RESUMO
Zebrafish is an attractive model organism for studying apoptosis development because of its genetic accessibility. Here we describe the induction of clonally derived apoptosis in transgenic zebrafish expressing mouse caspase-3 (CASP3) under control of the zebrafish beta-actin promoter (betap). Visualization of apoptotic cells, expressing a chimeric transgene encoding CASP3 fused to green fluorescent protein (GFP) gene, revealed that apoptosis arose in the thymus, spread locally into gill arches and retro-orbital soft tissue, and then disseminated into abdominal organs like testis, kidney. This transgenic model provides a platform for over-expression of caspase-3 induced extensive apoptosis in embryos and adult.
Assuntos
Apoptose , Caspases/metabolismo , Peixe-Zebra/anatomia & histologia , Actinas/genética , Animais , Animais Geneticamente Modificados , Caspase 3 , Caspases/genética , Embrião não Mamífero/anormalidades , Embrião não Mamífero/anatomia & histologia , Proteínas de Fluorescência Verde/genética , Proteínas de Fluorescência Verde/metabolismo , Camundongos , Especificidade de Órgãos , Regiões Promotoras Genéticas , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/metabolismo , Peixe-Zebra/anormalidades , Peixe-Zebra/genéticaRESUMO
Analyses of sediment and water indicate the presence of heavy metal pollutants like lead, zinc, copper, mercury and cadmium of the river Damodar of India. These metals are responsible for causing morphological deformities of antennae and other parts of chironomid larvae. Percentage of deformity correlated positively with the concentrations of Pb in water and sediment (r > 0.6) at the confluence point. A new severity index, SISS((antenna)) has been proposed here to assess deformity at the family or subfamily level.
