Biology subjects

Shimoda, M.

Publications and source records attributed to Shimoda, M..

5 recordsLinked to original sources

bioRxiv2023

High-quality genome of the zoophytophagous stinkbug, Nesidiocoris tenuis, informs their food habitadaptation

The zoophytophagous stink bug, Nesidiocoris tenuis, is a promising natural enemy of micropests such as whiteflies and thrips. This bug possesses both phytophagous and entomophagous food habits, enabling it to obtain nutrition from both plants and insects. This trait allows us to maintain its population density in agricultural fields by introducing insectary plants, even when the pest prey density is extremely low. However, if the bugs population becomes too dense, they can sometimes damage crop plants. This dual character seems to arise from the food preferences and chemosensation of this predator. To understand the genomic landscape of N. tenuis, we examined the whole genome sequence of a commercially available Japanese strain. We used long-read sequencing and Hi-C analysis to assemble the genome at the chromosomal level. We then conducted a comparative analysis of the genome with previously reported genomes of phytophagous and hematophagous stink bugs to focus on the genetic factors contributing to this species herbivorous and carnivorous tendencies. Our findings suggest that the gustatory gene set plays a pivotal role in adapting to food habits, making it a promising target for selective breeding. Furthermore, we identified the whole genomes of microorganisms symbiotic with this species through genomic analysis. We believe that our results shed light on the food habit adaptations of N. tenuis and will accelerate breeding efforts based on new breeding techniques for natural enemy insects, including genomics and genome editing.

genomics↗

bioRxiv2023

Prolonged Kaposi's Sarcoma-associated Herpesvirus vIL-6 Exposure Enhances Inflammatory Responses by Epigenetic Reprogramming

Kaposi sarcoma-associated herpesvirus (KSHV) inflammatory cytokine syndrome (KICS) is a newly described chronic inflammatory disease condition caused by KSHV infection and is characterized by high KSHV viral load and sustained elevations of serum KSHV-encoded IL-6 (vIL-6) and human IL-6 (hIL-6). KICS has significant immortality and possesses greater risks of having other complications, which include malignancies. Although prolonged inflammatory vIL-6 exposure by persistent KSHV infection is expected to have key roles in subsequent disease development, the biological effects of prolonged vIL-6 exposure remain elusive. Using thiol-Linked Alkylation for the Metabolic Sequencing and Cleavage Under Target & Release Using Nuclease analysis, we studied the effect of prolonged vIL-6 exposure in chromatin landscape and resulting cytokine production. The studies showed that prolonged vIL-6 exposure increased Bromodomain containing 4 (BRD4) and histone H3 lysine 27 acetylation co-occupancies on chromatin, and the recruitment sites were frequently co-localized with poised RNAPII with associated enzymes. Increased BRD4 recruitment on promoters was associated with increased and prolonged NF-KB p65 binding after the lipopolysaccharide stimulation. The p65 binding resulted in quicker and sustained transcription bursts from the promoters; this mechanism increased total amounts of hIL-6 and IL-10 in tissue culture. Pretreatment with the BRD4 inhibitor, OTX015, eliminated the enhanced inflammatory cytokine production. These findings suggest that persistent vIL-6 exposure may establish a chromatin landscape favorable for the reactivation of inflammatory responses in monocytes. This epigenetic memory may explain the greater risk of chronic inflammatory disease development in KSHV-infected individuals. Author summaryCombined and continuous cytokine stimulation triggers transcription reprogramming and is often used for specific tissue development. Continuous vIL-6 exposure occurs in KSHV-infected patients and leads to inflammatory cytokine storm with high mortality. However, possible epigenetic reprogramming by the vIL-6 and its association with pathogenesis remain unclear. Here we demonstrate the establishment of a new chromatin landscape mediated by BRD4 through prolonged vIL-6 exposure which contributes to more robust and rapid transcription and increased cytokines production. Inhibition of BRD4 suppressed this inflammatory response. Our results indicate that targeting the epigenetic effect of viral cytokines may lead to novel therapies for KSHV-induced inflammatory cytokine storms.

microbiology↗

bioRxiv2023

KSHV uses viral IL6 to expand infected immunosuppressive macrophages

Kaposis sarcoma-associated herpesvirus (KSHV) is an oncogenic double-stranded DNA virus and the etiologic agent of Kaposis sarcoma and hyperinflammatory lymphoproliferative disorders. Understanding the mechanism by which KSHV increases the infected cell population is crucial for curing KSHV-associated diseases. Here we demonstrate that KSHV preferentially infects CD14+ monocytes and sustains viral replication through the viral interleukin-6 (vIL6)-mediated activation of STAT1 and 3. Using vIL6-sufficient and vIL6-deficient recombinant KSHV, we demonstrated that vIL6 plays a critical role in promoting the proliferation and differentiation of KSHV-infected monocytes into macrophages. The macrophages derived from vIL6-sufficient KSHV infection showed a distinct transcriptional profile of elevated IFN-pathway activation with immune suppression and were compromised in T-cell stimulation function compared to those from vIL6-deficient KSHV infection or uninfected control. These results highlight a clever strategy, in which KSHV utilizes vIL6 to secure its viral pool by expanding infected dysfunctional macrophages. This mechanism also facilitates KSHV to escape from host immune surveillance and to establish a lifelong infection. 160 SummaryKSHV causes multiple inflammatory diseases, however, the underlying mechanism is not clear. Shimoda et al. demonstrate that KSHV preferentially infects monocytes and utilizes virally encoded interleukin-6 to expand and deregulate infected monocytes. This helps the virus escape from host immune surveillance.

immunology↗

bioRxiv2022

Deodorize with Bugs: Inoculation with black soldier fly larvae alters the microbiome and volatile organic compound profile of decomposing food waste

The black soldier fly (BSF; Hermetia illucens) is used in sustainable processing of many types of organic waste. However, organic waste being decomposed by BSF produces strong odors, hindering more widespread application. The odor components and how they are produced have yet to be characterized. We found that digestion of food waste by BSF significantly alters the microbial flora, based on metagenomic analyses, and the odor components generated, as shown by thermal desorption gas chromatography mass spectrometry analysis. Inoculation with BSF significantly decreased production of volatile organic sulfur compounds (dimethyl disulfide and dimethyl trisulfide), which are known to be released during methionine and cysteine metabolism by Lactobacillus and Enterococcus bacteria. BSF inoculation significantly changed the abundance of Lactobacillus and Enterococcus and decreased microbial diversity overall. These findings may help in optimizing use of BSF for deodorization of composting food waste.

microbiology↗

bioRxiv2021

Histidine-rich protein 2: a new pathogenic factor of Plasmodium falciparum malaria

Plasmodium falciparum causes serious malaria symptoms; when this protozoan parasite infects human erythrocytes, it produces and secretes large amounts of histidine-rich protein 2 (PfHRP2) into human blood. Thus, PfHRP2 is a well-known diagnostic marker for malaria infection. Here, however, we also identified PfHRP2 as a pathogenic factor produced by P. falciparum. PfHRP2 showed cell penetration and cytotoxicity against various human cells. In particular, PfHRP2 showed significant cytotoxicity over 5 days at the same concentration as in P. falciparum-infected patients blood (90-100 nM). This result is consistent with the mortality rate of P. falciparum malaria, which increases rapidly in untreated cases for 3-7 days. In addition, the cell penetration and cytotoxicity of PfHRP2 increased 2.5- and 2.6-fold, respectively, in the absence of serum, which suggests that low serum protein concentrations (occurring during malnutrition, for example) increase the risk of adverse effects from PfHRP2 (consistent with malnutrition increasing the lethality of malaria infection). We also showed that PfHRP2 bound to Ca2+ ions, localized to intracellular lysosomes, increased lysosomal Ca2+ levels, and inhibited the basal level of autophagy by inhibiting autolysosome formation. Furthermore, the Ca2+-dependent cytotoxicity of PfHRP2 was suppressed by the metal ion chelator ethylenediaminetetraacetic acid (EDTA). In summary, our findings suggest that PfHRP2 acts as a pathogenic factor in P. falciparum-infected patients and is associated with the exacerbation of malaria. Furthermore, EDTA is a promising candidate as a therapeutic agent for the suppression of PfHRP2 pathogenicity. Overall, this study provides new insights into P. falciparum malaria pathogenesis and treatment.

biochemistry↗