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Biology subjects

Otomo, K.

Publications and source records attributed to Otomo, K..

7 recordsLinked to original sources

A Data-Driven Correction Framework for Axial- and Radial-Position-Dependent Intensity Attenuation in Volumetric Fluorescence Microscopy

Accurate quantification of fluorescence signals in three-dimensional (3D) microscopy is often hindered by axial- and radial-position-dependent attenuation, limiting reliable measurements in live biological specimens. Here, we present a data-driven statistical correction model that compensates for signal loss arising from axial- and radial-position in 3D time-lapse imaging of Caenorhabditis elegans embryos. Our framework incorporates axial position (imaging depth, z), radial position (distance from the center of the field of view, r), together with cell cycle progression, to recover cell-specific fluorescence intensities independent of axial- and radial-positions. By leveraging repeated observations of biologically comparable states, the model infers attenuation directly from the data without requiring external calibration. Notably, the sign of the inferred radial-position-dependence in biological specimens was opposite to that observed in homogeneous fluorescent reference samples, underscoring the value of specimen-specific, data-driven correction. Validation using histone-tagged fluorescent proteins demonstrated that the method effectively removes geometric bias in nuclear fluorescence signals, enabling consistent quantification across cells and embryos. This approach provides a robust and generalizable solution for correcting intensity attenuation in volumetric microscopy datasets, thereby enabling more accurate and reproducible quantitative analyses in live imaging studies. Author summaryModern microscopy lets us watch living cells and embryos in three dimensions, but measuring brightness accurately is harder than it seems. Signals often become weaker not only when molecules are less abundant, but also when they lie deeper in the specimen or farther from the center of the image. This makes it difficult to tell whether differences in brightness reflect biology or simply the position of a cell within the microscope field. Existing correction methods typically rely on separately acquired reference measurement samples or on image-level statistical patterns. In this study, we took a different approach. Using the highly reproducible development of nematode (C. elegans) embryos, we compared cells that should be biologically equivalent across multiple embryos and used those repeated observations to estimate imaging bias directly from the biological images themselves. Our method corrects for both axial-dependent and radial attenuation simultaneously within a unified statistical framework, requiring no such reference data. Beyond simply improving consistency, we uncovered an unexpected result: the radial bias inferred from real embryos was opposite in sign to what calibration samples would predict. This underscores the need for specimen-specific, data-driven correction. Our framework should help make live imaging more quantitatively accurate for studying dynamic biological processes in complex three-dimensional specimens.

cell biology↗

In vivo deep-brain microscopy at submicrometer resolution with refractive index-matched prism interfaces

The mammalian brain is a thick and densely layered structure comprising a huge number of neurons that work together to process information and regulate brain functions. Although various optical methods have been developed to investigate deep brain dynamics, they are limited by technical constraints, invasiveness, suboptimal spatial resolution, and/or a restricted field of view. To overcome these limitations, we developed an implantable, optically optimized microprism interface with a refractive index matched to that of brain tissue and water, enabling minimally-invasive, wide-field two-photon imaging method with enhanced brightness and sub-micron resolution in deep prefrontal areas.

neuroscience↗

Cellular Responses to Photothermal Therapy: Heat-Induced ERK Signaling and Intercellular Communication in Solid Tumors

Nanoparticle-mediated photothermal therapy (PTT) shows promise as a standalone cancer treatment but faces clinical challenges due to inconsistent efficacy. Its translation is further hindered by a limited understanding of plasmon-induced heat effects, such as stress responses and intercellular signaling. Here, we investigate how plasmon-induced local heating affects cellular behavior and fate within tumor spheroids by focusing on the activity of the extracellular signal-regulated kinase (ERK). Spheroids were prepared from HeLa cells that express a FRET-based ERK sensor, and ERK activity changes under photothermal stimuli were tracked using a deep-learning program, 3DeeCellTracker. Gold nanostars were used as highly efficient photothermal transducers. Our results revealed significant alterations in ERK signaling patterns upon photothermal stimulation compared to spontaneous ERK activity in untreated spheroids, including changes in the activation frequency, timing, and duration. Notably, photothermal-induced ERK activity propagated across neighboring cells within the spheroid, suggesting intercellular communication. Furthermore, analysis of cell death and division further demonstrated that laser power modulates cellular fate during photothermal therapy. This study provides insights for predicting the therapeutic effects of PPT and guides the rational design of next-generation photothermal strategies. Additionally, our approach demonstrates the potential of FRET-based biosensors and deep-learning tools as powerful methods to study the effects of various therapeutic stimuli on solid tumors at the single-cell level.

cancer biology↗

Amyloid-β-induced Alteration of Fast and Localized Calcium Elevations in Cultured Astrocytes

Alzheimers disease (AD) is a progressive neurodegenerative disorder that causes cognitive decline. Uncovering the mechanisms of neurodegeneration in the early stages is essential to establish a treatment for AD. Recent research has proposed the hypothesis that amyloid-{beta} (A{beta}) oligomers elicit an excessive glutamate release from astrocytes toward synapses through intracellular free Ca2+ ([Ca2+]i) elevations in astrocytes, finally resulting in neuronal dendritic spine loss. Under physiological conditions, astrocytic [Ca2+]i elevations range spatially from microdomains to network-wide propagation and temporally from milliseconds to tens of seconds. Astrocytic localized and fast [Ca2+]i elevations might correlate with glutamate release; however, the A{beta}-induced alteration of localized, fast astrocytic [Ca2+]i elevations remains unexplored. In this study, we quantitatively investigated the A{beta} dimers-induced changes in the spatial and temporal patterns of [Ca2+]i in a primary culture of astrocytes by two-photon excitation spinning-disk confocal microscopy. The frequency of fast [Ca2+]i elevations occurring locally in astrocytes ([≤]0.5 s, [≤]35 {micro}m2) and [Ca2+]i event occupancy relative to cell area significantly increased after exposure to A{beta} dimers. The effect of A{beta} dimers appeared dose-dependently above 500 nM, and these A{beta} dimers-induced [Ca2+]i elevations were primarily mediated by a metabotropic purinergic receptor (P2Y1 receptor) and Ca2+ release from the endoplasmic reticulum. Our findings suggest that the A{beta} dimers-induced alterations and hyperactivation of astrocytic [Ca2+]i is a candidate cellular mechanism in the early stages of AD.

neuroscience↗

Autophagosome development and chloroplast segmentation occur synchronously for piecemeal degradation of chloroplasts

Plants distribute many nutrients to chloroplasts during leaf development and maturation. When leaves senesce or experience sugar starvation, the autophagy machinery degrades chloroplast proteins to facilitate efficient nutrient reuse. Here, we report on the intracellular dynamics of an autophagy pathway responsible for piecemeal degradation of chloroplast components. Through live-cell monitoring of chloroplast morphology, we observed the formation of chloroplast budding structures in sugar-starved leaves. These buds were then released and incorporated into the vacuolar lumen as an autophagic cargo termed a Rubisco-containing body. The budding structures did not accumulate in mutants of core autophagy machinery, suggesting that autophagosome creation is required for forming chloroplast buds. Simultaneous tracking of chloroplast morphology and autophagosome development revealed that the isolation membranes of autophagosomes interact closely with part of the chloroplast surface before forming chloroplast buds. Chloroplasts then protrude at the site associated with the isolation membranes, which divide synchronously with autophagosome maturation. This autophagy-related division does not require DYNAMIN-RELATED PROTEIN 5B, which constitutes the division ring for chloroplast proliferation in growing leaves. An unidentified division machinery may thus fragment chloroplasts for degradation in coordination with the development of the chloroplast-associated isolation membrane.

plant biology↗

descSPIM: Affordable and Easy-to-Build Light-Sheet Microscopy for Tissue Clearing Technique Users

Despite the easier use of multiple tissue clearing techniques in recent years, poor access to adequate light-sheet fluorescence microscopy remains a major obstacle for biomedical end users. Here, we propose a solution by developing descSPIM (desktop-equipped SPIM for cleared specimens) as a low-cost ($20,000-50,000), low-expertise (one-day installation by a non-expert), yet practically substantial do-it-yourself light-sheet microscopy. Academically open-sourced (https://github.com/dbsb-juntendo/descSPIM), descSPIM allows routine three-dimensional imaging of cleared samples in minutes.

bioengineering↗

Subthreshold repertoire and threshold dynamics of midbrain dopamine neuron firing in vivo.

The firing pattern of ventral midbrain dopamine neurons is controlled by afferent and intrinsic activity to generate prediction error signals that are essential for reward-based learning. Given the absence of intracellular in vivo recordings in the last three decades, the subthreshold membrane potential events that cause changes in dopamine neuron firing patterns remain unknown. By establishing stable in vivo whole-cell recordings of >100 spontaneously active midbrain dopamine neurons in anaesthetized mice, we identified the repertoire of subthreshold membrane potential signatures associated with distinct in vivo firing patterns. We demonstrate that dopamine neuron in vivo activity deviates from a single spike pacemaker pattern by eliciting transient increases in firing rate generated by at least two diametrically opposing biophysical mechanisms: a transient depolarization resulting in high frequency plateau bursts associated with a reactive, depolarizing shift in action potential threshold; and a prolonged hyperpolarization preceding slower rebound bursts characterized by a predictive, hyperpolarizing shift in action potential threshold. Our findings therefore illustrate a framework for the biophysical implementation of prediction error and sensory cue coding in dopamine neurons by tuning action potential threshold dynamics.

neuroscience↗