The expression of bacterial cold-shock proteins (CSPs) is highly induced in response to cold shock, and some CSPs are essential for cells to resume growth at low temperature. Bordetella bronchiseptica encodes five CSPs (named CspA to CspE) with significant amino acid homology to CspA of Escherichia coli. In contrast to E. coli, the insertional knock-out of a single csp gene (cspB) strongly affected growth of B. bronchiseptica independent of temperature. In the case of three of the csp genes (cspA, cspB, cspC) more than one specific transcript could be detected. The net amount of cspA, cspB and cspC transcripts increased strongly after cold shock, while no such effect could be observed for cspD and cspE. The exposure to other stress conditions, including translation inhibitors, heat shock, osmotic stress and nutrient deprivation in the stationary phase, indicated that the csp genes are also responsive to these conditions. The coding regions of all of the cold-shock genes are preceded by a long non-translated upstream region (59-UTR). In the case of the cspB gene, a deletion of parts of this region led to a significant reduction of translation of the resulting truncated transcript, indicating a role of the 59-UTR in translational control. The cold-shock stimulon was investigated by 2D-PAGE and mass spectrometric characterization, leading to the identification of additional cold-inducible proteins (CIPs). Interestingly, two cold-shock genes (cspC and cspD) were found to be under the negative control of the BvgAS system, the main transcriptional regulator of Bordetella virulence genes. Moreover, a negative effect of slight overexpression of CspB, but not of the other CSPs, on the transcription of the adenylate cyclase toxin CyaA of Bordetella pertussis was observed, suggesting cross-talk between the CSP-mediated stress response stimulon and the Bordetella virulence regulon.
The two-component system BvgAS positively controls transcription of the virulence genes of Bordetella pertussis and B. bronchiseptica, which include several genes for toxins and adhesins. On the other hand, the BvgAS system negatively controls the expression of a poorly characterized set of genes, the so-called virulence repressed ( vrg) genes. To investigate the function of this group of genes and their relationship to virulence, we identified several novel vrg genes of B. bronchiseptica via the generation of transcriptional fusions with gfp (the ORF encoding Green Fluorescent Protein) by transposon mutagenesis. Expression of all of the vrg genes was enhanced under phenotype-modulating growth conditions and in phase variants, demonstrating that their transcription is indeed controlled by the BvgAS system. In addition, transcription of most of these new vrg genes was found to be affected by the growth phase of the bacteria, with maximal expression being observed in the late logarithmic or stationary phase. The majority of these genes encode putative metabolic functions involved in redox reactions and amino acid transport. Interestingly, several vrg genes of B. bronchiseptica are not expressed or have been lost in B. pertussis, indicating that, possibly as a consequence of its adaptation to a single host organism, many vrg genes of B. pertussis are gradually decaying.
Several proteins encoded in the genomes of Bordetella species show significant sequence similarity to the autotransporter domains of surface exposed or secreted virulence factors of bordetellae such as pertactin, tracheal colonization factor or Vag8. One of these putative autotransporters, provisionally termed Phg, is encoded by the pertactin homologous gene (phg), which is highly conserved in Bordetella pertussis, B. bronchiseptica and B. parapertussis, but absent in B. avium and B. petrii. In contrast to homologues with documented functions in host interaction and virulence, several key amino acids probably involved in proteolytic processing of the autotransporter domain are not conserved in Phg. The transcription start site of phg was identified by primer extension analysis, but differential transcription of phg could not be detected in B. bronchiseptica strains under conditions that lead to enhanced expression of other known Bordetella autotransporter proteins. A mutant of B. pertussis was constructed in which major parts of phg are substituted by a kanamycin resistance cassette. Virulence testing of this mutant in a mouse respiratory infection model showed the same colonization properties as the wild-type strain.
Abstract. Tyrosine kinase 2 (TYK2) is a member of the janus kinase gene family and encodes an 1187 amino acid protein. All four members of the janus kinase family JAK1, JAK2, JAK3, and TYK2 associate with various cytokine receptors and mediate the signal transduction by tyrosine phosphorylation of downstream targets (YAMOAKA et al., 2004). Studies with tyk2 deficient mice demonstrated impairment of interferon α/β signaling (KARAGHIOSOFF et al., 2003). Mutations in the murine tyk2 gene are associated with increased susceptibility to infectious and autoimmune diseases (SHAW et al., 2003). The human TYK2 gene consists of 25 exons spanning 30,003 bp on human chromosome 19p13.2 starting at 10,322,209 bp. The objective of this study was to determine the chromosomal location of TYK2 in the horse by FISH and RH mapping.
Since the beginning of investigation in the horse genome in the early nineties, there has been a great progress, especially during the last five years. At the beginning the exploration of monogenic hereditary diseases was one of the main aims, and the causal mutations of several diseases in the horse have been unravelled. The inheritance of coat colours has been explored very detailed, and there exist gene tests for different coat colours. Information about coat colours and inherited diseases is very important for the breeders and helps avoiding the appearance of lethal genetic factors or undesirable diseases. The most important achievements of horse genome analysis were well-developed linkage, radiation hybrid and cytogenetic genome maps including more than 2950 loci. These maps support comparative analysis of equine hereditary diseases. The present known gene mutations for five diseases in horses have human homologs. Studies on multifactorial diseases such as osteochondrosis and navicular bone disease and on fertility and temperament are underway. At the moment, the whole equine genome is sequenced as it has been done for the human genome and also for other animal genomes. Horse breeding will greatly benefit from identification of QTL for multifactorial traits and gene mutations for congenital anomalies, diseases and performance traits.
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