármacos , Leucina Encefalina-2-Alanina/farmacologia , Ativação Enzimática/efeitos dos fármacos , Ativação Enzimática/fisiologia , Neurônios/efeitos dos fármacos , Neurônios/enzimologia , Neurônios/metabolismo , Cultura Primária de Células , Ratos , Ratos Sprague-Dawley , Receptores Opioides delta/fisiologia , Azida Sódica/toxicidade , Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
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