RESUMEN
BACKGROUND: Xanthomonas citri pv. citri (Xcc) is a citrus canker causing Gram-negative bacteria. Currently, little is known about the biological and molecular responses of Xcc to low temperatures. RESULTS: Results depicted that low temperature significantly reduced growth and increased biofilm formation and unsaturated fatty acid (UFA) ratio in Xcc. At low temperature Xcc formed branching structured motility. Global transcriptome analysis revealed that low temperature modulates multiple signaling networks and essential cellular processes such as carbon, nitrogen and fatty acid metabolism in Xcc. Differential expression of genes associated with type IV pilus system and pathogenesis are important cellular adaptive responses of Xcc to cold stress. CONCLUSIONS: Study provides clear insights into biological characteristics and genome-wide transcriptional analysis based molecular mechanism of Xcc in response to low temperature.
Asunto(s)
Respuesta al Choque por Frío/genética , Respuesta al Choque por Frío/fisiología , RNA-Seq , Xanthomonas/genética , Xanthomonas/fisiología , Flagelos/genética , Perfilación de la Expresión Génica , Lípidos de la Membrana/metabolismo , Xanthomonas/metabolismoRESUMEN
Gene leg1 (liver-enriched gene 1) was first identified as a novel gene whose expression was enriched in the liver of zebrafish. Further studies revealed that Leg1 protein was a novel secretory protein, which played a role in the liver development in zebrafish. Here we reported the analysis of expression pattern of zb-leg1 homologus gene mu-leg1. The cDNA of mu-leg1 was isolated from adult mouse liver by nested PCR. This gene encodes a putative protein, mu-Leg1, which shares 31% similarity with zb-Leg1 of zebrafish. Both Northern blotting and semi-quantitative RT-PCR demonstrated that the expression of mu-leg1 was enriched in the small intestine rather than in the liver in adult mouse. We also produced a recombined mu-Leg1 protein and a mu-Leg1 specific antibody. Western blottingdemonstrated that mu-Leg1 was a secretory protein. In addition, we have established a mu-leg1 conditional knock-out heterozygous mouse. Our work builds a basis for further studies of mu-leg1.
Asunto(s)
Proteínas/genética , Animales , Anticuerpos/inmunología , Clonación Molecular , ADN Complementario/química , ADN Complementario/genética , Femenino , Perfilación de la Expresión Génica , Orden Génico , Marcación de Gen , Vectores Genéticos , Heterocigoto , Hígado/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Proteínas/metabolismo , Proteínas Recombinantes de Fusión/genética , Proteínas Recombinantes de Fusión/inmunología , Proteínas Recombinantes de Fusión/aislamiento & purificaciónRESUMEN
Dickeya zeae is a causal agent of rice root rot disease. The pathogen is known to produce a range of virulence factors, including phytotoxic zeamines and extracellular enzymes, but the mechanisms of virulence regulation remain vague. In this study, we identified a SlyA/MarR family transcription factor SlyA in D. zeae strain EC1. Disruption of slyA significantly decreased zeamine production, enhanced swimming and swarming motility, reduced biofilm formation and significantly decreased pathogenicity on rice. Quantitative polymerase chain reaction (qPCR) analysis confirmed the role of SlyA in transcriptional modulation of a range of genes associated with bacterial virulence. In trans expression of slyA in expI mutants recovered the phenotypes of motility and biofilm formation, suggesting that SlyA is downstream of the acylhomoserine lactone-mediated quorum sensing pathway. Taken together, the findings from this study unveil a key transcriptional regulatory factor involved in the modulation of virulence factor production and overall pathogenicity of D. zeae EC1.