The present work reports the sequencing and analysis of the plasmid complement of L. garvieae IPLA 31405, a strain isolated from a traditional, Spanish, starter-free cheese made from raw-milk. It consists of pLG9 and pLG42, of 9,124 and 42,240 nucleotides, respectively. find more Based on sequence and structural homology in the putative origin of replication (ori) region, pLG9 and pLG42 are predicted to replicate via a theta
mechanism. Real-time, quantitative PCR showed the number of copies per chromosome equivalent of pLG9 and pLG42 to be around two and five, respectively. Sequence analysis identified eight complete open reading frames (orfs) in pLG9 and 36 in pLG42; these were organized into functional modules or cassettes this website containing different numbers of genes. These modules were flanked by complete or interrupted insertion sequence
(IS)-like elements. Among the modules of pLG42 was a gene cluster encoding specific components of a phosphoenolpyruvate-phosphotransferase (PEP-PTS) system, including a phospho-beta-galacosidase. The cluster showed a complete nucleotide identity respect to that in plasmids of L. lactis. Loss of pLG42 showed this to be involved in lactose assimilation. In the same plasmid, an operon encoding a type I restriction/modification (R/M) system was also identified. The specificity of this R/M system might be broadened by different R/M specificity subunits detected in pLG9 and in the bacterial chromosome. However, challenges of L. garvieae IPLA 31405 against L. lactis phages proved that the R/M system was not involved in phage resistance. Together, these results support the hypothesis that, as in L. lactis, pLG42 contribute towards the adaptation of L. garvieae to the dairy environment.”
“Objective. The (8;21)(q22;q22) chromosomal translocation, which involves AML1 gene on chromosome 21 and the ETO gene on chromosome 8, generates an AML1/ETO fusion. AML1/ETO is associated with 15% of acute myeloid leukemia (AML) cases. The fusion gene is a dominant inhibitor
of myeloid-specific GSK690693 clinical trial genes, notably AML1, CCAAT/enhancer-binding protein-alpha (C/EBP alpha), and myeloperoxidase (MPO). In this study, we investigated the role of antiapoptosis gene survivin as a target of AML1/ETO-related leukemia.\n\nMaterials and Methods. Through the combination of reporter assays, electrophoretic mobility shift assay, quantitative real-time polymerase chain reaction analysis, and short hairpin RNA (shRNA)- mediated knockdown of genes, we showed that survivin is a critical target of AML1/ETO. Biological studies were performed in cell lines and primary human CD 34(+) cells.\n\nResults. In this study, we have shown that ectopic expression of AML1/ETO induces survivin gene expression in both a cell line model and in the primary human hematopoietic CD34(+) cells.