bioRxiv Science⌕ Search

Biology subjects

Watanabe, Y.

Publications and source records attributed to Watanabe, Y..

At least 19 recordsLinked to original sources

An iPSC-based experimental framework for investigating phenotypic variation associated with Jomon ancestry in the present-day Japanese population

Ancestry-related genomic variation may contribute to phenotypic diversity. However, its cellular consequences remain difficult to evaluate. To address this, we developed a human induced pluripotent stem cell (hiPSC)-based framework for investigating such phenotypes. We used the Japanese population as a model of Jomon-related and continental East Asian ancestry admixture. Jomon ancestry, estimated using the Jomon allele score (JAS), was associated with clinical measures, including renal-related traits and serum triglycerides in 34,152 Tohoku Medical Megabank participants. Peripheral blood mononuclear cell transcriptomics of donors from the upper and lower extremes of the JAS distribution (n = 10) suggested group-level differences in immune-related gene expression. To test whether the serum triglyceride association coincided with hepatic cellular phenotypes, we differentiated hiPSCs from these donors into hepatocyte-like cells. Neither intracellular triglycerides nor lipid-related gene expression differed between groups. These findings highlight the value of a genetically characterized hiPSC-based framework for investigating ancestry-associated phenotypes across cellular contexts.

genomics↗

Female-biased continental farmer ancestry contribution to the modern Japanese genome

Modern mainland Japanese formed through admixture between the Jomon hunter- gatherers and continental farmers who arrived probably in northern Kyushu around 3,000 years ago (the dual-structure model). Although Jomon ancestry accounts for only [~]10-20% of the autosomes, the Jomon-associated Y-chromosome haplogroup D1a2a reaches [~]35% in present-day Japanese males--an "admixture paradox" often attributed to a larger contribution by Jomon males, though this has never been tested genome-wide. To test whether this admixture was sex-biased, here we compared the X chromosome with the autosomes. Using Jomon-derived variants as local-ancestry markers, we separated the modern Japanese genome into Jomon-related and continental East Asian-related ancestry components and computed the Keinan-type autosome-to-X drift ratio (Q, neutral expectation 0.75) for each. The continental East Asian-related component gave a significantly higher Q than the Jomon-related component ({Delta} = Qfarming - QHG = 0.10, P = 9.1 x 10 {square}3). Relative to the neutral value of 0.75, the Jomon-related component was indistinguishable from neutrality (Q = 0.78, P = 0.34), whereas the continental East Asian-related component was significantly higher (Q = 0.88, P = 4.2 x 10{square} {square}). Under a single-pulse founder model, this pattern implies a continental farmer contribution that was significantly more female-biased than the Jomon hunter-gatherer contribution, with no detectable departure from sex balance in the latter. Monte Carlo simulations showed that the inferred sex ratios account for much of the observed D1a2a frequency, although the remaining discrepancy indicates that additional demographic processes may have contributed. The ancestry asymmetry in the modern Japanese genome was thus driven primarily by a female-biased contribution of continental farming migrants, rather than by the male-biased Jomon contribution conventionally invoked to explain the admixture paradox.

evolutionary biology↗

Spontaneous and stimulus-driven arousal produce distinct acetylcholine dynamics across sensory and prefrontal cortex

Acetylcholine (ACh) release from the basal forebrain has traditionally been viewed as a slow, spatially diffuse signal regulating cortical arousal across sleep and wakefulness1-3. Recent characterizations with higher resolution optical sensors have revealed rapid, local cholinergic modulation supporting dynamic changes in sensory processing, associative learning, and behavioral state4-7. However, sensory events that recruit cortical ACh often also change arousal and evoke movements, making it difficult to determine whether ACh transients reflect sensory features of environmental stimuli or the behavioral state changes that accompany sensory stimulation. To separate these contributions, we performed optic fiber recordings of a genetically encoded ACh fluorescent sensor in the auditory, visual, and prefrontal cortex of awake, head-fixed mice while monitoring pupil size and facial movements. Across cortical areas, ACh release tracked spontaneous fluctuations in arousal state, as indexed by pupil dilation and orofacial movements. Sensory stimuli also evoked rapid ACh transients, with sounds producing larger and more widespread responses than visual stimuli. Because sounds also elicited time-locked pupil dilations and facial movements, we used multivariate modeling to estimate the relative contributions of stimulus features, arousal, and behavior to cortical ACh dynamics. We identified a regional dissociation: sound-evoked ACh release in prefrontal cortex was largely explained by arousal- and movement-related variables, whereas auditory cortical ACh release retained a stronger relationship to stimulus features. These findings show that cortical ACh signaling reflects both shared arousal state and area-specific sensory processing and demonstrate that sound is especially effective at recruiting rapid, widespread cholinergic modulation across cortex.

neuroscience↗

Structures of the Pseudomonas aeruginosa MlaC-MlaD complexes reveal a conformational switch mediated by the C-terminal helix of MlaC

Gram-negative bacteria maintain an asymmetric outer membrane that protects cells from environmental stresses and antibiotics. The maintenance of lipid asymmetry (Mla) pathway contributes to outer membrane lipid homeostasis through phospholipid transport between the outer and inner membranes. Although the periplasmic lipid carrier MlaC is thought to transfer phospholipids to the inner membrane MlaFEDB transporter via the hexameric protein MlaD, the molecular mechanism underlying this process remains unclear. Here we show crystal structures of two distinct MlaC-MlaD complexes from Pseudomonas aeruginosa that reveal distinct conformational states of MlaC. In these structures, an ordered conformation of the C-terminal 8 helix of MlaC positions MlaC distally from the central pore of the MlaD hexamer and limits accessibility of the lipid-binding cavity, whereas partial disordering of the 8 helix allows closer association with the MlaD hexamer and increased exposure of the cavity. Structure-based biochemical analyses further demonstrate that the C-terminal region negatively regulates MlaC- MlaD interaction while stabilizing phospholipid binding. These findings identify the C-terminal 8 helix as a conformational switch that couples MlaC positioning with lipid cavity accessibility, providing structural insight into phospholipid transfer at the MlaC-MlaD interface.

biochemistry↗

High-fat diet-induced obesity differentially alters circadian gene expression across peripheral tissues

Circadian rhythms regulate diverse physiological processes, including metabolism, and their disruption has been implicated in metabolic disorders such as obesity. However, the tissue-specific effects of obesity on peripheral circadian clocks remain incompletely understood. Here, we investigated the impact of high-fat diet (HFD)-induced obesity on circadian gene expression in skeletal muscle, liver, and white adipose tissue (WAT). Mice were fed either a regular diet (RD) or HFD for 6 weeks, followed by tissue collection at 4-hour intervals over a 24-hour period. Under RD conditions, key circadian regulators and their downstream targets exhibited robust 24-hour oscillations across all tissues. In contrast, HFD feeding induced distinct, tissue-specific alterations. In the liver, Per2, Dbp, and Rev-erb showed phase-advanced expression patterns, whereas in WAT, rhythmic expression was markedly attenuated. Notably, skeletal muscle largely preserved circadian gene expression patterns, indicating relative resistance to HFD-induced circadian disruption. In addition, HFD feeding altered metabolic gene expression in adipose tissue, characterized by reduced Pgc1 expression and increased Leptin expression. Together, these findings demonstrate that HFD-induced obesity differentially disrupts peripheral circadian clocks in a tissue-specific manner and highlight skeletal muscle as a relatively resilient tissue. These results provide insight into how circadian dysregulation contributes to metabolic abnormalities in obesity.

physiology↗

Functional divergence of DSCAM family in vertebrates through domain-specific evolutionary pressures

The Down syndrome cell adhesion molecule (DSCAM) family, conserved across metazoans, plays key roles in neural development by mediating cell-cell recognition. Invertebrate Dscam evolved extensive molecular diversity through isoform diversification, whereas the vertebrate paralogs DSCAM and DSCAML1 followed a distinct evolutionary trajectory. However, how these vertebrate paralogs evolved after duplication, particularly with respect to functional divergence, remains poorly understood. Here, we investigated the evolutionary history and post-duplication divergence of these paralogs using phylogenetic, molecular evolutionary, sequence comparison, and transcriptomic analyses. Our phylogenetic analyses suggest an ancestral gene duplication predating the split between gnathostomes and cyclostomes. We found distinct patterns of selective constraint between the paralogs, particularly in the intracellular domain. In tetrapods, the intracellular domain of DSCAM showed strengthened purifying selection, whereas no comparable reinforcement was evident for DSCAML1, despite strong constraint in mammals. We also found distinct patterns of lineage- and site-specific positive selection between DSCAM and DSCAML1. Consistent with these evolutionary differences, comparative analysis of the intracellular domains revealed distinct repertoires of short linear motifs (SLiMs) predicted to mediate protein-protein interactions. Reanalysis of published transcriptomic data further suggested distinct downstream responses elicited by the intracellular domains of DSCAM and DSCAML1. Together, these findings suggest that post-duplication functional divergence of vertebrate DSCAM paralogs may have contributed to the evolution of molecular mechanisms underlying vertebrate neural development and circuit formation.

evolutionary biology↗

The epidermal stem cell-supporting matricellular protein fibulin 7 modulates skin inflammatory response in a psoriasis model

ECM composition and organization are greatly altered during inflammation but it is still elusive if ECM dynamics may protect tissue stem cells against aberrant inflammation. Fibulin 7 (encoded by Fbln7) is part of the basement membrane ECM where epidermal stem cells (EpSCs) reside. It supports the long-term potential of fast-cycling EpSCs and moderates aging-related inflammatory markers in keratinocytes. Here, we assessed fibulin 7s role during imiquimod (IMQ)-induced inflammation in 1-year-old mouse dorsal skin. We found that loss of Fbln7 aggravates epidermal inflammation, marked by increased epidermal thickness, proliferation, and phosphorylation of JNK (c-Jun N-terminal kinase). Fast-cycling EpSCs labeled with Slc1a3-creER-TdTomato demonstrated that IMQ-induced proliferation in Fbln7 KO mice is contributed by cell divisions in the suprabasal layers, a hallmark of inflammatory epidermal responses. EpSC transcriptomes further reveal IMQ-modulated genes that are more substantially affected in Fbln7 KO mice, including IL-17 pathway-related genes known in psoriasis pathogenesis. Mechanistically, fibulin 7 directly binds to IL-17A and decreases IL-17A-mediated p38 MAPK activation. In public human psoriasis datasets, FBLN7 is reduced in lesional skin compared with non-lesional or normal skin, and it is significantly correlated with common psoriasis-associated genes. Altogether, fibulin 7 is potentially beneficial to protect against skin inflammation.

cell biology↗

Chromatin landscape and epigenetic heterogeneity of acute myeloid leukemia

Acute myeloid leukemia (AML) is an aggressive hematologic cancer characterized by proliferation of immature myeloblasts. It shows profound molecular heterogeneity, which has been primarily studied through genetic abnormalities, providing the basis for disease classification, prognostication, and therapeutic choice. However, genetic factors alone may not fully explain AML pathogenesis and diversity, while leaving the role of abnormal epigenome, particularly chromatin state, largely unexplored in a large cohort of patients. Here we show that AML is classified into 16 subgroups with distinct chromatin accessibility profiles based on ATAC-seq in 1,563 AML cases, including novel AML subgroups not previously recognized in conventional genomic classifications. By integrating multi-omics analyses of genome, transcriptome, and major histone marks, we show that these epigenetic subgroups exhibit unique features in clinical presentation, gene mutations, differentiation states, gene expression, and super-enhancer profiles, which are validated across independent cohorts. Single-cell sequencing demonstrates the presence of subgroup-specific ATAC signatures that are shared by all leukemic cells, confirming the definitive role of the epigenome in the ATAC-based classification. Mechanistically, each subgroup is associated with a distinct gene regulatory network centered on key transcription factors, where subgroup-specific super-enhancers play a pivotal role. These ATAC subgroups also have prognostic significance independent of genomic classification, and help reveal unexpected drug sensitivities. In summary, ATAC-based chromatin profiling in this large sample set, combined with multi-omics data, provides new insights into AML pathogenesis beyond genomic profiling and also serves as an invaluable resource for AML research.

cancer biology↗

High-Coverage Jomon Genomes Provide Insights into Population Structure and Genetic Traits of Ancient Japanese Hunter-Gatherers

We analyzed eight high-coverage Jomon genomes spanning 9,000-2,800 years ago across the Japanese archipelago. Population genomic analyses revealed substantial genetic homogeneity across time and space reflecting post-glacial isolation, yet temporal stratification emerged: Initial Jomon (Iyai) individuals formed the earliest branch with weaker affinities to present-day Japanese. Using genomes from Todoroki and Chidorikubo sites, we estimated Jomon ancestry in mainland Japanese at [~]20%, substantially higher than previous estimates ([~]13%). Polygenic score analyses, based on the direct analysis of Jomon genomes, provided the genetic evidence for their phenotypic predispositions, including elevated BMI and metabolic trait scores, reduced immune-related scores, and larger cardiac dimensions, patterns consistent with hunter-gatherer adaptations. These ancestral genetic influences, including elevated risks for obesity and dyslipidemia, persist in present-day Japanese. Our findings demonstrate that Jomon populations maintained genetic continuity despite ecological diversity, while their greater-than-expected contribution to present-day Japanese reshapes population history models and reveals how ancient adaptations continue influencing contemporary disease susceptibility.

genomics↗

Structural basis of substrate recognition and membrane association by the bacterial lysyl-phosphatidylglycerol hydrolase AcvB

Bacteria adapt to environmental stresses via membrane phospholipid remodeling; however, the underlying molecular mechanism remains largely elusive. In Agrobacterium tumefaciens, the lysyl-phosphatidylglycerol (Lys-PG) synthase LpiA and periplasmic hydrolase AcvB genes form an operon that controls Lys-PG levels. We determined the crystal structures of mature AcvB and its C-terminal catalytic domain at 3.1 [A] and 1.8 [A] resolution, respectively. The catalytic domain forms a negatively charged cavity that recognizes the positively charged Lys-PG head group through multiple acidic residues, including Asp271, Asp340, and Asp370. A hydrophobic protruding loop containing Trp378 and Leu379 mediates transient membrane association and contributes to Lys-PG acyl-chain recognition. Further, AcvB interacts with LpiA via its C-terminal domain, suggesting a cooperative module for Lys-PG turnover. These findings reveal the structural basis of Lys-PG hydrolysis and provide mechanistic insight into adaptive lipid modification at the bacterial membrane interface, and may guide future development of antibacterial agents against plant-pathogenic bacteria.

biochemistry↗

Shugoshin holds the potential to inhibit APC/C and thereby prevents separase activation

Accurate chromosome segregation during mitosis and meiosis depends on shugoshin protein which localizes at the centromere of chromosomes. Sgo1, a meiosis-specific shugoshin in fission yeast, collaborates with the PP2A phosphatase enzyme to remove phosphate groups from Rec8 cohesin, thereby preventing its cleavage by separase during meiosis. Here we show that ectopic expression of Sgo1 causes chromosome segregation errors during mitosis, especially in cut1-206 separase mutant cells, but that the D-box mutant Sgo1 has no effect in cut1-206 cells. Our molecular genetic analyses suggest that the D-box of Sgo1 directly binds Slp1/CDC20 and inhibits APC/C-dependent separase activation, thereby preventing cleavage of Rad21 cohesin. In contrast, during meiosis, the Sgo1 D-box mutant makes the cut1-206 mutant more difficult to cleave Rec8 cohesin. This is because the D-box mutation increases the amount of Sgo1 protein during meiosis, thereby enhancing its canonical protective ability against Rec8 cohesin. Thus, our studies using a separase mutant have revealed that Sgo1 has multiple faces to protect coheisn.

cell biology↗

Protection and deprotection of the Rec8 cohesin complex during meiosis

In the first meiotic division, the cohesin Rec8 is cleaved by separase along the chromosome arms but is protected at the centromere by shugoshin (Sgo1), maintaining centromeric cohesion throughout meiosis I. Another meiotic regulator, meikin (Moa1), supports the protective function of Sgo1 primarily by phosphorylating S450 of Rec8. Both Sgo1 and Moa1 are meiosis I-specific proteins. Unlike fission yeast Sgo1, mammalian shugoshin (SGO2) persists at centromeres throughout meiosis I and II, but REC8 cohesin is protected only during meiosis I. Here, we show that fission yeast Moa1 and Sgo1 appear at kinetochores/centromeres from prophase I to metaphase I and are degraded during anaphase I by the APC/C-Slp1 pathway. We expressed non-degradable versions of Moa1 and Sgo1 in meiosis II and investigated how these proteins protect the cohesin Rec8 during meiosis II. Our analyses suggest that the localization of Sgo1 and the phosphorylation of Rec8 at S449 and S450 are necessary and sufficient events for protecting Rec8 cohesin during meiosis II. The absence of either event leads to deprotection at meiosis II.

cell biology↗

The interferon-stimulated gene product HERC5 inhibits human LINE-1 retrotransposition with an ISGylation-independent mechanism

Text AbstractMobilization of long interspersed element-1 (LINE-1 or L1) compromises genome stability and can cause sporadic genetic disease. Accordingly, cells have evolved multiple mechanisms to restrict L1 retrotransposition. Several interferon-stimulated genes (ISGs) that interact with cytoplasmic L1 ribonucleoproteins (RNPs), which contain the L1-encoded proteins ORF1p and ORF2p, have been identified as suppressors of L1 retrotransposition. We previously reported that the ISG protein HECT and RLD domain containing E3 ubiquitin-protein ligase 5 (HERC5) efficiently inhibits L1 retrotransposition. While HERC5 is known to restrict numerous viruses through ISGylation, how HERC5 inhibits L1 remains to be elucidated. Here, we show that HERC5 inhibits L1 retrotransposition through an ISGylation-independent mechanism. HERC5 interacts with L1 RNA and reduces ORF1p levels, a function that requires the ORF1 coding sequence. We further demonstrate that HERC5 decreases L1 translation efficiency and prevents the assembly of L1 RNPs. Our comparative analysis suggests that HERC5 may have acquired its L1-inhibitory function during the evolution of the small HERC family. These findings uncover a previously unidentified mechanism by which an ISG protein recognizes and inhibits L1 and suggest a role for HERC5 as an evolutionarily adapted restriction factor that expands the repertoire of cellular defenses against retrotransposons.

molecular biology↗

G3BP1 Maintains Lysosomal Homeostasis to Limit Tau Aggregate Accumulation

Tau aggregation is a pathological hallmark of a group of neurodegenerative diseases collectively termed tauopathies. While impaired proteostasis is known to drive the accumulation of abnormal proteins, the molecular factors influencing Tau aggregate clearance remain incompletely understood. In this study, we employed a cell-based Tau reporter assay combined with a lentivirus-based pooled CRISPR-Cas9 loss-of-function library to identify genes that regulate Tau aggregation. Genome-wide screening revealed that candidate genes were significantly enriched in categories related to mRNA metabolic processes and autophagy. Among them, we focused on the RNA-binding protein G3BP1, which is functionally associated with both processes. Detailed analyses showed that G3BP1 deficiency promoted the accumulation of Tau aggregates without affecting stress granule formation or autophagic flux. Instead, G3BP1 dysfunction resulted in impaired lysosomal homeostasis, as evidenced by reduced lysosomal abundance and acidification. Furthermore, lysosomal damage induced by L-leucyl-L-leucine methyl ester (LLOMe) enhanced Tau aggregation, particularly in G3BP1-deficient cells. Conversely, pharmacological activation of TFEB by the curcumin analog C1 restored lysosomal function and suppressed Tau aggregate accumulation to wild-type levels. These findings highlight a role of G3BP1 in maintaining lysosomal homeostasis and promoting Tau clearance. Our results further suggest that therapeutic strategies aimed at enhancing lysosomal biogenesis, such as TFEB activation, may hold promise for the treatment of tauopathies.

cell biology↗

Computed Tomography-Derived Elastic Modulus as a Noninvasive Marker of Aortic Wall Integrity: Correlation with Histopathology in the Ascending Aorta

BackgroundAscending aortic aneurysms and dissections are life-threatening conditions often requiring prophylactic surgeries. Current guidelines rely primarily on aortic diameter for intervention; however, many dissections occur without severe dilation. Mechanical properties, such as elastic modulus have emerged as potential predictors of disease progression; nonetheless, noninvasive clinical applications remain limited. This study evaluated the relationship between the computed tomography (CT)-derived elastic modulus of the ascending aorta and the histopathological characteristics of the aortic media. MethodsThirty patients who underwent surgical ascending aorta replacement were included in this study. Preoperative CT was used to calculate the aortic elastic modulus based on geometric measurements and pulse pressure. Resected aortic specimens were subjected to histological and immunohistochemical analyses to assess elastin, collagen, vascular smooth muscle cells (VSMCs), and smoothelin expression. Correlation analyses between the CT-derived elastic modulus and aortic media composition were conducted after adjusting for age and aortic diameter. ResultsThe CT-derived elastic modulus exhibited a significant negative correlation with elastin area and a positive correlation with collagen area. Additionally, a moderate negative correlation was observed between the elastic modulus and elastin fiber waviness. A strong negative correlation was detected between the elastic modulus and the proportion of contractile-type (smoothelin-positive) VSMCs. These findings remained significant after adjusting for confounders. ConclusionsCT-derived elastic modulus of the ascending aorta reflects the underlying pathological changes, including extracellular matrix remodeling and VSMC phenotypic modulation. Noninvasive assessment of aortic mechanical properties may provide novel insights into aortic disease progression and therapeutic responses.

pathology↗

Effects of contrast water therapy on performance, circulatory function, and fatigue in collegiate freestyle swimmers

This study aimed to examine the effects of contrast water therapy (CWT) on recovery following high-intensity interval training in competitive collegiate swimmers. Fifteen male freestyle swimmers (mean age: 19.3 {+/-} 1.1 years) participated in a crossover design, performing five 100-meter maximal-effort intervals under two conditions: CWT and passive rest (PAS). Each session included standardized warm-up, pre- and post-intervention measurements of blood pressure (BP), blood lactate concentration (LA), and subjective fatigue (FAS), followed by a second interval set. CWT consisted of 10 cycles of hot (40-41 {degrees}C, 60 s) and cold (20-21 {degrees}C, 30 s) full-body immersion. Performance metrics--swim time, stroke count, stroke length, and stroke velocity--were recorded during both interval sets. The results showed no significant differences between CWT and PAS in swim performance or blood pressure. However, a significant interaction was observed in stroke length during the first interval set, indicating a potential subtle benefit of CWT on swimming mechanics. Importantly, blood lactate concentrations were significantly lower after CWT compared to PAS (p < .001), and subjective fatigue was also reduced. These findings suggest that CWT promotes metabolic recovery, likely through enhanced peripheral circulation and lactate clearance, without negatively affecting cardiovascular parameters. Although CWT did not enhance immediate performance, its ability to reduce physiological and perceptual fatigue indicates its value in managing accumulated fatigue during training cycles. In conclusion, contrast water therapy appears to be a practical and effective recovery strategy for competitive swimmers, especially in supporting lactate clearance and reducing fatigue following high-intensity training. Future studies should explore optimal immersion protocols and assess long-term benefits across varied performance levels.

physiology↗

Cold-induced suppression of myogenesis in skeletal muscle stem cells contributes to delayed muscle regeneration during hibernation

Mammalian hibernators experience profound cold stress and prolonged physical inactivity during torpor periods; however, it is unclear how skeletal muscle stem cells (satellite cells; SCs) respond to these challenges. In this study, we demonstrate that SCs from a mammalian hibernator, Syrian hamster exhibit remarkable resistance to cold-induced cell death, which is associated with intrinsically higher expression of the antioxidant enzyme GPX4, which likely contributes to the suppression of ferroptosis. RNA-seq analysis revealed widespread downregulation of myogenesis-related genes following cold exposure, which suggests suppression of the myogenic program. Consistently, SCs exposed to cold stress exhibited reduced activation and differentiation capacities upon subsequent rewarming, with an increased number of quiescent Pax7-positive/MyoD-negative cells. Muscle regeneration was markedly delayed during hibernation, accompanied by decreased SC activation and macrophage infiltration, suggesting that cold-induced suppression of SC function underlies limited regenerative capacity in hibernating hamsters. Our results provide insight into the unique physiology of mammalian hibernators: SC viability is preserved, whereas regenerative activity is selectively suppressed during hibernation.

physiology↗

Allometric studies on human- and pig-sized Delphinidae to understand resting metabolic rates with respiratory measurements

Exponential relationships between basal metabolic rate (BMR) and body mass are known in both terrestrial and marine mammals, with elevated BMR in the latter. However, it remains unclear whether the exponential relationship in marine mammals is different from that in terrestrial mammals. Metabolic rates of animals while resting at the water surface (resting metabolic rates: RMRs) were measured by breath-by-breath respirometry in two species of Delphinidae from temperate regions to elucidate the relationship between RMR and body mass in pantropical spotted dolphins (Stenella attenuate) and Rissos dolphins (Grampus griseus) with body masses ranging from 71 to 386 kg. The RMRs of rough-toothed dolphins (83-123 kg), common bottlenose dolphins (143-220 kg), and killer whales (3,364-5,318 kg) were obtained from the literature for allometric analyses. Measured RMRs were 344 {+/-} 39 and 1398 {+/-} 160 ml O2 min-1, respectively, which were 1.2-2.1 times higher than those predicted for similar-sized terrestrial mammals. A linear mixed-effects model showed the allometric mass exponent of 0.65 (95% CI: 0.54-0.76), which was closer to the 2/3-power of body mass than that of the widely observed 3/4-power commonly reported across a broad range of taxa. The new scaling relationship observed in the Delphinidae indicates that larger dolphins require less energy in aquatic environments, which is consistent with the theory of heat loss associated with a narrower surface area relative to larger volumes. This study suggested a different scaling relationship between aquatic and terrestrial mammals.

zoology↗