Hfq regulates the expression of the thermostable direct hemolysin gene in <Emphasis Type="Italic">Vibrio parahaemolyticus</Emphasis>

Background  

The hfq gene is conserved in a wide variety of bacteria and Hfq is involved in many cellular functions such as stress responses and the regulation of gene expression. It has also been reported that Hfq is involved in bacterial pathogenicity. However, it is not clear whether Hfq regulates virulence in Vibrio parahaemolyticus. To evaluate this, we investigated the effect of Hfq on the expression of virulence-associated genes including thermostable direct hemolysin (TDH), which is considered to be an important virulence factor in V. parahaemolyticus, using an hfq deletion mutant.     

Pleiotropic phenotypes of a <Emphasis Type="Italic">Yersinia enterocolitica flhD</Emphasis> mutant include reduced lethality in a chicken embryo model

Background  

The Yersinia enterocolitica flagellar master regulator FlhD/FlhC affects the expression levels of non-flagellar genes, including 21 genes that are involved in central metabolism. The sigma factor of the flagellar system, FliA, has a negative effect on the expression levels of seven plasmid-encoded virulence genes in addition to its positive effect on the expression levels of eight of the flagellar operons. This study investigates the phenotypes of flhD and fliA mutants that result from the complex gene regulation.     

The use of metabolome analysis to identify the cause of an unexplained disease of Japanese gentians (<Emphasis Type="Italic">Gentiana triflora</Emphasis>)

Introduction

Gentian spotted bleaching disease (GSBD), a novel disease of unknown etiology, affects Gentiana triflora plants that are cultivated as ornamental flowers in Japan. This disease leads to the production of necrotic leaf spots, a delay in flowering, and has thus become a serious problem for gentian production.

Objectives

The objective of this study was to identify the cause of GSBD in G. triflora by analyzing differences between healthy and GSBD-affected leaves.

Method

Selected metabolite concentrations in healthy and GSBD-affected leaves were quantified using capillary electrophoresis and liquid chromatography-mass spectrometry, and statistically significant differences in metabolite concentrations were assessed. GSBD-affected metabolic pathways were identified followed by examination of pathway-related gene expression and enzyme activities. Furthermore, the effects of root hypoxia on metabolite concentrations and gene expression were investigated.

Results

We found that concentrations of Calvin cycle intermediates and ribulose 1,5-bisphosphate carboxylase/oxygenase (RubisCO) activity were significantly lower in GSBD-affected leaves, whereas sucrose cleavage and Ala accumulation were enhanced. Since these metabolic changes are frequently observed in plants exposed to hypoxia, the expression of hypoxia-responsive genes was investigated. Expression levels of hypoxia-responsive genes were higher in GSBD-affected plants than in the controls. Furthermore, root hypoxia induced similar symptoms and metabolic changes as those observed in GSBD-affected plants.

Conclusion

Our results indicate that GSBD was likely induced by root hypoxia and that metabolome analysis is an effective tool for identifying the cause of plant disease with unknown etiologies.

     

Gene and pathway identification with <Emphasis Type="Italic">L</Emphasis><Subscript><Emphasis Type="Italic">p</Emphasis></Subscript>penalized Bayesian logistic regression

Background  

Identifying genes and pathways associated with diseases such as cancer has been a subject of considerable research in recent years in the area of bioinformatics and computational biology. It has been demonstrated that the magnitude of differential expression does not necessarily indicate biological significance. Even a very small change in the expression of particular gene may have dramatic physiological consequences if the protein encoded by this gene plays a catalytic role in a specific cell function. Moreover, highly correlated genes may function together on the same pathway biologically. Finally, in sparse logistic regression withL _p (p< 1) penalty, the degree of the sparsity obtained is determined by the value of the regularization parameter. Usually this parameter must be carefully tuned through cross-validation, which is time consuming.     

Alternative pre-mRNA processing regulates cell-type specific expression of the <Emphasis Type="Italic">IL4l1</Emphasis> and <Emphasis Type="Italic">NUP62</Emphasis> genes

Background  

Given the complexity of higher organisms, the number of genes encoded by their genomes is surprisingly small. Tissue specific regulation of expression and splicing are major factors enhancing the number of the encoded products. Commonly these mechanisms are intragenic and affect only one gene.     

Differential selection on gene translation efficiency between the filamentous fungus <Emphasis Type="Italic">Ashbya gossypii</Emphasis> and yeasts

Background  

The filamentous fungus Ashbya gossypii grows into a multicellular mycelium that is distinct from the unicellular morphology of its closely related yeast species. It has been proposed that genes important for cell cycle regulation play central roles for such phenotypic differences. Because A. gossypii shares an almost identical set of cell cycle genes with the typical yeast Saccharomyces cerevisiae, the differences might occur at the level of orthologous gene regulation. Codon usage patterns were compared to identify orthologous genes with different gene regulation between A. gossypii and nine closely related yeast species.     

Two non-homologous brain diseases-related genes, <Emphasis Type="Italic">SERPINI1</Emphasis> and <Emphasis Type="Italic">PDCD10</Emphasis>, are tightly linked by an asymmetric bidirectional promoter in an evolutionarily conserved manner

Background  

Despite of the fact that mammalian genomes are far more spacious than prokaryotic genomes, recent nucleotide sequencing data have revealed that many mammalian genes are arranged in a head-to-head orientation and separated by a small intergenic sequence. Extensive studies on some of these neighboring genes, in particular homologous gene pairs, have shown that these genes are often co-expressed in a symmetric manner and regulated by a shared promoter region. Here we report the identification of two non-homologous brain disease-related genes, with one coding for a serine protease inhibitor (SERPINI1) and the other for a programmed cell death-related gene (PDCD10), being tightly linked together by an asymmetric bidirectional promoter in an evolutionarily conserved fashion. This asymmetric bidirectional promoter, in cooperation with some cis-acting elements, is responsible for the co-regulation of the gene expression pattern as well as the tissue specificity of SERPINI1 and PDCD10.     

Two Frequenins in <Emphasis Type="Italic">Drosophila</Emphasis>: unveiling the evolutionary history of an unusual Neuronal Calcium Sensor (NCS) duplication

Background  

Drosophila Frequenin (Frq), the homolog of the mammalian Neuronal Calcium Sensor-1 (NCS-1), is a high affinity calcium-binding protein with ubiquitous expression in the nervous system. This protein has an important role in the regulation of neurotransmitter release per synapse, axonal growth and bouton formation. In D. melanogaster, Frequenin is encoded by two genes (frq1 and frq2), a very unexpected feature in the Frq/NCS-1 subfamily. These genes are located in tandem in the same genomic region, and their products are 95% identical in their amino acid sequence, clearly indicating their recent origin by gene duplication. Here, we have investigated the factors involved in this unusual feature by examining the molecular evolution of the two frq genes in Drosophila and the evolutionary dynamics of NCS family in a large set of bilaterian species.     

The <Emphasis Type="Italic">Tnfrh1</Emphasis> (<Emphasis Type="Italic">Tnfrsf23</Emphasis>) gene is weakly imprinted in several organs and expressed at the trophoblast-decidua interface

Background  

The Tnfrh1 gene (gene symbol Tnfrsf23) is located near one end of a megabase-scale imprinted region on mouse distal chromosome 7, about 350 kb distant from the nearest known imprinting control element. Within 20 kb of Tnfrh1 is a related gene called Tnfrh2 (Tnfrsf22) These duplicated genes encode putative decoy receptors in the tumor necrosis factor (TNF) receptor family. Although other genes in this chromosomal region show conserved synteny with genes on human Chr11p15.5, there are no obvious human orthologues of Tnfrh1 or Tnfrh2.     

Functional dissection of the <Emphasis Type="Italic">ash2</Emphasis> and <Emphasis Type="Italic">ash1</Emphasis> transcriptomes provides insights into the transcriptional basis of wing phenotypes and reveals conserved protein interactions

Background  

The trithorax group (trxG) genes absent, small or homeotic discs 1 (ash1) and 2 (ash2) were isolated in a screen for mutants with abnormal imaginal discs. Mutations in either gene cause homeotic transformations but Hox genes are not their only targets. Although analysis of double mutants revealed that ash2 and ash1 mutations enhance each other's phenotypes, suggesting they are functionally related, it was shown that these proteins are subunits of distinct complexes.