Badapanda, C. | bioRxiv Science

bioRxiv2019

Rice Bean (Vigna umbellata) draft genome sequence: unravelling the late flowering and unpalatability related genomic resources for efficient domestication of this underutilized crop.

Rice bean is a less well known and underutilized legume crop that has proved to be highly favourable due to its rich nutritional value in comparison with other members of the Vigna family. As an initiative to compose rice bean (Vigna umbellata) genomic resource, the size of 414 mega-base pairs with an estimate of 31276 highly confidential genes from 15521 scaffolds and functional coverage of 96.08% was sequenced from 30X coverage data from Illumina and PacBio platform. Rice bean genome assembly was found to be exquisitely close to V. angularis (experimental control/outgroup), V. radiata and V. unguiculata, however, V. angularis being the closest. Heuristically, the assembled genome was further aligned with 31 leguminous plants (13 complete genomes and 18 partial genomes), by collinearity block mapping. Further, we predicted similar discriminant results by complete CDS alignment. In contrast, 17 medically influential genomes from NIGMS-NIH, when compared with rice bean assembly for LCB clusters led to identification of more than 18000 genes from the entire selected medicinal genomes. Empirical construction of all genome comparisons revealed symplesiomorphic character in turn uncovering the lineage of genetic and functional features of rice beans. Signifiacantly, we found deserving late-flowering genes, palatably-indexed uncommon genes that regulate various metabolite pathways, related to abiotic and biotic stress pathways and those that are specific to photoperiod and disease resistance and so on. Further, we developed a repository for underutilised crop genome facility using D3.js at www.nicg.in. Therefore, the findings from this report addresses the genomic value of rice bean to be escalated via breeding by allied and applied approaches.\n\n\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=104 SRC=\"FIGDIR/small/816595v1_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (22K):\norg.highwire.dtl.DTLVardef@a8b2fforg.highwire.dtl.DTLVardef@17fafcborg.highwire.dtl.DTLVardef@1ee6861org.highwire.dtl.DTLVardef@106ee9c_HPS_FORMAT_FIGEXP M_FIG C_FIG

genomics↗

bioRxiv2019

The pneumococcal two-component system VisRH is linked to enhanced intracellular survival of Streptococcus pneumoniae in influenza-infected pneumocytes

The virus-bacterial synergism implicated in secondary bacterial infections caused by Streptococcus pneumoniae following infection with epidemic or pandemic influenza A virus (IAV) is well documented. However, the molecular mechanisms behind such synergism remain largely ill-defined. In pneumocytes infected with influenza A virus, subsequent infection with S. pneumoniae leads to enhanced pneumococcal intracellular survival. The pneumococcal two-component system VisRH appears essential for such enhanced survival. Through comparative transcriptomic analysis between the {Delta}visR and wt strains, a list of 179 differentially expressed genes was defined. Among those, the clpL protein chaperone gene and the psaB Mn+2 transporter gene, which are involved in the stress response, are important in enhancing S. pneumoniae survival in influenza-infected cells. The {Delta}visR, {Delta}clpL and {Delta}psaB deletion mutants display increased susceptibility to acidic and oxidative stress and no enhancement of intracellular survival in IAV-infected pneumocyte cells. These results suggest that the VisRH two-component system senses IAV-induced stress conditions and controls adaptive responses that allow survival of S. pneumoniae in IAV-infected pneumocytes.\n\nAuthor summaryS. pneumoniae is an inhabitant of the human nasopharynx that is capable of causing a variety of infections contributing to an estimated 1.6 million deaths each year. Many of these deaths occur as result of secondary S. pneumoniae infections following seasonal or pandemic influenza. Although S. pneumoniae is considered a typical extracellular pathogen, an intracellular survival mechanism has been more recently recognized as significant in bacterial pathogenesis. The synergistic effects between influenza A and S. pneumoniae in secondary bacterial infection are well documented; however, the effects of influenza infections on intracellular survival of S. pneumoniae are ill-defined. Here, we provide evidence that influenza infection increases S. pneumoniae intracellular survival in pneumocytes. We demonstrate that the poorly understood VisRH signal transduction system in pneumococcus controls the expression of genes involved in the stress response that S. pneumoniae needs to increase intracellular survival in influenza A-infected pneumocytes. These findings have important implications for understanding secondary bacterial pathogenesis following influenza and for the treatment of such infections in influenza-stricken patients.

microbiology↗