RESUMEN
The suitability of F1 progeny insect larvae of the irradiated male parent, Spodoptera litura (Fabr.) for infective juveniles (IJs) of entomopathogenic nematodes (EPN), Steinernema thermophilum was assessed to comprehend the feasibility of combining EPNs with nuclear pest control tactic. As compared to the control, the IJs induced faster host mortality with reduced proliferation in F1 host larvae. IJs derived from F1 host larvae exhibited almost similar proliferation capacity on normal hosts as in control. Further, the molecular basis of EPNs induced mortality in F1 host larvae was evaluated. Dual stress of EPN infection and irradiation induced downregulation of the relative mRNA expression of antimicrobial genes and upregulated expression of antioxidative genes. A pronounced effect of EPNs in association with irradiation stress was apparent on host mortality. Radiation induced sterile F1 insect larvae of S. litura acted as a reasonably suitable host for EPNs and also provided the environment for developing viable EPNs for their potential use as biocontrol agents.
Asunto(s)
Rayos gamma , Larva , Spodoptera , Animales , Masculino , Larva/efectos de la radiación , Virulencia , Rabdítidos/genética , Rabdítidos/crecimiento & desarrollo , Rabdítidos/fisiología , Rabdítidos/efectos de la radiación , Control Biológico de Vectores , Interacciones Huésped-ParásitosRESUMEN
Mycobacterial species is known for inhabiting various niches ranging from soil to harsh intracellular environment of animal hosts and their survival through constant changes. For survival and persistence, these organisms must quickly adapt by bringing shift in their metabolism. Metabolic shifts are brought by sensing the environmental cues usually by membrane localized sensor molecules. These signals are transmitted to regulators of various metabolic pathways leading to post-translational modifications of regulators ultimately resulting in altered metabolic state of the cell. Multiple regulatory mechanisms have been unearthed so far that play crucial role in adapting to these situations, and among them, the signal-dependent transcriptional regulators mediated responses are integral for the microbes to perceive environmental signals and generate appropriate adaptive responses. LysR-type transcriptional regulators (LTTRs) form the largest family of transcriptional regulators, which are present in all kingdoms of life. Their numbers vary among bacterial genera and even in different mycobacterial species. To understand the evolutionary aspect of pathogenicity based on LTTRs, we performed phylogenetic analysis of LTTRs encoded by several mycobacterial species representing non-pathogenic (NP), opportunistic (OP), and totally pathogenic (TP) mycobacteria. Our results showed that LTTRs of TP clustered separately from LTTRs of NP and OP mycobacteria. In addition, LTTRs frequency per Mb of genome was reduced in TP when compared with NP and OP. Further, the protein-protein interactions and degree-based network analysis showed concomitant increased interactions per LTTRs with increase in pathogenicity. These results suggested the increase in regulon of LTTRs during evolution of TP mycobacteria.
RESUMEN
Previous studies implicate cyclin-dependent kinase 5 in cell adhesion and migration of epithelial cells of the cornea and lens. To explore molecular interactions underlying these functions, we performed yeast two-hybrid screening of an embryonic rat lens library for proteins that interact with cyclin-dependent kinase 5 and its regulators, p35 and p39. This screen identified a specific interaction between p39 and muskelin, an intracellular protein known to affect cytoskeletal organization in adherent cells. Immunohistochemistry detected muskelin in the developing lens and in other tissues, including brain and muscle. Glutathione S-transferase pull-down experiments and co-immunoprecipitations confirmed the specificity of the p39-muskelin interaction. Deletion analysis of p39 showed that muskelin binds to the p39 C terminus, which contains a short insertion (amino acids 329-366) absent from p35. Similar analysis of muskelin mapped the interaction with p39 to the fifth kelch repeat. Co-expression of p39 and muskelin in COS1 cells or lens epithelial cells altered the intracellular localization of muskelin, recruiting it to the cell periphery. These findings demonstrate a novel interaction between muskelin and the cyclin-dependent kinase 5 activator p39 and suggest that p39 may regulate the subcellular localization of muskelin.
Asunto(s)
Quinasas Ciclina-Dependientes/metabolismo , Proteínas/metabolismo , Proteínas Proto-Oncogénicas c-jun/metabolismo , Actinas/química , Animales , Sitios de Unión , Encéfalo/metabolismo , Células COS , Adhesión Celular , Moléculas de Adhesión Celular , Línea Celular , Movimiento Celular , Quinasa 5 Dependiente de la Ciclina , Citoesqueleto/metabolismo , ADN Complementario/metabolismo , Células Epiteliales/metabolismo , Eliminación de Gen , Biblioteca de Genes , Glutatión Transferasa/metabolismo , Immunoblotting , Inmunohistoquímica , Inmunoprecipitación , Péptidos y Proteínas de Señalización Intracelular , Cristalino/metabolismo , Microscopía Fluorescente , Músculos/metabolismo , Oligonucleótidos/química , Péptidos/química , Fosfotransferasas/metabolismo , Plásmidos/metabolismo , Unión Proteica , ARN/química , ARN Mensajero/metabolismo , Conejos , Ratas , Proteínas Recombinantes de Fusión/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factores de Tiempo , Transfección , Técnicas del Sistema de Dos HíbridosRESUMEN
Resuscitation from hemorrhagic shock initiates profound changes in the liver that are likely to contribute to end organ damage and resultant dysfunction after shock. Extensive research in this area has indicated the potential of free radical scavenging strategy for better management of the pathophysiology following hemorrhage-resuscitation (H/R) injury. We studied the effect of a novel pharmacological agent, picroliv, on hepatocellular injury and redox status, as well as its possible mechanism of action in a H/R model in adult rats. Anesthetized rats were subjected to hemorrhagic shock by bleeding 30 mL/kg body weight. After 60 min of shock, rats were resuscitated with twice the shed blood volume of lactated Ringer's solution and were sacrificed 2 h after resuscitation. We observed that picroliv (12 mg/kg) pretreatment, given orally for 7 days, resulted in a significant decrease in serum aspartate transaminase and gamma-glutamyl transpeptidase levels. Picroliv also inhibited the lipid peroxidation and nitric oxide release that occurred after H/R and altered the activity of glutathione reductase in a favorable manner, thereby suggesting better antioxidant status. Picroliv significantly down-regulated the stress-sensitive transcription factor AP1 and decreased the level of c-fos mRNA as well as c-jun and c-fos proteins in liver tissue, indicating that its actions could be mediated through AP1 and associated signal transduction pathways. These findings suggest that picroliv has the potential to be developed as a protective agent against H/R injury.