Biology subjects

Kato, A.

Publications and source records attributed to Kato, A..

At least 19 recordsLinked to original sources

bioRxiv2026

A genome-wide catalog of sites where peripheral DNA methylation reflects the brain

Epigenetic studies of psychiatric and neurological disorders rely largely on peripheral tissues, yet where peripheral DNA methylation (DNAm) reflects the brain remains unclear. We generated a paired brain and peripheral DNAm dataset from 148 donors in three cohorts and combined it with five published cohorts for consensus brain-peripheral correlations. By cross-validation across cohorts, we defined brain epigenome shared sites (BrESS), more than 100,000 CpGs per tissue at which peripheral DNAm reproducibly predicts brain DNAm. BrESS lay at promoters active in both brain and periphery and in housekeeping genes, and most were not explained by genetic effects. BrESS did not contribute to the heritability of seven disorders, and CpGs from epigenome-wide association studies of these disorders were not enriched at BrESS. Peripheral DNAm reflects the brain mainly in a regulatory compartment shared across tissues, outside which disease signals largely lie, and BrESS separate peripheral signals attributable to the brain from others.

neuroscience↗

bioRxiv2026

Solute selectivity and functional divergence of aquaporins in reef-building corals

Reef-building corals are increasingly threatened by environmental stressors, including ocean warming, acidification, and osmotic stress caused by fluctuations in seawater salinity, highlighting the need for a better understanding of coral physiology. However, the molecular mechanisms by which corals regulate water and solute transport remain poorly understood. To investigate the role of aquaporins (Aqps) in coral physiology, we examined the evolutionary history and transport properties of the Aqp family in reef-building corals. Comparative genomic analyses across cnidarians revealed that the nine-member core hexacorallian aqp repertoire, comprising aqp4L1.1, aqp4L1.2, aqp4L1.3, aqp4L2, aqp4L3, glp1, glp2.1, glp2.2, and aqp12L1, has been highly conserved since the common ancestor of reef-building corals and sea anemones, whereas aqp8L was consistently absent across all examined hexacorallian species. Conservation of synteny and exon-intron structures further confirmed that major components of the aqp family architecture originated deep in metazoan evolution. Functional characterization of Acropora millepora Aqp4L and Glp proteins demonstrated that most transport properties were consistent with phylogenetic predictions, with the majority of Aqp4L proteins exhibiting water-selective permeability, whereas Glp proteins transported both water and small solutes such as glycerol. Unexpectedly, Aqp4L1.2, which belongs to the water-specific aquaporin lineage, transported not only water but also glycerol, urea, and boric acid, suggesting functional co-option after gene duplication and underscoring the evolutionary flexibility of the Aqp4L lineage. These findings suggest that the hexacorallian aqp family evolved through a combination of deep evolutionary conservation and lineage-specific functional innovation, providing new insight into the molecular foundations of coral physiology.

evolutionary biology↗

bioRxiv2026

SIK3 links synaptic strength to sleep pressure through RhoA signaling

Sleep is regulated by homeostatic sleep pressure, which accumulates during wakefulness, triggering sleep, and dissipates during sleep, leading to wakefulness. Although recent evidence suggests that synaptic potentiation encodes sleep pressure, the intracellular mechanisms linking synaptic strength to sleep pressure remain unclear. Here we demonstrate that the sleep-promoting kinase SIK3 links synaptic strength and sleep pressure through RhoA signalling. We found that SIK3 is required for dendritic spine enlargement induced by chemical long-term potentiation (cLTP) in cultured cortical pyramidal neurons and positively regulates spine size in the prefrontal cortex in vivo. cLTP reduced RhoA activity in an SIK3-dependent manner during spine enlargement, whereas activation of RhoA reduced EEG delta density in vivo during non-rapid eye movement sleep (NREMS), an indicator of sleep pressure. SIK3 substrate screening identified several RhoA regulators including GEF-H1, and further biochemical analyses found that phosphorylation by SIK3 activates GEF-H1. However, contrary to our expectation, RhoA facilitation through pharmacological activation of GEF-H1 enlarged spine size in cultured neurons, and expression of constitutively active GEF-H1 increased NREMS delta density in a RhoA-dependent fashion. Together, these results indicate that SIK3 enlarges spine size and enhances NREMS delta density through two RhoA-dependent pathways, driving mutually opposing intermediate phenotypes. Our findings identify two clashing SIK3-RhoA signalling pathways that couple synaptic regulation to sleep homeostasis.

neuroscience↗

bioRxiv2026

Evolutionary history of aquaporin-10 pseudogenization in Cetartiodactyla

Aquaporin-10 (AQP10) is an aquaglyceroporin that transports small, uncharged molecules, such as water and glycerol. In some species, such as mice and cattle, the AQP10 gene (Aqp10) is pseudogenized. In rodents, pseudogenization of Aqp10 is limited to the Myomorpha suborder, while Aqp10 remains intact in other rodent lineages. The order Cetartiodactyla encompasses diverse species, including Suina, Tylopoda, Ruminantia, and Whippomorpha. The distribution of intact Aqp10 across the entire Cetartiodactyla and analyses estimating the timing of Aqp10 pseudogenization have not been sufficiently investigated. In this study, we identified species within Cetartiodactyla that retain intact Aqp10 and analyzed the detailed patterns of pseudogenization to elucidate the specifics of pseudogenization within this order. We collected Aqp10 loci by BLAST and synteny analyses of publicly available genome databases of 51 cetartiodactyl species from 17 families. Dot plot and alignment analyses revealed that seudogenization of Aqp10 occurred in 42 Cetartiodactyla species, including the Camelidae, warthog (Suidae), Antilocapridae, okapi (Giraffidae), Cervidae, Bovidae, Hippopotamidae, and Cetacea. In contrast, nine species retained an intact Aqp10: pig and babirusa (Suidae), peccary (Tayassuidae), mouse deeres (Tragulidae), giraffes (Giraffidae), and musk deers (Moschidae). The timing of pseudogenization was estimated by comparing patterns of exon deletions, frameshifts, and nonsense mutations in Aqp10 pseudogenes. RT-PCR analysis of cattle and sheep tissues revealed that these species express Aqp3 and Aqp7 in their intestines, but not Aqp10. Collectively, these findings indicate that Aqp10 pseudogenization occurred independently in multiple cetartiodactyl lineages and provide new insights into the evolutionary history of Aqp10 loss within this order.

evolutionary biology↗

bioRxiv2026

Single neurons in the human substantia nigra encode social learning signals

Humans are remarkable at adapting to changing norms, yet we know little about how the human brain encodes these social signals at the single neuron level. Here, we recorded the activity of single neurons in the substantia nigra and globus pallidus in neurosurgical participants as they played an iterative ultimatum game versus human and computer avatars. Using computational modeling of behavior, we found that putative dopaminergic units in the substantia nigra tracked the valence of norm prediction errors, with greater encoding during gameplay with human versus computer avatars. Analogous analyses in the globus pallidus, a nucleus adjacent to the substantia nigra, found no significant effect. Our results identify a novel role for the substantia nigra in encoding social learning signals.

neuroscience↗

bioRxiv2026

Basolateral localization of Kcnj15 in branchial ionocytes of the seawater pufferfish Takifugu rubripes

In marine teleosts, gill ionocytes play central roles in the excretion of excess monovalent ions (Na+, Cl-, and K+). Basolateral K+ channels are considered essential for sustaining ion secretion by maintaining K+ homeostasis and membrane potential; however, the molecular identity of basolateral K+ channels in teleost gill ionocytes remains incompletely understood. Kcnj15 is a K+ channel expressed in multiple osmoregulatory tissues of the Japanese pufferfish (Takifugu rubripes), and its localization changes depending on tissue type and osmotic conditions; however, its localization in the gills has remained unresolved. Here, we determined the cellular localization of Kcnj15 in the gills and examined its expression in response to changes in environmental salinity. In seawater-acclimated fish, Kcnj15 was localized to the basolateral membrane of Nka- and Nkcc1-positive ionocytes. Following acclimation to hypoosmotic brackish water (1 ppt), transcript levels of cftr, nkcc1, and kcnj1a decreased, whereas kcnj15 expression remained unchanged. Under this condition, Kcnj15 was localized to the basolateral membrane of Nka-positive ionocytes. These results demonstrate that Kcnj15 is localized to the basolateral membrane of gill ionocytes and suggest that it may function as a basolateral K+ leak channel supporting ionocyte homeostasis under both seawater and low-salinity conditions.

physiology↗

bioRxiv2026

Calmodulin controls the tempo of HSV-1 gene-expression cascade to reshape infection heterogeneity

Viral replication exhibits substantial heterogeneity among individual cells. Although temporally ordered gene-expression cascades are thought to contribute to such heterogeneity in DNA viruses, whether and how their tempo is regulated, and how cell-to-cell variability shapes population-level infection outcomes, remain unknown. Here, we developed a high-throughput live-cell imaging platform to track HSV-1 gene-expression dynamics in individual cells and, in combination with single-cell RNA sequencing, identified calmodulin (CaM) as a host regulator of HSV-1 gene-expression tempo. CaM accelerates progression from immediate-early to early and late phases at the single-cell level by advancing their onset. By increasing the fraction of virus-producing cells without altering burst size, CaM reshapes the distribution of infection outcomes, thereby promoting population-level viral replication. Pharmacological inhibition of CaM protects mice from lethal infection, exceeding acyclovir. These findings establish CaM-mediated temporal control as a key determinant of population-level viral output and a regulator of infection heterogeneity.

microbiology↗

bioRxiv2026

Aqp1aa and Aqp4a mediate collecting duct water permeability in a marine teleost

Regulation of water permeability in the collecting duct is important for osmoregulatory acclimation in teleost fish. In hyperosmotic environments such as seawater (SW), the teleost kidney functions as a site of divalent ion excretion. The collecting ducts reabsorb Na+, Cl-, and water, thereby reducing urine volume and producing small amounts of isotonic urine with high concentrations of divalent ions. In hypoosmotic environments such as freshwater (FW) or low-salinity brackish water (BW), the kidney produces large volumes of hypotonic urine and serves as a site of water excretion; under these conditions, the collecting ducts reabsorb Na+ and Cl- but not water. To identify aquaporins (Aqps) involved in regulating water permeability in the collecting ducts of teleosts, we analyzed renal Aqp expression in a euryhaline marine fish, the Japanese pufferfish (Takifugu rubripes), which possesses 16 Aqp genes in its genome, seven of which (Aqp1aa, 1ab, 3a, 4a, 7, 8bb, and 11a) are expressed in the kidney. Quantitative RT-PCR analysis showed that Aqp1aa and Aqp4a were highly expressed in collecting duct tissues, and that Aqp1aa expression was markedly reduced in fish acclimated to BW. Immunohistochemistry revealed apical localization of Aqp1aa and basolateral localization of Aqp4 in collecting duct cells, with apical Aqp1aa downregulated in BW. These results suggest that Aqp1aa and Aqp4 mediate water reabsorption in SW and that downregulation of Aqp1aa contributes to hypotonic urine production in BW. NEW & NOTEWORTHYRegulation of water permeability in the collecting duct is important for osmoregulation in teleost fish. Expression analyses of aquaporins (Aqps) in the marine pufferfish Takifugu rubripes showed that Aqp1aa and Aqp4a are highly expressed in the collecting duct and localized to the apical and basolateral membranes, respectively. Renal Aqp1aa expression was markedly reduced in fish acclimated to hypoosmotic brackish water. These results indicate that collecting duct water permeability is regulated by Aqp1aa expression.

physiology↗

bioRxiv2026

The circadian clock gates lateral root development

Lateral root (LR) formation remodels root architecture, yet how temporal information integrates with hormonal cues remains unclear. We show that the circadian clock component EARLY FLOWERING 3 (ELF3) acts as a temporal gatekeeper of root organogenesis in Arabidopsis thaliana. Time-resolved transcriptomics, imaging, and genetics reveal that ELF3 restrains hormone-induced pericycle proliferation by maintaining rhythmic expression of key regulators under callus-inducing conditions. Loss of ELF3 disrupts rhythmic gene expression, enhancing callus growth and accelerating LR development. ELF3 functions through its target LNK1 to regulate the MADS-box genes AGL14 and AGL20. Notably, callus-inducing signals partially restore rhythmicity in elf3 mutants, revealing feedback from hormonal signaling to the circadian system. These findings identify ELF3 as an integrator of circadian and hormonal inputs that temporally constrains root developmental plasticity.

plant biology↗

bioRxiv2025

Dopamine and serotonin transients predict depressive symptom relief following deep brain stimulation of human subcallosal cingulate cortex

Recent advances in deep brain stimulation (DBS) of the subcallosal cingulate (SCC) show promise in mitigating the symptoms of treatment-resistant depression (TRD) in humans1-3. Monoamines, such as dopamine and serotonin, mediate the effects of pharmacological treatments of depression. However, their roles in recovery following DBS remain elusive, largely due to technical limitations of measuring these neurotransmitters in the living human brain. Here, by leveraging machine learning-enhanced electrochemistry4-7, we show that dopamine and serotonin signaling following DBS to the SCC predicted later depressive symptom relief in humans with TRD. We found that both dopamine and serotonin levels increased following subtherapeutic intraoperative SCC stimulation, with each neurotransmitter showing selective responses to distinct decision-making tasks. Furthermore, acute dopamine increases predicted later mood improvements during a social decision-making task, while serotonin enhancement predicted faster responses during a non-social learning task longitudinally. Critically, changes in dopamine and serotonin levels during the social decision-making task jointly predicted depressive symptom remission at 6-month follow-up. These findings illustrate the contribution of both dopamine and serotonin signaling in predicting behavioral improvement and depressive symptom remission in humans with TRD. Such neurochemical plasticity may serve as potential mechanistic biomarkers for SCC DBS mechanism and TRD treatment response. Significance statementO_LIDopamine and serotonin levels increased following acute DBS to the SCC in humans. C_LIO_LIAcute dopamine and serotonin changes predicted later mood and response speed changes. C_LIO_LISustained TRD recovery was predicted by acute increases in both dopamine and serotonin estimates. C_LI

neuroscience↗

bioRxiv2025

Multi-Class Classification of Cannabis and Alcohol Use Disorder: Identifying Common and Substance-Specific Neural Circuits.

Machine learning approaches have advanced the identification of neural signatures of substance use, particularly through case-control comparisons and network-level analyses. However, most studies have focused on single substances in isolation, making it difficult to directly compare shared and distinct network computations and limiting their generalizability, given that many individuals engage in polysubstance use. Here, we introduce an explainable, connectivity-based multiclass classification framework that models distributed brain network organization to delineate both shared and substance-specific mechanisms of addiction. This design enables direct comparison among cannabis users, alcohol users, and controls, revealing network computations that uniquely differentiate each group. Using functional connectivity features from cue-induced craving tasks, we classified cannabis users (n=166), alcohol users (n=101), and healthy controls (n=238), achieving high out-of-sample accuracy (87% for cannabis, 69% for alcohol, and 73% for controls). Functional connectivity-based models consistently outperformed activation-based models, highlighting the importance of inter-regional network properties for biomarker development. Network analysis further revealed dorsal prefrontal, cingulate, and precuneus hubs consistent with meta-analytic craving networks and substance-specific connectivity motifs enhanced prefrontal coupling in cannabis users and greater insular-striatal integration in alcohol users. These results demonstrate that distinct network configurations define different substance-use profiles, advancing interpretable biomarkers for addiction neuroscience.

neuroscience↗

bioRxiv2025

Age-related decline of synaptic plasticity is regulated by neuro-androgen and neuro-estrogen in normal aging of hippocampus

We revealed a good relationship between age-dependent decrease in the hippocampal dendritic spine density and age-dependent decrease in hippocampal androgen and estrogen levels with normal aging of male rats. Approximately 25% decrease in the spine density was observed in hippocampal CA1 region by going from 3 month-old (3m; young adult) to 24 month-old (24m; aged). We found a significant age-induced decrease in hippocampal neuro-androgen levels by going from 3m to 24 m using mass-spectrometric analysis. The hippocampal levels of testosterone (T) and dihydrotestosterone (DHT) dramatically decreased from 17 nM T and 7 nM DHT at 3 m to 17/100 nM T and 7/15 nM DHT at 24 m. On the other hand, hippocampal estradiol (E2) was moderately decreased with aging, from 8 nM at 3 m to 2 nM at 24m. Comprehensive analysis of mRNAs of hippocampal steroidogenic enzymes and receptors showed an age-dependent decrease in their expression levels by approximately 50% (P450(17)), 25% (17-hydroxysteroid dehydrogenase) and 0% (5-reductase and P450arom). Androgen receptor AR was moderately decreased but estrogen receptor ER was not decreased with aging. The 25% decrease in the spine density with aging may be due to a balance between considerably decreased T and DHT levels (spine decrease factor) and remained moderately high E2 level (spine increase factor) in the 24m hippocampus. Aged hippocampus still has moderate capacity of sex-steroid synthesis and their functions. Interestingly, DHT-supplementation and T-supplementation recovered the spine density at 24m.

neuroscience↗

bioRxiv2025

Identification of Viral Activators of the HSV-2 UL13 Protein Kinase

Although previous studies reported that the herpes simplex virus 2 (HSV-2) UL13 protein kinase mediates the phosphorylation of elongation factor 1{delta} (EF-1{delta}) in infected cells, we show here that individual expression of UL13 was insufficient to induce phosphorylation of EF-1{delta} in mammalian cells. This led us to hypothesize that HSV-2 UL13 requires viral cofactors for full kinase activity and prompted us to identify such cofactors. Our results were as follows. (i) Co-expression of UL13 with UL55 or Us10 significantly enhanced phosphorylation of EF-1{delta} compared to UL13 alone. (ii) UL13 was co-precipitated with UL55 or Us10 upon co-expression, and its kinase activity was significantly increased in their presence, as demonstrated by in vitro kinase assays. (iii) In HSV-2-infected cells, UL13 was specifically co-precipitated with Us10 and UL55. (iv) The UL55-null mutation significantly reduced phosphorylation of EF-1{delta} in HSV-2-infected cells, whereas the Us10-null mutation had little effect; however, the double-null mutation further decreased the phosphorylation compared to the UL55-null mutation alone. (v) The UL55-null mutation, but not the Us10-null mutation, significantly reduced HSV-2 replication and cell-cell spread in U2OS cells to levels comparable to those observed with the UL13 kinase-dead mutation. These results suggest that UL55 acts as a principal activator of UL13 in HSV-2-infected cells, whereas Us10 serves as an auxiliary activator. Moreover, the role of UL13 kinase activity in HSV-2 replication and cell-cell spread in U2OS cells appears to be largely dependent on UL55. ImportanceHerpesviruses encode conserved protein kinases (CHPKs) that often target cellular cyclin-dependent kinase (CDK) phosphorylation sites. CHPKs from beta-and gammaherpesviruses can exhibit these CDK-like functions even when individually expressed in mammalian cells. In contrast, CHPKs from alphaherpesviruses display these CDK-like functions in infected cells, but not upon individual expression, suggesting that they require additional viral factors to exhibit full kinase activity. In this study, we focused on HSV-2 UL13, an alphaherpesvirus CHPK, and identified HSV-2 UL55 and Us10 as viral activators of UL13. In HSV-2-infected cells, UL55 functions as a principal activator of UL13, while Us10 serves as an auxiliary activator. Importantly, the contribution of UL13 kinase activity to HSV-2 replication and cell-cell spread appears to be largely dependent on the presence of UL55. Our findings uncover a previously unrecognized mechanism of CHPK regulation in alphaherpesviruses and provide new insights into the evolutionary diversification of viral kinase control.

microbiology↗

bioRxiv2025

The glomerulus as a selective gate for tumor-derived extracellular vesicles in urine

Urinary small extracellular vesicles (sEVs), which can reflect systemic conditions, hold great promise for non-invasive cancer diagnostics, yet the mechanism by which tumor-derived sEVs reach urine remains unclear. Here, we demonstrate that the glomerulus actively transcytoses circulating tumor-derived sEVs into urine. Using CRISPR gRNA-tagged glioma sEVs and bioluminescent/fluorescent GeNL-tagged lung and pancreatic cancer sEVs, we tracked their journey from tumors to urine in multiple mouse models. In vivo and in vitro analyses revealed endocytic uptake and transcytotic release by glomerular cells, accompanied by changes in sEV size and surface composition. GeNL-tagged sEVs consistently showed higher signals in urine than plasma, indicating selective excretion. These findings redefine the glomerulus as a dynamic regulator of EV processing and establish a mechanistic foundation for urinary liquid biopsy.

cancer biology↗

bioRxiv2025

Bacterial pathogen deploys iminosugar galactosyrin to manipulate plant glycobiology

The extracellular space (apoplast) of plants is an important molecular battleground during infection by many pathogens. We previously found that a plant-secreted {beta}-galactosidase BGAL1 acts in immunity by facilitating the release of immunogenic peptides from bacterial flagellin and that Pseudomonas syringae suppresses this enzyme by producing a small molecule inhibitor called galactosyrin. Here, we elucidated the structure and biosynthesis of galactosyrin and uncovered its multifunctional roles during infection. Structural elucidation by cryo-EM and chemical synthesis revealed that galactosyrin is an iminosugar featuring a unique geminal diol attached to the pyrrolidine moiety that mimics galactose binding to the {beta}-galactosidase active site. Galactosyrin biosynthesis branches off from purine biosynthesis and involves three enzymes of which the first is a reductase that is unique in iminosugar biosynthesis. Besides inhibiting BGAL1 to avoid detection, galactosyrin also changes the glycoproteome and metabolome of the apoplast. The manipulation of host glycobiology may be common to plant-associated bacteria that carry putative iminosugar biosynthesis clusters.

plant biology↗

bioRxiv2025

Striatal Gradient in Value-Decay Explains Regional Differences in Dopamine Patterns and Reinforcement Learning Computations

Dopamine has been suggested to encode reward-prediction-error (RPE) in reinforcement learning (RL) theory, but also shown to exhibit heterogeneous patterns depending on regions and conditions: some exhibiting ramping response to predictable reward while others only responding to reward-predicting cue. It remains elusive how these heterogeneities relate to various RL algorithms proposed to be employed by animals/humans, such as RL under predictive state representation, hierarchical RL, and distributional RL. Here we demonstrate that these relationships can be coherently explained by incorporating the decay of learned values (value-decay), implementable by the decay of dopamine-dependent plastic changes in the synaptic strengths. First, we show that value-decay causes ramping RPE under certain state representations but not under others. This accounted for the observed gradual fading of dopamine ramping across repeated reward navigation, attributed to the gradual formation of predictive state representations. It also explained the cue-type and inter-trial-interval-dependent temporal patterns of dopamine. Next, we constructed a hierarchical RL model composed of two coupled systems--one with value-decay and one without. The model accounted for distinct patterns of neuronal activity in parallel striatal-dopamine circuits and their proposed roles in flexible learning and stable habit formation. Lastly, we examined two distinct algorithms of distributional RL with and without value-decay. These algorithms explained how distinct dopamine patterns across striatal regions relate to the reported differences in the strength of distributional coding. These results suggest that within-striatum differences--specifically, a medial-to-lateral gradient in value or synaptic decay--tune regional RL computations by generating distinct patterns of dopamine/RPE signals.

neuroscience↗

bioRxiv2024

Reinforcement learning of state representation and value: the power of random feedback and biological constraints

Representation of external and internal states in the brain plays a critical role in enabling suitable behavior. Recent studies suggest that state representation and state value can be simultaneously learnt through Temporal-Difference-Reinforcement-Learning (TDRL) and Backpropagation-Through-Time (BPTT) in recurrent neural networks (RNNs) and their readout. However, neural implementation of such learning remains unclear as BPTT requires offline update using transported downstream weights, which is suggested to be biologically implausible. We demonstrate that simple online training of RNNs using TD reward prediction error and random feedback, without additional memory or eligibility trace, can still learn the structure of tasks with cue-reward delay and timing variability. This is because TD learning itself is a solution for temporal credit assignment, and feedback alignment, a mechanism originally proposed for supervised learning, enables gradient approximation without weight transport. Furthermore, we show that biologically constraining downstream weights and random feedback to be non-negative not only preserves learning but may even enhance it because the non-negative constraint ensures loose alignment - allowing the downstream and feedback weights to roughly align from the beginning. These results provide insights into the neural mechanisms underlying the learning of state representation and value, highlighting the potential of random feedback and biological constraints.

neuroscience↗

bioRxiv2024

Innovative Use of Depth Data to Estimate Energy Intake and Expenditure in Adelie Penguins

Energy governs species life histories and pace of living, requiring individuals to make trade-offs. However, measuring energetic parameters in the wild is challenging, often resulting in data collected from heterogeneous sources. This complicates comprehensive analysis and hampers transferability within and across case studies. We present a novel framework, combining information obtained from eco-physiology and bio-logging techniques, to estimate both energy expended and acquired on 48 Adelie penguins (Pygoscelis adeliae) during the chick-rearing stage. We employ the machine learning algorithm random forest (RF) to predict accelerometry-estimated foraging behaviour using depth data (our proxy for energy acquisition). We also build a time-activity model calibrated with doubly labelled water data to estimate energy expenditure. Using depth-derived time spent diving and amount of vertical movement in the sub-surface phase, we accurately predict energy expenditure (R{superscript 2} = 0.70). Movement metrics derived from depth data modelled with the RF algorithm were able to accurately (accuracy = 0.82) detect the same foraging behaviour predicted from accelerometry. The RF more accurately predicted accelerometry-estimated time spent foraging (R{superscript 2} = 0.81) compared to historical proxies like number of undulations (R{superscript 2} = 0.51) or dive bottom duration (R{superscript 2} = 0.31). The proposed framework is accurate, reliable and simple to implement, enabling to couple energy intake and expenditure, which is crucial to further assess individual trade-offs. We provide universal guidelines for predicting these parameters based on widely used bio-logging technology in marine species. Our work allows us to revisit historical data, to study how long-term environmental changes affect animals energetics. Summary statementUsing machine learning, we estimated energy expenditure and foraging activity of free-ranging Adelie penguins using depth data recorded with bio-logging devices.

ecology↗