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Biology subjects

Shima, H.

Publications and source records attributed to Shima, H..

11 recordsLinked to original sources

Symmetry breaking and social coordination in children: Using group theory to understand emergent patterns of multi-agent coordination

Predicting patterns of behavioural coordination that emerge in small interacting groups is challenging because goal-directed social action is shaped by complex reciprocal and compensatory dynamics. In this study, we examined whether formal symmetry principles derived from group theory could explain coordination patterns among children performing a triadic jumping task. We investigated how geometric symmetries of the task environment and dispositional (a)symmetries associated with leader-follower tendencies jointly constrain collective behaviour. Forty-seven children were classified into symmetric or asymmetric triads based on teacher evaluations of leadership dispositions. Each triad completed multiple trials of a synchronized jumping game requiring movement between adjacent hoops arranged in triangular or square configurations. Results showed that temporal asymmetries in inter-child movement (first, second, or last to jump) were consistent with group-theoretic predictions. In triangular configurations, observed asymmetries corresponded to the highest-order subgroup defined by task and dispositional symmetries. These findings demonstrate that environmental symmetry exerts a hierarchically dominant constraint on collective coordination, within which actor dispositional (a)symmetries further modulate emerging patterns.

animal behavior and cognition↗

Spatial turnover amplifies with trophic level in hyperdiverse food webs

One of the most intuitive ideas in ecology is that diversity at lower trophic levels in food webs provides niches to support diversity at higher trophic levels. This accumulation of diversity can be limited by survival of species in the landscape, but revealing these limits has been challenging. We analyze spatial turnover in a hyperdiverse parasitoid-caterpillar-plant food web across 75,000 km2 of continuous lowland rainforest in Papua New Guinea. Species turnover across sites is higher in parasitoids than in their caterpillar hosts. Furthermore, turnover of interactions is also higher in parasitoid-caterpillar than caterpillar-plant networks. Spatial turnover thus amplifies upwards across trophic levels, forcing parasitoids to live closer to spatial persistence limits. Consequently, progressing rainforest fragmentation can especially endanger parasitoids.

ecology↗

The nuclear role of methionine adenosyltransferase 2A in immunoglobulin class switch recombination

Methionine adenosyltransferase synthesizes S-adenosylmethionine (SAM), the universal methyl donor. Its ubiquitous isozyme MAT2 is present in the nucleus and regulates gene expression through histone methylation. However, the physiological significance of its nuclear enzymatic activity remains unclear. Here, we investigate the role of nuclear MAT2 in antibody class switch recombination (CSR), a crucial process in adaptive immunity. We established murine B-cell lines expressing either wild-type (WT) or catalytically-inactive (D134A) MAT2A subunits, targeted to the nucleus with nuclear localization signal (NLS). Inhibition of nuclear MAT2 enzymatic activity by expressing NLS-MAT2A(D134A) significantly suppressed CSR from IgM to IgA and reduced intracellular SAM levels. Chromatin immunoprecipitation revealed that MAT2A localized to the IgA switch region. Interestingly, while the expression of germline transcripts was enhanced, the expression of activation-induced cytidine deaminase (AID), an essential enzyme for CSR, was downregulated in NLS-MAT2A(D134A) cells. Our findings demonstrate that the enzymatic activity of MAT2 in the nucleus is indispensable for CSR, likely by ensuring proper AID expression subsequent to germline transcription, thus revealing a critical link between nuclear SAM metabolism and adaptive immunity.

biochemistry↗

Data-Driven Feed Optimization for Sustainable Aquaculture through Integrated Omics Analysis and Two-stage Bayesian optimization

In aquaculture and livestock farming, developing feed that promotes efficient growth while minimizing environmental impact is crucial for sustainability. We developed a data-driven feed optimization system (DFOS) that integrates omics analysis with machine learning-based optimization technologies. First, DFOS employed Bayesian optimization (BO) to identify the optimal proportions of proteins and lipids, which are crucial feed components. Simultaneously, omics analysis was conducted to assess the physiological response of the targets to a given feed and identify key dietary components essential for growth. Next, BO was used to efficiently modify the combination and proportion of the specific additives identified in the first stage. We demonstrated the efficacy of DFOS by applying it to develop a new feed for the high-demand leopard coral grouper (Plectropomus leopardus) in Southeast Asia. This system provides an efficient data-driven framework for feed optimization across aquaculture and livestock, contributing significantly to more sustainable and productive farming practices.

ecology↗

Cysteine restriction induces ferroptosis depending on the polyamine biosynthetic pathway in hepatic cancer cells

Background and AimsMetabolic activities are also known to affect responses and disease processes of the liver which is a central organ for organismal metabolism. Liver diseases such as intestinal failure associated liver disease (IFALD) and hepatocellular carcinoma are known to be affected by nutrition contents, but the mechanisms behind them remain unclear. In this study, we aimed to reveal the relationship between the concentration of sulfur-containing amino acids and hepatocellular response, and further investigated the mechanism focusing on methionine adenosyltransferase (MAT), which plays the central role in methionine metabolism by synthesizing S-adenosylmethionine (SAM). MethodsMouse hepatoma Hepa1 cells were cultured in media with reduced amounts of cysteine, methionine, or both. Cell death was monitored using propidium iodide (PI) and annexin V staining followed by flow cytometry. Inhibitors of ferroptosis (Fer-1), autophagy (GSK872), SAM synthesis (cycloleucine), or polyamine synthesis (sardomozide and DFMO) were used. ResultsCysteine restriction induced marked cell death, whereas simultaneous restriction of cysteine and methionine fully suppressed the cell death. Cysteine restriction-induced cell death was suppressed with Fer-1 and GSK872, suggesting the involvement of ferroptosis in this process. Cysteine restriction-induced cell death was also suppressed by knockdown of MAT2A or its inhibitor cycloleucine. Furthermore, inhibitors of several enzymes in the polyamine biosynthetic pathway also suppressed the cell death. In contrast, primary culture of mouse hepatocytes did not show cell death upon cysteine restriction. ConclusionsThese results suggest that SAM-polyamine metabolism is a critical modulator of ferroptosis of hepatic cancer cells. Since normal liver cells were more resistant to ferroptosis than cancer cells, cysteine restriction may be exploited in treating hepatic cancer by inducing ferroptosis specifically in cancer cells without affecting normal cells in the liver. Graphical abstrct O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=61 SRC="FIGDIR/small/582667v1_ufig1.gif" ALT="Figure 1"> View larger version (13K): org.highwire.dtl.DTLVardef@bcb32borg.highwire.dtl.DTLVardef@96d39corg.highwire.dtl.DTLVardef@1eaa25org.highwire.dtl.DTLVardef@1346f82_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

TANK binding kinase 1 promotes BACH1 degradation through both phosphorylation-dependent and -independent mechanisms without relying on heme and FBXO22

BTB and CNC homology 1 (BACH1) represses the expression of genes involved in the metabolism of iron, heme and reactive oxygen species. While BACH1 is rapidly degraded when it is bound to heme, it remains unclear how BACH1 degradation is regulated under other conditions. We found that FBXO22, a ubiquitin ligase previously reported to promote BACH1 degradation, polyubiquitinated BACH1 only in the presence of heme in a highly purified reconstitution assay. In parallel to this regulatory mechanism, TANK binding kinase 1 (TBK1), a protein kinase that activates innate immune response and regulates iron metabolism via ferritinophagy, was found to promote BACH1 degradation when overexpressed in 293T cells. While TBK1 phosphorylated BACH1 at multiple serine and threonine residues, BACH1 degradation was observed with not only the wild-type TBK1 but also catalytically impaired TBK1. The BACH1 degradation in response to catalytically impaired TBK1 was not dependent on FBXO22 but involved both autophagy-lysosome and ubiquitin-proteasome pathways judging from its suppression by using inhibitors of lysosome and proteasome. Chemical inhibition of TBK1 in hepatoma Hepa1 cells showed that TBK1 was not required for the heme-induced BACH1 degradation. Its inhibition in Namalwa B lymphoma cells increased endogenous BACH1 protein. These results suggest that TBK1 promotes BACH1 degradation in parallel to the FBXO22- and heme-dependent pathway, placing BACH1 as a downstream effector of TBK1 in iron metabolism or innate immune response.

biochemistry↗

How to control unpredictable others in court-net sports

Competition in sports does not involve a single solution because individuals aim to behave unpredictably, thereby preventing others from predicting their actions. This study determined how individuals in court net sports tried to control others unpredictable behavior, thereby addressing the gap of the lack of clarity about strategies employed by individuals in competitive situations. We employed a switching hybrid dynamics model, considering external inputs when analyzing individual behaviors. The study shows that skilled individuals, unlike intermediate players, exhibit greater regularity in their behavior, lead others to anticipate this regularity, and employ strategies to disrupt these expectations. This strategy exploits the principles of active human inference, implying that competition involves cooperation. We revealed this by analyzing both human decision-making and behavior in actual matches as discrete and continuous dynamical systems. This strategy helps policymakers adopt a new policy targeting cooperation with competitors, which would increase competitiveness in our daily lives.

biophysics↗

Relationship Between Domain and Function of the Yeast RNase T2, Rny1p, Which Mediates rRNA Degradation upon Starvation

RNase T2 is ubiquitous across diverse organisms, playing essential roles despite its simple enzymatic activity. In Saccharomyces cerevisiae, RNase T2, known as Rny1p, localizes in vacuoles and mediates rRNA degradation during autophagy of ribosomes. In this study, we elucidated novel aspects of ribosome degradation mechanisms and the function of Rny1p. First, we discovered that most ribosomes are degraded by selective autophagy, where Rsa1p is the specific receptor of ribosomes to be degraded. Complex structure prediction suggested that Rsa1p also interacts with Atg8p. Furthermore, we observed that the accumulation of rRNA in vacuoles, due to the lack of Rny1p, leads to a decrease in bulk autophagic activity. This decrease in autophagic activity may explain the inability of Rny1p-deficient strains to adapt to starvation conditions. Second, our structural prediction and biochemical analyses indicate that a C-terminal extension, characteristic in fungal RNase T2 including Rny1p, is not necessary for rRNA degradation but for anchoring to the cell wall. Together with molecular phylogenetic analysis, a species-specific role of RNase T2 conferred by the C-terminal extension is suggested.

molecular biology↗

Distinctive nuclear zone for RAD51-mediated homologous recombinational DNA repair

Genome-based functions are inseparable from the dynamic higher-order architecture of the cell nucleus. In this context, the repair of DNA damage is coordinated by precise spatiotemporal controls that target and regulate the repair machinery required to maintain genome integrity. However, the mechanisms that pair damaged DNA with intact template for repair by homologous recombination (HR) without illegitimate recombination remain unclear. This report highlights the intimate relationship between nuclear architecture and HR in mammalian cells. RAD51, the key recombinase of HR, forms spherical foci in S/G2 phases spontaneously. Using super-resolution microscopy, we show that following induction of DNA double-strand breaks RAD51 foci at damaged sites elongate to bridge between intact and damaged sister chromatids; this assembly occurs within bundle-shaped distinctive nuclear zones, requires interactions of RAD51 with various factors, and precedes ATP-dependent events involved the recombination of intact and damaged DNA. We observed a time-dependent transfer of single-stranded DNA overhangs, generated during HR, into such zones. Our observations suggest that RAD51-mediated homologous pairing during HR takes place within the distinctive nuclear zones to execute appropriate recombination.

cell biology↗

The haploinsufficient tumor suppressor Tip60 negatively regulates the oncogenic Aurora B kinase

The Aurora kinases represent a group of serine/threonine kinases which are crucial regulators of mitosis. Dysregulated Aurora kinase B (AurkB) expression, stemming from genomic amplification, increased gene transcription or overexpression of its allosteric activators, is capable of initiating and sustaining malignant phenotypes. Although AurkB level in cells is well-orchestrated, studies that relate to its stability or activity, independent of mitosis, are lacking. We report that AurkB undergoes acetylation in vitro by lysine acetyltransferases (KATs) belonging to different families, namely by p300 and Tip60. The haploinsufficient tumor suppressor Tip60 acetylates two highly conserved lysine residues within the kinase domain of AurkB which not only impinges the protein stability but also its kinase activity. These results signify a probable outcome on the increase in \"overall activity\" of AurkB upon Tip60 downregulation, as observed under cancerous conditions. The present work, therefore, uncovers an important functional interplay between AurkB and Tip60, frailty of which may be an initial event in carcinogenesis.

biochemistry↗

Aurora kinase A mediated phosphorylation of mPOU is critical for skeletal muscle differentiation

Aurora kinases are Ser/Thr-directed protein kinases which play pivotal roles in mitosis. Recent evidences highlight the importance of these kinases in non-mitotic biological events like skeletal myogenesis. Our earlier study identified POU6F1 (or mPOU) as a novel Aurora kinase A (AurkA) substrate. Here, we report that AurkA phosphorylates POU6F1 at Ser197 and inhibits its DNA binding ability. Delving into POU6F1 physiology, we find that the phospho-mimic (S197D) POU6F1 mutant exhibits enhancement, while wild type (WT) or phospho-deficient (S197A) mutant shows retardation in C2C12 myoblast differentiation. Interestingly, POU6F1 depletion phenocopies S197D-POU6F1 overexpression in the differentiation context. Collectively, our results signify mPOU as a negative regulator of skeletal muscle differentiation and strengthens the importance of AurkA in skeletal myogenesis.

cell biology↗