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1.
PLoS One ; 13(4): e0196520, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29698535

RESUMEN

Potato common scab, which is caused by soil-borne Streptomyces species, is a severe plant disease that results in a significant reduction in the economic value of potatoes worldwide. Due to the lack of efficacious pesticides, crop rotations, and resistant potato cultivars against the disease, we investigated whether biological control can serve as an alternative approach. In this study, multiple Bacillus species were isolated from healthy potato tubers, and Bacillus amyloliquefaciens Ba01 was chosen for further analyses based on its potency against the potato common scab pathogen Streptomyces scabies. Ba01 inhibited the growth and sporulation of S. scabies and secreted secondary metabolites such as surfactin, iturin A, and fengycin with potential activity against S. scabies as determined by imaging mass spectrometry. In pot assays, the disease severity of potato common scab decreased from 55.6 ± 11.1% (inoculated with S. scabies only) to 4.2 ± 1.4% (inoculated with S. scabies and Ba01). In the field trial, the disease severity of potato common scab was reduced from 14.4 ± 2.9% (naturally occurring) to 5.6 ± 1.1% after Ba01 treatment, representing evidence that Bacillus species control potato common scab in nature.


Asunto(s)
Bacillus amyloliquefaciens/metabolismo , Agentes de Control Biológico/metabolismo , Enfermedades de las Plantas/prevención & control , Solanum tuberosum/microbiología , Bacillus amyloliquefaciens/clasificación , Bacillus amyloliquefaciens/genética , Agentes de Control Biológico/química , Agentes de Control Biológico/farmacología , Pruebas Antimicrobianas de Difusión por Disco , Lipopéptidos/química , Lipopéptidos/metabolismo , Lipopéptidos/farmacología , Espectrometría de Masas , Péptidos Cíclicos/química , Péptidos Cíclicos/metabolismo , Péptidos Cíclicos/farmacología , Filogenia , Enfermedades de las Plantas/microbiología , ARN Ribosómico 16S/clasificación , ARN Ribosómico 16S/metabolismo , Solanum tuberosum/crecimiento & desarrollo , Streptomyces/efectos de los fármacos , Streptomyces/crecimiento & desarrollo
2.
eNeuro ; 5(6)2018.
Artículo en Inglés | MEDLINE | ID: mdl-30627660

RESUMEN

Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by degeneration of spinal motor neurons resulting in variable degrees of muscular wasting and weakness. It is caused by a loss-of-function mutation in the survival motor neuron (SMN1) gene. Caenorhabditis elegans mutants lacking SMN recapitulate several aspects of the disease including impaired movement and shorted life span. We examined whether genes previously implicated in life span extension conferred benefits to C. elegans lacking SMN. We find that reducing daf-2/insulin receptor signaling activity promotes survival and improves locomotor behavior in this C. elegans model of SMA. The locomotor dysfunction in C. elegans lacking SMN correlated with structural and functional abnormalities in GABAergic neuromuscular junctions (NMJs). Moreover, we demonstrated that reduction in daf-2 signaling reversed these abnormalities. Remarkably, enhancing GABAergic neurotransmission alone was able to correct the locomotor dysfunction. Our work indicated that an imbalance of excitatory/inhibitory activity within motor circuits and underlies motor system dysfunction in this SMA model. Interventions aimed at restoring the balance of excitatory/inhibitory activity in motor circuits could be of benefit to individuals with SMA.


Asunto(s)
Trastornos Neurológicos de la Marcha/etiología , Trastornos Neurológicos de la Marcha/terapia , Atrofia Muscular Espinal/complicaciones , Ácido gamma-Aminobutírico/metabolismo , Adyuvantes Inmunológicos/farmacología , Animales , Animales Modificados Genéticamente , Fenómenos Biomecánicos/efectos de los fármacos , Fenómenos Biomecánicos/genética , Caenorhabditis elegans , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/metabolismo , Inhibidores de la Colinesterasa/farmacología , Modelos Animales de Enfermedad , Factores de Transcripción Forkhead/genética , Factores de Transcripción Forkhead/metabolismo , Trastornos Neurológicos de la Marcha/patología , Levamisol/farmacología , Longevidad/efectos de los fármacos , Longevidad/genética , Atrofia Muscular Espinal/genética , Atrofia Muscular Espinal/terapia , Unión Neuromuscular/efectos de los fármacos , Unión Neuromuscular/patología , Bromuro de Piridostigmina/farmacología , Interferencia de ARN/fisiología , Transducción de Señal/efectos de los fármacos , Transducción de Señal/genética , Análisis de Supervivencia , Proteína 1 para la Supervivencia de la Neurona Motora/genética
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