RESUMO
To understand the effects of disease-resistant maize varieties and new cropping systems on the population of Curvularia lunata, 52 isolates of C. lunata were collected in China from 2011 to 2013. The isolates were analyzed in terms of phylogenetic relationships, morphology, and pathogenicity. Phylogenetic analysis showed that the 52 isolates clustered into 2 distinct clusters with further subdivisions, suggesting the emergence of new genetic divergence within C. lunata. Results of morphology and pathogenicity analyses demonstrated that there were significant differences among these isolates: 27 isolates were classified as fast growing, 5 as slow growing, and 20 as moderate growing. Three isolates had white-colored colonies, 13 had yellowish green-colored colonies, and the remaining isolates had dark green-colored colonies. Furthermore, conidiation rates were assessed: 30 isolates were characterized as having low conidiation rates, 15 as having medium conidiation rates, and the remaining 7 isolates as having high conidiation rates. Eleven of the isolates appeared to be strongly pathogenic against maize, 15 isolates proved to be weakly pathogenic against maize, and the remaining isolates were regarded to be moderately pathogenic. Interestingly, correlation analysis demonstrated a negative correlation between the growth rate and the pathogenicity of the isolates, while a positive correlation was observed between the conidiation rate and the pathogenicity. No correlation was observed between the colony color and the pathogenicity of the isolates.
Assuntos
Ascomicetos/genética , Ascomicetos/patogenicidade , Doenças das Plantas/microbiologia , Zea mays/microbiologia , China , Filogenia , VirulênciaRESUMO
Exposure of humans to low levels of environmental oxygen results in alveolar hypoxia and normally causes chronic pulmonary hypertension and morphological alterations of precapillary pulmonary vessels. In this study, the microarray dataset GSE11341 was used to identify potential differentially expressed genes related with human lung microvascular endothelial cell hypoxia. In addition, gene ontology term enrichment analysis was performed to explore their underlying functions. In addition, we also investigated the small molecules by comparing with the Connectivity Map. We found that hypoxia samples of 3, 24, and 48 h relative to 0 h displayed 22, 21, and 29 differentially expressed genes, respectively. Among them, six genes (ADM, HMOX1, VEGFA, EGLN3, APOLD1, and ANGPTL4) were closely related to pulmonary microvascular endothelial cell hypoxia response. Three drugs (pindolol, sulfapyridine, and ciclopirox) were selected as candidates to treat hypoxia-related pulmonary diseases. In conclusion, our results provide some underlying drug targets for treatment of hypoxic pulmonary patients.