Biology subjects

Aida, M.

Publications and source records attributed to Aida, M..

4 recordsLinked to original sources

bioRxiv2026

Photosynthesis-derived carbon gates cell cycle activation to enable hormone-autonomous shoot regeneration

Shoot regeneration is a powerful model for cell fate reprogramming but how it occurs in nature remains poorly understood because studies in Arabidopsis thaliana conventionally rely on in vitro assays supplemented with exogenous hormones and sugars. In this study, we established the Hormone-autonomY Direct Regeneration Assay (HYDRA) in which removal of the shoot apical meristem (SAM) initiates shoot regeneration from the cotyledon-hypocotyl boundary domain without hormone or sugar supplementation. We show that photosynthesis-derived carbon and the boundary domain are two separable but convergent requirements for shoot regeneration in HYDRA. Carbon availability increases in the boundary domain where it activates cell cycle progression via the RETINOBLASTOMA-RELATED1 (RBR1) pathway. Carbon deprivation blocks regeneration despite induction of SAM marker genes, indicating that carbon-dependent cell cycle activation is a limiting factor for regeneration. In parallel, perturbation of the boundary domain or its regulators reduces regeneration despite sufficient carbon, indicating that boundary domain identity is independently required. Additionally, exogenous carbon supply overcomes the requirement for SAM removal to induce shoot formation, indicating that carbon availability also acts as an initiation cue. Together, this study reveals an inherent capacity for hormone-autonomous shoot regeneration and identifies photosynthesis-derived carbon as a central regulator of this process.

Plant Biology↗

bioRxiv2023

Immunostimulatory effects of Bacillus coagulans SANK70258

Specific intestinal bacteria modulate immunoresponses through various pathways, and several probiotic bacteria have been identified as immunostimulants by screening. In the present study, we evaluated the immunomodulating effects of Bacillus coagulans SANK70258 (B. coagulans SANK70258), a spore-forming and lactic acid-producing bacterium usable as food supplement for human and animals. We found that treatment of mouse splenocytes with {gamma}-ray irradiated B. coagulans SANK70258 induced high amount of IFN-{gamma} in comparison with 7 kinds of typical lactic acid bacteria. Further analyses using splenocytes revealed that NK cell is a major source of IFN-{gamma}, and B. coagulans SANK70258-induced IFN-{gamma} production was inhibited by neutralization of IL-12 or IL-23, depletion of CD11c+ cells, and inhibition of NF{kappa}B. B. coagulans SANK70258 also induced release of IFN-{gamma} from activated CD8+ T cells, and increased expression of chemokine receptors in CD8+ T cells. B. coagulans SANK70258-treatment induced production of cytokines from bone marrow-derived dendritic cells, which is reduced by knockdown of Tlr2 and Nod2. B. coagulans SANK70258-treatment also induced IgA production from Peyers patch cells with high level among tested lactic bacteria. The oral intake of {gamma}-ray irradiated B. coagulans SANK70258 significantly increased intestinal IgA levels and IgA-expressing B cells in the Peyers patch of mice. Taken together, we conclude that B. coagulans SANK70258 possesses high activity as immunostimulant inducing production of IFN-{gamma} and IgA.

immunology↗

bioRxiv2021

Reversible brain edema in experimental cerebral malaria is associated with transcellular blood-brain barrier disruption and delayed microhemorrhages

Brain swelling occurs in cerebral malaria (CM) and may either reverse or result in fatal outcome. It is currently unknown how brain swelling in CM reverses, as investigations have been hampered by inadequate animal models. In this study, we show that reversible brain swelling in experimental murine cerebral malaria (ECM) can be induced reliably after single vaccination with radiation-attenuated sporozoites as revealed by in vivo high-field (9.4T) magnetic resonance imaging. Our results provide evidence that parenchymal fluid increase and consecutive brain swelling results from transcellular blood-brain barrier disruption (BBBD), as revealed by electron microscopy. This mechanism enables reversal of brain swelling but does not prevent persistent focal brain damage, evidenced by microhemorrhages, in areas of most severe BBBD. In a cohort of 27 pediatric and adult CM patients (n=4 fatal, n=23 non-fatal) two out of four fatal CM patients (50%) and 8 out of 23 non-fatal CM patients (35%) showed microhemorrhages on MRI at clinical field strength of 1.5T, emphasizing the translational potential of the experimental model. Our data suggest that targeting transcellular BBBD may represent a promising adjunct therapeutic approach in cerebral brain swelling to reduce edema and may ultimately lead to a reduced permanent brain damage and a better longtime neurological outcome. Author summaryBrain swelling, which occurs in diseases such as cerebral malaria, is not necessarily fatal, and may reverse. Even upon reversal of brain swelling, neurological sequelae can still occur. The factors contributing to the reversibility of brain edema are not known, and treatment options remain therefore limited. Identifying the mechanisms leading to such reversibility could inform clinical management aimed at decreasing brain swelling and consecutive brain injury. Here we introduce a reproducible and simple animal model that allows comprehensive in vivo studies of reversible brain swelling in cerebral malaria at the peak of disease and upon recovery. We identify a specific type of blood-brain barrier disruption (BBBD) as a mechanism that occurs in brain swelling. We show that BBBD can reverse, but also highlight remaining brain damage in areas of most severe BBBD. As the ECM model introduced here bares crucial similarities to the CM in humans, our findings open strategies to study new therapeutic avenues and point to compounds that specifically target transcellular BBBD to reduce brain edema, and increase survival rates.

neuroscience↗

bioRxiv2021

The Boundary-Expressed EPIDERMAL PATTERNING FACTOR-LIKE2 Gene Encoding a Signaling Peptide Promotes Cotyledon Growth during Arabidopsis thaliana Embryogenesis

The shoot organ boundaries have important roles in plant growth and morphogenesis. It has been reported that a gene encoding a cysteine-rich secreted peptide of the EPIDERMAL PATTERNING FACTOR-LIKE (EPFL) family, EPFL2, is expressed in the boundary domain between the two cotyledon primordia of Arabidopsis thaliana embryo. However, its developmental functions remain unknown. This study aimed to analyze the role of EPFL2 during embryogenesis. We found that cotyledon growth was reduced in its loss-of-function mutants, and this phenotype was associated with the reduction of auxin response peaks at the tips of the primordia. The reduced cotyledon size of the mutant embryo recovered in germinating seedlings, indicating the presence of a factor that acted redundantly with EPFL2 to promote cotyledon growth in late embryogenesis. Our analysis indicates that the boundary domain between the cotyledon primordia acts as a signaling center that organizes auxin response peaks and promotes cotyledon growth.

plant biology↗