Biology subjects

Nagashima, S.

Publications and source records attributed to Nagashima, S..

3 recordsLinked to original sources

bioRxiv2024

A Nonsecretory Antimicrobial Peptide Mediates Inflammatory Organ Damage in Drosophila Renal Tubules

An excessive immune response damages organs, yet its molecular mechanism is incompletely understood. In this study, we used Drosophila renal tubules as a model to screen a factor mediating organ damage upon genetic activation of an innate immune Imd signalling pathway. We identified an antimicrobial peptide, Attacin-D (AttD), which causes organ damage upon Imd activation in the Malpighian tubules. Loss of AttD function suppresses most of the pathological phenotypes induced by Imd activation, such as cell death, compensatory stem cell proliferation, bloating of whole animal, susceptibility to a high salt diet, elevation of purine levels, and mortality, without compromising the immune activation. AttD is required for the immune-induced damage specifically in the Malpighian tubules but not the midgut. Interestingly, AttD uniquely lacks the signal peptide and is not secreted out from cells. Suppression of AttD almost completely attenuates mortality induced by gut tumour-induced immune activation. Our study elucidates the mechanistic effector of immune-induced organ damage.

immunology↗

bioRxiv2023

Role of Immature Choroid Plexus in the Pathology of Autism Spectrum Disorder

During gestation, the choroid plexus (ChP) produces protein-rich cerebrospinal fluid and matures prior to brain development. It is assumed that ChP dysfunction has a profound effect on developmental neuropsychiatric disorders, such as Autism Spectrum Disorder (ASD). However, the mechanisms linking immature ChP to the onset of ASD remain unclear. In this study, we found that ChP-specific CAMDI-knockout mice developed an immature ChP, alongside decreased multiciliogenesis and expression of differentiation marker genes following disruption of the cerebrospinal fluid barrier. These mice exhibited ASD-like behaviors, including impaired socialization with delayed critical period. Additionally, administration of Metformin, an FDA-approved drug, before the critical period achieved ChP maturation and restored social behaviors. Furthermore, ASD model mice and ASD patient-derived organoids developed immature ChP. These results indicate towards involvement of immature ChP in the pathogenesis of ASD and suggest the targeting of functional maturation of ChP as a therapeutic strategy for ASD.

neuroscience↗

bioRxiv2020

Anoxygenic phototrophic Chloroflexota member uses a Type I reaction center

Scientific exploration of phototrophic bacteria over nearly 200 years has revealed large phylogenetic gaps between known phototrophic groups that limit understanding of how phototrophy evolved and diversified. Through Boreal Shield lake water incubations, we cultivated an anoxygenic phototrophic bacterium from a previously unknown order within the Chloroflexota phylum that represents a highly novel transition form in the evolution of photosynthesis. Unlike all other known phototrophs, this bacterium uses a Type I reaction center (RCI) for light energy conversion yet belongs to the same bacterial phylum as organisms that use a Type II reaction center (RCII) for phototrophy. Using physiological, phylogenomic, and environmental metatranscriptomic data, we demonstrate active RCI-utilizing metabolism by the strain alongside usage of chlorosomes and bacteriochlorophylls related to those of RCII-utilizing Chloroflexota members. Despite using different reaction centers, our phylogenomic data provide strong evidence that RCI- and RCII-utilizing Chloroflexia members inherited phototrophy from a most recent common phototrophic ancestor that used RCI, RCII, or both reaction center classes, substantially revising our view of the diversity and evolution of phototrophic life. The Chloroflexota phylum preserves an evolutionary record of interaction between RCI and RCII among anoxygenic phototrophs that gives new context for exploring the origins of phototrophy on Earth.

microbiology↗