Biology subjects

Oshima, Y.

Publications and source records attributed to Oshima, Y..

11 recordsLinked to original sources

bioRxiv2026

Photosynthesis-derived carbohydrate supply sustains CuCl2-induced phytoalexin production in rice leaves

Phytoalexins are antimicrobial metabolites whose biosynthesis is triggered by signaling activated by both biotic and abiotic elicitors, but the physiological conditions that sustain their production remain poorly understood. Here, we examined how light and carbohydrate availability affect CuCl2-induced production of diterpenoid (phytocassanes and momilactones) and flavonoid (sakuranetin) phytoalexins in rice (Oryza sativa L.) leaf disks. Darkness strongly suppressed both the accumulation of all three phytoalexin groups and the induction of their biosynthetic genes. In darkness, endogenous sucrose, glucose, and fructose declined to 3%-8% of the levels in the light, whereas early accumulation of jasmonic acid and jasmonoyl-L-isoleucine (JA-Ile) was not detectably reduced. Exogenous sucrose restored phytoalexin accumulation in darkness in a dose-dependent manner, together with the expression of the suppressed biosynthetic genes, whereas equimolar mannitol had no effect. Glucose also restored sakuranetin accumulation in darkness but only partially restored diterpenoid accumulation, whereas the glucose analog 2-deoxy-D-glucose did not, and it suppressed CuCl2-induced accumulation in the light in a dose-dependent manner. In the light, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), an inhibitor of photosynthetic electron transport, depleted soluble sugars and suppressed phytoalexin accumulation, and sucrose reversed this suppression. Sugars alone induced little phytoalexin accumulation, indicating that carbohydrates act permissively rather than as elicitors. Diterpenoid phytoalexins depended more strongly on light than sakuranetin, yet both classes depended on carbohydrate availability. These results indicate that photosynthesis-derived carbohydrate supply sustains elicitor-induced phytoalexin production in rice leaves and largely accounts for its light dependence.

plant biology↗

bioRxiv2026

Differential associations of insulin resistance with anterior hippocampal volume in mild cognitive impairment and Alzheimer's disease

Insulin resistance is increasingly recognized as a metabolic factor associated with Alzheimers disease (AD); however, its relevance to hippocampal structural changes--a key pathological feature of AD--across disease stages is not fully understood. To address this issue, we investigated the relationship between insulin resistance, hippocampal gray matter volume, and cognitive performance using data from the Alzheimers Disease Neuroimaging Initiative (ADNI), a large-scale neuroimaging dataset. Insulin resistance was assessed using the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), and its relationship with brain structure and cognitive performance was evaluated across diagnostic groups. In the mild cognitive impairment (MCI) group, higher insulin resistance was associated with larger anterior hippocampal gray matter volume, whereas in the AD group this association was reversed in direction. Furthermore, in the MCI group, anterior hippocampal gray matter volume was also positively associated with higher Mini-Mental State Examination (MMSE) scores, and an exploratory mediation analysis suggested a significant indirect association linking HOMA-IR, anterior hippocampal volume, and cognitive performance through anterior hippocampal volume. These findings suggest that the relationship between insulin resistance and AD-related brain changes differs across diagnostic groups, highlighting the importance of considering metabolic alterations in relation to disease status.

neuroscience↗

bioRxiv2026

Changes in dysbiosis and gene expression in the gut of wharf roach (Ligia Spp.) fed with expanded polystyrene

The East Asian region, known for its high levels of human and fishery activities, experiences serious plastic pollution in the marine environment, especially in seawater and along coastlines. Wharf roaches (Ligia spp.) collected from the coast of western Japan frequently ingest expanded polystyrene (EPS), which is then excreted as microplastic through their feces. However, the impact of EPS exposure and ingestion on the gut microbiome of wharf roaches remains unclear. Thus, this study aimed to investigate the effects of EPS ingestion on the gut microbiota of wharf roaches by examining their gut microbiota and gene expression. The expression levels of more than 400 genes, including those associated with xenobiotic metabolism, and the abundance of gut microbial community were altered. Microbial analysis revealed that at least five archaeal types, two to four bacterial types, three to seven eukaryotic types, and three viral types were involved in a correlation network composed of strong associations. Among them, Haloquadratum, Halalkalicoccus, and Methanospirillum (archaea); Volvox (eukaryote); and Varicellovirus and T4-like viruses showed significantly increased abundance. Furthermore, covariance structure analysis indicated that the viruses and methanogens played key causal roles as characteristic factors related to EPS administration. In conclusion, EPS disrupts the intestinal environment of wharf roaches and serves as a potential material for viral activation and methane production. Building on our previous field study that identified wharf roaches as potential indicators of coastal EPS pollution, this study provides novel insights into the ecological impacts of EPS ingestion and consequences of plastic pollution.

pharmacology and toxicology↗

bioRxiv2025

TEP-1, a glial thioester protein is required for cilia organization and intraflagellar transport in ensheathed sensory neurons

Age-related macular degeneration (AMD), the leading cause of blindness in the elderly, is characterized by progressive degeneration of retinal photoreceptors. Traditional disease models suggest that defective repression of thioester protein C3 activity by complement factor H (CFH) is a major contributor to pathogenesis in AMD and a related disease, early-onset drusen maculopathy (EODM). Our previous study identified novel functions for human CFH and C. elegans CFH-1 in the maintenance of inversin compartment integrity in photoreceptors and mechanosensory neurons, indicating that CFH has a novel, evolutionarily conserved role in cilia compartment organization that is distinct from its established function in alternative complement pathway regulation. Here, we investigate the C. elegans thioester protein TEP-1, an ancestral relative of C3 and other members of the AMCOM family (C4, C5, CD109, and alpha-2-macroglobulin). TEP-1 localizes to select glial cell surfaces and regulates inversin compartment organization and intraflagellar transport (IFT) within the cilia of ensheathed sensory neurons. In addition to revealing a novel role for an AMCOM family member in sensory neuron structure and protein transport, the localization of C3 and CFH on human photoreceptors provides support for non-canonical models of AMD and EODM pathogenesis in which defects in cilia structure and protein transport contribute directly to the progressive photoreceptor dysfunction that characterizes these diseases.

cell biology↗

bioRxiv2025

Complement Factor H and its C. elegans homolog regulate IFT52/OSM-6 and CNG channel localization in sensory neurons

Age-related macular degeneration (AMD), the leading cause of blindness in the elderly, is characterized by progressive degeneration of retinal photoreceptors. Current disease models propose AMD pathogenesis is a consequence of cytolytic damage and tissue inflammation that result from defective repression of alternative complement pathway activity by complement factor H (CFH). However, recent studies demonstrate functions for CFH that are outside of its established role in the alternative complement pathway, suggesting that novel CFH-mediated mechanisms may influence AMD initiation and progression. Our previous demonstration that CFH and its nematode homolog, CFH-1, modulate inversin/NPHP-2 accumulation in vertebrate photoreceptor and C. elegans sensory neuron cilia during aging suggests that AMD patients with CFH loss-of-function mutations have cilia defects that may contribute to photoreceptor dysfunction. Here, we investigate the consequences of CFH and CFH-1 loss-of-function mutations on the dynamics and localization of intraflagellar transport (IFT) train and visual cycle components in these cells. In C. elegans sensory neurons, IFTB1 components IFT52/OSM-6 and IFT88/OSM-5 are transported at similar rates in WT animals but IFT52/OSM-6 transport slows significantly in cfh-1 mutant animals while IFT88/OSM-5 is unaffected. Defective localization of IFT52/OSM-6 in photoreceptors of CFH knockout mice and in human photoreceptors from AMD high-risk CFH Y402H homozygotes, suggest an evolutionarily conserved role for CFH in promoting IFT52/OSM-6 transport and localization in sensory neuron cilia. In addition, distribution of CNG channel subunits in C. elegans cfh-1 mutant sensory neurons and CFH Y402H high-risk human photoreceptors are distinct from their WT and Y402 low-risk counterparts. Together, the data indicate previously unappreciated functions for CFH in IFT train organization and cilia protein localization and suggest a novel mechanism for photoreceptor segment thinning, an early AMD biomarker that has been linked to CFH high-risk variants.

cell biology↗

bioRxiv2024

LATE MERISTEM IDENTITY2 regulates cuticle formation on the seed surface and influences seed longevity

The seed coat protects the embryo from severe external environment. Like the aerial plant parts, the exterior surface of the seed coat is surrounded by a cuticle consisting of lipid polyesters and wax. However, the protective role of the cuticle in mature seeds has not been characterized. We herein study the transcriptional regulation of cuticle formation on the seed surface, which influences seed longevity. A chimeric repressor of Arabidopsis thaliana R2R3 MYB transcription factor gene LATE MERISTEM IDENTITY2 (LMI2) and a Torenia fournieri ortholog (TfMYBML3) was expressed in A. thaliana and T. fournieri, respectively. These lines and A. thaliana LMI2 T-DNA insertion lines were analyzed for cuticle deficiencies. A. thaliana LMI2 mutants and chimeric repressor lines exhibited a similar cuticle deficiency in immature seeds. Transmission electron microscopy observations, polyester composition analyses, and gene expression investigations revealed that LMI2 plays an essential role in cuticle development in the seed coat epidermis by regulating cutin biosynthesis. The lmi2-2 mutant exhibited shorter seed longevity than the wild-type controls in an accelerated aging test. These results indicate that LMI2 is a key regulator of cuticle formation in the seed coat, and is important for maintaining seed longevity. Significance statementCuticle is well known to have multiple important roles for surviving in the terrestrial environment, but their specific role on the seed coat and transcriptional regulation have not yet been elucidated. Here we show that LATE MERISTEM IDENTITY 2, encoding a transcription factor regulating floral meristem transition, is required for seed cuticle formation and maintaining seed longevity, providing evidence for a link between surface cuticle and seed longevity.

plant biology↗

bioRxiv2023

Outer mitochondrial membrane E3 Ub ligase MARCH5 controls mitochondrial steps in peroxisome biogenesis.

Peroxisome de novo biogenesis requires yet unidentified mitochondrial proteins. We report that the outer mitochondrial membrane (OMM)-associated E3 Ub ligase MARCH5 is vital for generating mitochondria-derived pre-peroxisomes. MARCH5 knockout results in accumulation of immature peroxisomes and lower expression of various peroxisomal proteins. Upon fatty acid-induced peroxisomal biogenesis, MARCH5 redistributes to newly formed peroxisomes; the peroxisomal biogenesis under these conditions is inhibited in MARCH5 knockout cells. MARCH5 activity-deficient mutants are stalled on peroxisomes and induce accumulation of peroxisomes containing high levels of the OMM protein Tom20 (mitochondria-derived pre-peroxisomes). Furthermore, depletion of peroxisome biogenesis factor Pex14 leads to the formation of MARCH5- and Tom20-positive peroxisomes, while no peroxisomes are detected in Pex14/MARCH5 dko cells. Reexpression of WT, but not MARCH5 mutants, restores Tom20-positive pre-peroxisomes in Pex14/MARCH5 dko cells. Thus, MARCH5 acts upstream of Pex14 in mitochondrial steps of peroxisome biogenesis. Our data validate the hybrid, mitochondria-dependent model of peroxisome biogenesis and reveal that MARCH5 is an essential mitochondrial protein in this process. SummaryThe authors found that mitochondrial E3 Ub ligase MARCH5 controls the formation of mitochondria-derived pre-peroxisomes. The data support the hybrid, mitochondria-dependent model of peroxisome biogenesis and reveal that MARCH5 is an essential mitochondrial protein in this process.

cell biology↗

bioRxiv2023

Diurnal variation of brain activity in the human suprachiasmatic nucleus

The suprachiasmatic nucleus (SCN) is the central clock for circadian rhythms. Animal studies have revealed daily rhythms in the neuronal activity in the SCN. However, the circadian activity of the human SCN has remained elusive. In this study, to reveal the diurnal variation of the SCN activity in humans, the SCN was localized, and its activity was investigated using perfusion imaging. We scanned each participant four times a day, every six hours, and higher activity was observed at noon while lower activity was recorded in the early morning. The SCN activity was then measured every thirty minutes for six hours from midnight to dawn and showed a decreasing trend and was comparable with the rodent SCN activity after switching off the lights. These results suggest that the diurnal variation of the human SCN follows the zeitgeber cycles of mammals and is modulated by physical lights rather than the local time.

neuroscience↗

bioRxiv2023

Nutrient-regulated dynamics of chondroprogenitors in the postnatal murine growth plate

Longitudinal bone growth relies on endochondral ossification in the cartilaginous growth plate where chondrocytes accumulate and synthesize the matrix scaffold that is replaced by bone. The chondroprogenitors in the resting zone maintain the continuous turnover of chondrocytes in the growth plate. Malnutrition is a leading cause of growth retardation in children; however, after recovery from nutrient deprivation, bone growth is accelerated beyond the normal rate, a phenomenon termed catch-up growth. Though nutritional status is a known regulator of long bone growth, it is largely unknown if and how chondroprogenitor cells respond to deviations in nutrient availability. Here, using fate-mapping analysis in Axin2CreERT2 mice, we showed that dietary restriction increased the number of Axin2+ chondroprogenitors in the resting zone and simultaneously inhibited their differentiation. Once nutrient deficiency was resolved, the accumulated chondroprogenitor cells immediately restarted differentiation and formed chondrocyte columns, contributing to accelerated growth. Furthermore, we showed that nutrient deprivation reduced the level of phosphorylated Akt in the resting zone, and that exogenous IGF-1 canceled this reduction and stimulated differentiation of the pooled chondroprogenitors, decreasing their numbers. Our study of Axin2CreERT2 revealed that nutrient availability regulates the balance between accumulation and differentiation of chondroprogenitors in the growth plate, and further demonstrated that IGF-1 partially mediates this regulation by promoting the committed differentiation of the chondroprogenitor cells.

developmental biology↗

bioRxiv2021

Liver ductal organoids reconstruct intrahepatic biliary trees in decellularized liver grafts.

Three-dimensional scaffolds decellularized from native organs are a promising technique to establish engineered liver grafts and overcome the current shortage of donor organs. However, limited sources of bile duct cells and inappropriate cell distribution in bioengineered liver grafts have hindered their practical application. Organoid technology is anticipated to be an excellent tool for the advancement of regenerative medicine. In the present study, we reconstructed intrahepatic bile ducts in a rat decellularized liver graft by recellularization with liver ductal organoids. Using an ex vivo perfusion culture system, we demonstrated the biliary characteristics of repopulated mouse liver organoids, which maintained bile duct markers and reconstructed biliary tree-like networks with luminal structures. We also established a method for the co-recellularization with engineered bile ducts and primary hepatocytes, revealing the appropriate cell distribution to mimic the native liver. We then utilized this model in human organoids to demonstrate the reconstructed bile ducts. Our results show that liver ductal organoids are a potential cell source for bile ducts from bioengineered liver grafts using three-dimensional scaffolds.

bioengineering↗

bioRxiv2020

Production of a tributyltin-binding protein 2 knockout mutant strain of Japanese medaka, Oryzias latipes

Tributyltin-binding proteins (TBT-bps), members of the lipocalin family, bind TBT in fish blood and are presumed to contribute to detoxification of TBT. Recent studies have shown that many fish species have TBT-bp genes, and that these genes are induced by stresses such as exposure to chemicals or fish pathogenic bacteria. However, the function of TBT-bps, and the mechanisms of their induction and detoxification activity are still unclear. Here, towards elucidating the functions of TBT-bp2, we produced a TBT-bp2 knockout (TBT-bp2-/-) strain of Japanese medaka, Oryzias latipes, by using the CRISPR/Cas9 system. Gene expression of the mutated TBT-bp2 was reduced, and the cDNA sequencing and predicted protein structure suggested possible loss of function. However, the fish could be grown under normal conditions. Exposure of the TBT-bp2-/- strain of medaka to various stresses in future experiments is expected to contribute to our understanding of this novel detoxification system in aquatic organisms.

pharmacology and toxicology↗