E-like ascospore excision mutants in Neurospora tetrasperma resistant to either p-DL-fluorophenylalanine or methyl benzimidazol-2-y1 carbamate

E-like ascospore excision mutants in Neurospora tetetrasperma resistant to either p-DL-fluorophenylalanine or methyl benzimidazol-2-y1 carbamat

The Roles and Acting Mechanism of Caenorhabditis elegans DNase II Genes in Apoptotic DNA Degradation and Development

DNase II enzymes are acidic endonucleases that have been implicated in mediating apoptotic DNA degradation, a critical cell death execution event. C. elegans genome contains three DNase II homologues, NUC-1, CRN-6, and CRN-7, but their expression patterns, acting sites, and roles in apoptotic DNA degradation and development are unclear. We have conducted a comprehensive analysis of three C. elegans DNase II genes and found that nuc-1 plays a major role, crn-6 plays an auxiliary role, and crn-7 plays a negligible role in resolving 3′ OH DNA breaks generated in apoptotic cells. Promoter swapping experiments suggest that crn-6 but not crn-7 can partially substitute for nuc-1 in mediating apoptotic DNA degradation and both fail to replace nuc-1 in degrading bacterial DNA in intestine. Despite of their restricted and largely non-overlapping expression patterns, both CRN-6 and NUC-1 can mediate apoptotic DNA degradation in many cells, suggesting that they are likely secreted nucleases that are retaken up by other cells to exert DNA degradation functions. Removal or disruption of NUC-1 secretion signal eliminates NUC-1's ability to mediate DNA degradation across its expression border. Furthermore, blocking cell corpse engulfment does not affect apoptotic DNA degradation mediated by nuc-1, suggesting that NUC-1 acts in apoptotic cells rather than in phagocytes to resolve 3′ OH DNA breaks. Our study illustrates how multiple DNase II nucleases play differential roles in apoptotic DNA degradation and development and reveals an unexpected mode of DNase II action in mediating DNA degradation

An\ue1lisis microbiol\uf3gico y molecular del "lloro primaveral" del kiwi: \ubfEs posible detectar con antelaci\uf3n el agente causal del cancro bacteriano (Pseudomonas syringae pv. actinidiae)?

En este art\uedculo los autores se\uf1alan la necesidad de desarrollar un modelo de prevenci\uf3n de PSA que reduzca la diseminaci\uf3n del cancro bacteriano. As\ued mismo explica un modelo de detecci\uf3n desarrollado en Italia y experimentado en Chile que se basa en el muestreo y an\ue1lisis del \u201clloro primaveral\u201d del kiwi, es decir, del flujo xilem\ue1tico que se libera por los cortes de poda de las plantas