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Biology subjects

Haraguchi, T.

Publications and source records attributed to Haraguchi, T..

At least 19 recordsLinked to original sources

Identification of tail-binding proteins of Arabidopsis class VIII myosin ATM1 using TurboID proximity labeling and AlphaFold3

Higher plants possess two classes of myosin molecular motors, class XI and class VIII, both unique to the plant lineage. The diverse cellular functions of class XI myosins, including organelle transport and nuclear positioning, have been elucidated largely through systematic identification of cargo adaptor proteins that bind to their globular tail domains (GTDs). In contrast, no proteome-wide screen for class VIII myosin tail-binding proteins has been reported; the few known interacting proteins were each discovered through studies focused on the binding partner rather than on the myosin itself, leaving the full repertoire of class VIII myosin-associated proteins largely unknown. Here, we employed TurboID-based proximity labeling to systematically identify proteins associated with the GTD of the class VIII myosin ATM1 in Arabidopsis thaliana, as this approach covalently biotinylates neighboring proteins in vivo, enabling their identification even after proteolytic degradation during cell lysis. We identified 233 non-redundant candidate ATM1-proximal proteins. Candidates were prioritized by AlphaFold3-based protein complex structure prediction and validated by co-immunoprecipitation. We identified two ATM1-associated proteins: C3H61/AtTZF5, a tandem zinc finger protein involved in mRNA turnover at processing bodies and stress granules; and SFH7, a Sec14-nodulin domain protein that mediates phosphatidic acid transfer from the endoplasmic reticulum to chloroplasts. These findings provide initial evidence linking ATM1 to proteins involved in post-transcriptional gene regulation and interorganellar lipid transport, raising the possibility of previously unrecognized connections between class VIII myosins and these cellular processes.

plant biology↗

Identification of loop regions as motifs determining cellular and organ chirality in Myosin 1C

Left-right (LR) asymmetry occurs throughout the animal kingdom, from microscopic to macroscopic scales; however, how microscale LR asymmetry (chirality) is integrated into higher-order structural LR asymmetry remains unclear. In Drosophila, the actin motor proteins Myosin1D and Myosin1C impose opposite chirality states on cell shape and intracellular F-actin flow, thereby directing dextral and sinistral morphogenesis, respectively. However, the protein motifs that confer their distinct activities in specifying chiral states have remained unknown. Here, we show that loop motifs within the myosin head domain that form actin-binding sites determine enantiomeric chirality. By swapping these loop motifs between Myosin1D and Myosin1C, we demonstrate that Myosin1D acquires sinistral activity when carrying Myosin1C loops. AlphaFold3 and molecular dynamics analyses reveal differences in loop structure and actin-binding energetics that may account for the contrasting chiral activities of Myosin1D and Myosin1C. Our findings identify specific protein motifs that dictate the handedness of actin flow and organ asymmetry, providing a mechanistic link between molecular interactions and macroscopic left-right patterning.

cell biology↗

Class I myosins direct circumferential F-actin flows to define cell chirality

Eukaryotic cells possess intrinsic chirality in their structure, motility, and intracellular dynamics, which are designated cell chirality. Cell chirality participates in the left-right asymmetric morphogenesis and tissue integrity. However, the mechanisms of cell chirality formation remain elusive. In Drosophila, two evolutionarily conserved myosin I genes, Myosin 1D (Myo1D) and Myosin 1C (Myo1C), respectively, dictate the dextral and sinistral chirality of the cells and body. Here, we reported that Myo1D and Myo1C respectively directed the clockwise and counterclockwise circumferential flow of F-actin in Drosophila macrophages. Both induced the corresponding circular cytoplasm flows and depended on Myosin2 (Myo2). In a modified in vitro motility assay using near-physiological actin concentrations, Myo1D triggered the self-organization of the F-actin ring (chiral F-actin ring) that rotated clockwise; conversely, Myo1C induced the random flow of F-actin. The chiral F-actin ring implied that the F-actin bundle was parallelly and annularly polarized concerning its barbed pointed end. Considering that Myo1D and Myo1C are localized to the dorsal plasma membrane of macrophages, Myo1D and Myo1C might organize the parallelly polarized F-actin in macrophages. Our results suggest that Myo2 might drive the clockwise circumferential flow of F-actin along its parallel and annular polarity induced by Myo1D, which may be a molecular basis of cell and organ chirality.

cell biology↗

Intestinal fructose metabolism/GLP-1/β-cell axis counteracts hyperglycemia after short-term fructose ingestion

Fructose ingestion increases circulating GLP-1 and insulin, yet the specific contributions of these hormonal responses to glycaemic control remain incompletely defined. We hypothesised that fructose metabolism in intestinal L-cells triggers GLP-1 secretion, which then potentiates insulin secretion and counteracts fructose-induced hyperglycaemia. To test this hypothesis, we systematically characterised metabolic responses across multiple mouse strains after 24 h ad libitum fructose ingestion. In both lean (NSY.B6-a/a) and obese diabetic (NSY.B6-Ay/a) mice, fructose elevated plasma insulin, glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP). The insulin response was preserved in GIP receptor-deficient mice (Gipr-/-) but was abolished in proglucagon-deficient mice (Gcg-/-) by pharmacological GLP-1 receptor antagonism, indicating a requirement for GLP-1, but not GIP. Across strains, fructose-induced insulin response correlated with attenuation of post-fructose glycaemia, consistent with insulin being essential for suppressing fructose-induced hyperglycaemia. To explore the mechanism underlying fructose-induced GLP-1 secretion, we combined ATP-sensitive potassium channel-deficient mice (Kcnj11-/-), GLUTag L-cell line, and metabolic tracing of 13C-labelled fructose in freshly isolated intestinal crypts. These complementary approaches support a model in which fructolysis increases the ATP/ADP ratio in L-cells, closes KATP channels, and stimulates GLP-1 secretion. In obese diabetic mice, increased fructolytic flux and a higher ATP/ADP ratio were associated with elevated GLP-1 levels, further corroborating this model. Collectively, our findings indicate that intestinal fructose metabolism drives GLP-1 secretion required to potentiate insulin secretion, thereby establishing a gut-pancreas axis that counter-regulates fructose-induced hyperglycaemia. KEY POINTS SUMMARYO_LIFructose ingestion acutely increases plasma insulin levels, but the underlying mechanisms and physiological significance remain elusive. C_LIO_LIOur study demonstrates that short-term (24h) fructose ingestion in mice elevates both insulin and glucagon-like peptide 1 (GLP-1) levels in the blood, with the plasma insulin response being GLP-1-dependent. C_LIO_LIWe found that fructose metabolism in intestinal L-cells triggered GLP-1 secretion by increasing the ATP/ADP ratio and closing ATP-sensitive K+ channels (KATP channels). C_LIO_LIThis intestinal fructose metabolism/GLP-1/{beta}-cell axis plays a crucial role in preventing fructose-induced hyperglycaemia, an effect that is compromised in obese diabetic mice. C_LIO_LIThese insights highlight the previously unclear metabolic responses following short-term fructose ingestion and their importance in glucose homeostasis. C_LI 1. ABSTRACT FIGURE LEGENDThis study investigated the hormonal effects of short-term fructose consumption in mice, allowing them ad-lib access to fructose solution for 24 h. Fructose metabolism in intestinal L-cells increases the intracellular ATP/ADP ratio, leading to GLP-1 secretion via KATP channel closure and Ca2+ influx. GLP-1 promotes insulin secretion from pancreatic {beta}-cells. The fructose metabolism/GLP-1/insulin pathway is essential for mitigation of fructose-induced hyperglycaemia. Figures were drawn using BioRender.com.

physiology↗

Elucidating Chiral Myosin-Induced Actin Dynamics: From Single Filament Behavior to Collective Structures

The myosin superfamily comprises over 70 classes, each with multiple subclasses, and shows substantial diversity in properties such as velocity, ATPase activity, duty ratio, and directionality. This functional diversity enables the specialized roles of each myosin in various organisms, organs, and cell types. Recent studies have revealed that certain myosins induce chiral curved motions of actin filaments. However, this newly identified property remains largely unexplored. Here, we investigated this chiral motion in vitro using Chara corallina myosin XI (CcXI), which drives fast counterclockwise (CCW) movement of actin filaments. This chiral motion arises from asymmetric displacement at the filaments leading tip, and its curvature depends on the surface density of myosin. Surprisingly, at near-physiological actin concentrations, actin filaments exhibiting chiral curved motion undergo collective motion, spontaneously forming a novel structure--termed the actin chiral ring (ACR)--that exhibits persistent CCW rotation. ACRs display remarkable stability, continuing to rotate at their formation site until ATP is depleted, while maintaining their structure even after rotation ceases. This stability is unprecedented among reported collective motions of cytoskeletal proteins driven by various motors. Our findings demonstrate that myosins with chiral activity can autonomously organize actin filaments into stable, chiral structures through collective motion, providing new insights into actin self-organization by unconventional myosins. This study advances our understanding of the diverse functional roles of unconventional myosins and introduces a new paradigm for cytoskeletal organization. Significance StatementMyosins are motor proteins that move along actin filaments and support various intracellular functions. Recently, some myosins have been found to drive actin filaments along chiral curved paths, but the mechanisms and significance of this behavior remain poorly understood. Here, we analyzed this activity and discovered that it not only drives chiral curved motion of single actin filaments, but also organizes them into stable, unidirectionally rotating ring structures through collective motion. These rings, termed actin chiral rings (ACRs), spontaneously emerge at near-physiological actin concentrations. Our findings uncover a previously unrecognized organizing principle of actin self-assembly driven by myosin with chiral activity and provide a new framework for understanding how cytoskeletal chirality is made.

cell biology↗

The Calmodulin-like proteins, CML13 and CML14 Function as Myosin Light Chains for the Class XI Myosins in Arabidopsis

Myosins are a crucial motor protein associated with the actin cytoskeleton in eukaryotic cells. Structurally, myosins form heteromeric complexes, with smaller light chains such as calmodulin (CaM) bound to isoleucine-glutamine (IQ) domains in the neck region. These interactions facilitate mechano-enzymatic activity. Recently, we identified Arabidopsis CaM-like (CML) proteins CML13 and CML14 as interactors with proteins containing multiple IQ domains, that function as the myosin VIII light chains. This study demonstrates that CaM, CML13, and CML14 specifically bind to the neck region of all 13 Arabidopsis myosin XI isoforms, with some preference among the CaM/CML-IQ domains. Additionally, we observed distinct residue preferences within the IQ domains for CML13, CML14, and CaM. In vitro experiments revealed that recombinant CaM, CML13, and CML14 exhibit calcium-independent binding to the IQ domains of myosin XIs. Furthermore, when co-expressed with MAP65-1-myosin fusion proteins containing the IQ domains of myosin XIs, CaM, CML13, and CML14 co-localize to microtubules. In vitro actin motility assays demonstrated that recombinant CML13, CML14, and CaM function as myosin XI light chains. A cml13 T-DNA mutant exhibited a shortened primary root phenotype that was complemented by the wild-type CML13 and was similar to that observed in a triple myosin XI mutant (xi3KO). Overall, our data indicate that Arabidopsis CML13 and CML14 are novel myosin XI light chains that likely participate in a breadth of myosin XI functions. HighlightMyosin XI proteins play a crucial role in the plant cytoskeleton, but their associated light chains have remained unidentified. Here, we show that calmodulin-like proteins, CML13 and CML14, serve as light chains for myosin XI, similar to their role for myosin VIII proteins

plant biology↗

TRBP regulates poly(I:C)-mediated apoptotic pathway by modulating miRNA biogenesis

Interferon (IFN) response is usually triggered by the invasion of viral RNAs, and is known to suppress RNA silencing triggered by microRNAs (miRNAs). However, the detailed mechanism regulating RNA silencing during IFN response has not been elucidated. We previously reported that a virus sensor protein, LGP2, which is an upregulated protein during IFN response, interacts with an RNA-binding protein, TRBP. Since TRBP is an RNA-binding protein which enhances miRNA biogenesis in collaboration with Dicer, the interaction of TRBP with LGP2 inhibits the interaction with Dicer and suppresses the TRBP-mediated miRNA biogenesis. During Sendai virus infection, we found that the inhibition of miRNA maturation caused by TRBP depletion resulted in the induction of apoptosis. However, the global gene expression network regulated by miRNAs during viral infection is not understood. In this study, we analyzed comprehensive data from RNA-sequencing and small RNA-sequencing during the antiviral response induced by poly(I:C) transfection, and investigated how TRBP regulates expression profiles of miRNAs and the downstream mRNAs. A group of miRNAs, including miRNAs preferably bind to TRBP, were downregulated by poly(I:C) transfection. Although about 60 % of miRNAs were situated in the introns of their host genes, the expression levels of mature miRNAs were not correlated with those of host genes. Therefore, the downregulation of the expression levels of mature miRNAs was considered to be not caused by transcriptional inhibition of host genes but by the inhibition of TRBP-mediated miRNA processing. Target prediction analysis suggested that the downregulated miRNAs in the presence of TRBP but not in the absence of TRBP mainly targeted transcription factors. Furthermore, these transcription factors were included in the regulators of apoptosis- and cell cycle-related factors. Some of these regulators were also predicted to be the direct targets of downregulated miRNAs in the presence of TRBP. Thus, it was revealed that the downregulation of miRNAs in the presence of TRBP regulates the expression of apoptosis- and cell cycle-related genes either directly or indirectly through adjusting the expression levels of transcription factors. These results suggest that TRBP has a pivotal role in the determination of cell fates during viral infection regulating the miRNA-mRNA regulatory networks through modifying miRNA biogenesis.

molecular biology↗

Reconstruction of artificial nuclei with nuclear import activity in living mouse oocytes

The cell nucleus is a dynamic structure repeating disassembly and reformation during mitosis. Reformation of the nucleus is essential for cell proliferation, and therefore, the factors required for nuclear reformation are fundamental for eukaryotes. Although various factors have been identified in in vitro systems using frog egg extracts and in vivo imaging of somatic cells, little is known about the factors required for the formation of functional nuclear structures in living mouse eggs. To identify such factors, we used a reconstruction approach to construct an artificial nucleus around DNA in mouse eggs. T4 phage DNA (166 kbp) was microinjected into living mouse oocytes. Amounts of DNA injected and injection timing were examined to determine the conditions appropriate for the formation of functional nuclei. Microinjection of 100-500 ng/{micro}l DNA during metaphase through telophase of the second meiosis, but not the subsequent interphase, was important for the formation of artificial nucleus. This T4 DNA-derived artificial nucleus had the structure of nuclear lamina and nuclear pore complexes, and nuclear transport activity, similar to natural nuclei. These results suggest that exogenous DNA can form a functional nucleus in mouse oocytes, regardless of the sequence or the source of DNA.

cell biology↗

Orc6 dissociation from chromatin prevents premature loading of MCM at G2 and tetraploid production

DNA replication is tightly regulated to occur only once per cell cycle, as untimely re-initiation can lead to aneuploidy, which is associated with early senescence and cancer. The pre-replication complex (comprising Orc1-6, Cdc6, Cdt1, and MCM) is essential for the initiation of DNA replication, but the dynamics and function of Orc6 during the cell cycle remain elusive. Here, we demonstrate that Orc6 associates with chromatin during G1-phase and dissociates upon S-phase entry. The dissociation of Orc6 from chromatin is dependent on proteasome activity, and inhibition of the proteasome leads to the accumulation of chromatin-bound Orc6, which promotes abnormal MCM loading after S-phase entry without undergoing mitosis in human immortalized hTERT-RPE1 cells. Following release from proteasome inhibition, cells with elevated levels of chromatin-bound Orc6 and MCM proceed to the next replication phase as tetraploid cells. Our findings suggest that the proteasome-dependent dissociation of Orc6 after DNA replication is critical for preventing inappropriate MCM reloading and tetraploid formation.

cell biology↗

Nuclear membrane protein Bqt4 maintains nuclear envelope integrity by recruiting phosphatidic acid

The nuclear envelope (NE) is a permeable barrier that maintains nuclear-cytoplasmic compartmentalization and ensures nuclear function; however, it ruptures in various situations such as mechanical stress and mitosis. Although the protein components for sealing a ruptured NE have been identified, the mechanism by which lipid components are involved in this process remains to be elucidated. Here, we found that an inner nuclear membrane (INM) protein Bqt4 directly interacts with phosphatidic acid (PA) and serves as a platform for NE maintenance in the fission yeast Schizosaccharomyces pombe. The intrinsically disordered region (IDR) of Bqt4, proximal to the transmembrane domain, binds to PA and forms a solid aggregate in vitro. Excessive accumulation of Bqt4 IDR in INM results in membrane overproliferation and lipid droplet formation in the nucleus, leading to centromere dissociation from the NE and chromosome missegregation. Our findings suggest that Bqt4 IDR controls nuclear membrane homeostasis by recruiting PA to the INM, thereby maintaining the structural integrity of the NE.

cell biology↗

Functional Characterization of Calmodulin-like Proteins, CML13 and CML14, as Novel Light Chains of Arabidopsis Class VIII Myosins

Myosins are important motor proteins that associate with the actin cytoskeleton. Structurally, myosins function as heteromeric complexes where smaller light chains, such as calmodulin (CaM), bind to isoleucine-glutamine (IQ) domains in the neck regions to facilitate mechano-enzymatic activity. We recently identified Arabidopsis CaM-like (CML) proteins, CML13 and CML14 as interactors of proteins containing multiple IQ domains, including a member of the myosin VIII class. Here, using in vivo and in vitro assays we demonstrate that CaM, CML13, and CML14 bind the neck region of all four Arabidopsis myosin VIII isoforms. Among ten CML isoforms tested for in planta binding to myosins VIIIs, CaM, CML13, and CML14 gave the strongest signals using in planta split-luciferase protein-interaction assays. In vitro, recombinant CaM, CML13, and CML14 showed specific, high-affinity, calcium-independent binding to the IQ domains of myosin VIIIs. Subcellular localization analysis indicated that CaM, CML13, and CML14 co-localized to plasma membrane-bound puncta when co-expressed with RFP-myosin fusion proteins containing IQ- and tail-domains of myosin VIIIs. In addition, in vitro actin-motility assays using recombinant myosin holoenzymes demonstrated that CaM, CML13, and CML14 function as light chains for myosin VIIIs. Collectively, our data indicate that Arabidopsis CML13 and CML14 are novel myosin VIII light chains. HighlightMyosins are key proteins in the plant cytoskeleton, but the identity of their light chain components is unknown. Here, we show that calmodulin-like proteins function as novel myosin light chains.

plant biology↗

A ubiquitin-proteasome pathway degrades the inner nuclear membrane protein Bqt4 to maintain nuclear membrane homeostasis

Aberrant accumulation of inner nuclear membrane (INM) proteins is associated with deformed nuclear morphology and mammalian diseases. However, the mechanisms underlying the maintenance of INM homeostasis remain poorly understood. In this study, we explored the degradation mechanisms of the INM protein, Bqt4, in the fission yeast Schizosaccharomyces pombe. We have previously shown that Bqt4 interacts with the transmembrane protein Bqt3 at the INM and is degraded in the absence of Bqt3. Here, we revealed that excess Bqt4, unassociated with Bqt3, was targeted for degradation by the ubiquitin-proteasome system localized in the nucleus and Bqt3 antagonized this process. The degradation process involved the Doa10 E3 ligase complex at the INM. Bqt4 is a tail-anchored protein and extraction from the membrane by the Cdc48 complex is required for its degradation. The C-terminal transmembrane domain of Bqt4 is necessary and sufficient for proteasome-dependent protein degradation. Accumulation of Bqt4 at the INM impaired cell viability with nuclear envelope deformation, suggesting that quantity control of Bqt4 plays an important role in nuclear membrane homeostasis. Summary statement Appropriate levels of the inner nuclear membrane protein Bqt4 are maintained by ubiquitin-proteasome-mediated degradation. Aberrant accumulation of Bqt4 disturbs nuclear membrane homeostasis.

cell biology↗

Rec8 cohesin-mediated loop-axis chromatin architecture is required for meiotic recombination

During meiotic prophase, cohesin-dependent axial structures are formed in the synaptonemal complex (SC). However, the functional correlation between these structures and cohesion remains elusive. Here, we examined the formation of cohesin-dependent axial structures in the fission yeast Schizosaccharomyces pombe. This organism forms atypical SCs composed of linear elements (LinEs) resembling the lateral elements of SC but lacking the transverse filaments. Hi-C analysis using a highly synchronous population of meiotic S. pombe cells revealed that the axis-loop chromatin structure formed in meiotic prophase was dependent on the Rec8 cohesin complex. In contrast, the Rec8-mediated formation of the axis-loop structure occurred in cells lacking components of LinEs. To dissect the functions of Rec8, we identified a rec8-F204S mutant that lost the ability to assemble the axis-loop structure without losing cohesion of sister chromatids. This mutant showed defects in the formation of the axis-loop structure and LinE assembly and thus exhibited reduced meiotic recombination. Collectively, our results demonstrate that the Rec8-dependent axis-loop structure provides a structural platform essential for LinE assembly, facilitating meiotic recombination of homologous chromosomes, independently of its role in sister chromatid cohesion.

cell biology↗

Chromatin loading of MCM hexamers is associated with di-/tri-methylation of histone H4K20 toward S phase entry

DNA replication is a key step in initiating cell proliferation. Loading hexameric complexes of minichromosome maintenance (MCM) helicase onto DNA replication origins during the G1 phase is essential for initiating DNA replication. Here, we examined MCM hexamer states during the cell cycle in human hTERT-RPE1 cells using multicolor immunofluorescence-based, single-cell plot analysis, and biochemical size fractionation. Experiments involving cell-cycle arrest at the G1 phase and release from the arrest revealed that a double MCM hexamer was formed via a single hexamer during G1 progression. A single MCM hexamer was recruited to chromatin in the early G1 phase. Another single hexamer was recruited to form a double hexamer in the late G1 phase. We further examined relationship between the MCM hexamer states and the methylation levels at lysine 20 of histone H4 (H4K20) and found that the double MCM hexamer state was correlated with di/trimethyl-H4K20 (H4K20me2/3). Inhibiting the conversion from monomethyl-H4K20 (H4K20me1) to H4K20me2/3 retained the cells in the single MCM hexamer state. Non-proliferative cells, including confluent cells or Cdk4/6 inhibitor-treated cells, also remained halted in the single MCM hexamer state. We propose that the single MCM hexamer state is a halting step in the determination of cell cycle progression.

cell biology↗

Microtubule inhibitors enhance DNA transfection efficiency through autophagy receptor p62/SQSTM1

Ectopic gene expression is an indispensable tool in biology and medicine, but is often limited by the low efficiency of DNA transfection. We previously reported that depletion of the autophagy receptor p62/SQSTM1 enhances DNA transfection efficiency by preventing the degradation of transfected DNA. Therefore, p62 is a potential target for drugs to increase transfection efficiency. To identify such drugs, a non-biased high-throughput screening was applied to over 4,000 compounds from the Osaka University compound library, and their p62-dependency was evaluated. The top-scoring drugs were mostly microtubule inhibitors, such as colchicine and vinblastine, and all of them showed positive effects only in the presence of p62. To understand the p62-dependent mechanisms, the time required for p62-dependent ubiquitination, which is required for autophagosome formation, was examined using polystyrene beads that were introduced into cells as materials that mimicked transfected DNA. Microtubule inhibitors caused a delay in ubiquitination. Furthermore, the level of phosphorylated p62 at S405 was markedly decreased in the drug-treated cells. These results suggest that microtubule inhibitors inhibit p62-dependent autophagosome formation. Our findings demonstrate for the first time that microtubule inhibitors suppress p62 activation as a mechanism for increasing DNA transfection efficiency and provide solutions to increase efficiency.

cell biology↗

Discovery of the fastest myosin, its amino acid sequence, and structural features

Cytoplasmic streaming with extremely high velocity (~70 m s-1) occurs in cells of the characean algae (Chara). Because cytoplasmic streaming is caused by organelle-associated myosin XI sliding along actin filaments, it has been suggested that a myosin XI, which has a velocity of 70 m s-1, the fastest myosin measured so far, exists in Chara cells. However, the previously cloned Chara corallina myosin XI (CcXI) moved actin filaments at a velocity of around 20 m s-1, suggesting that an unknown myosin XI with a velocity of 70 m s-1 may be present in Chara. Recently, the genome sequence of Chara braunii has been published, revealing that this alga has four myosin XI genes. In the work reported in this paper, we cloned these four myosin XIs (CbXI-1, 2, 3, and 4) and measured their velocities. While the velocities of CbXI-3 and CbXI-4 were similar to that of CcXI, the velocities of CbXI-1 and CbXI-2 were estimated to be 73 and 66 m s-1, respectively, suggesting that CbXI-1 and CbXI-2 are the main contributors to cytoplasmic streaming in Chara cells and showing that CbXI-1 is the fastest myosin yet found. We also report the first atomic structure (2.8 [A] resolution) of myosin XI using X-ray crystallography. Based on this crystal structure and the recently published cryo-EM structure of acto-myosin XI at low resolution (4.3 [A]), it appears that the actin-binding region contributes to the fast movement of Chara myosin XI. Mutation experiments of actin-binding surface loop 2 support this hypothesis. Significance statementIt has been suggested for more than 50 years that the fastest myosin in the biological world, with a velocity of 70 m s-1, exists in the alga Chara because cytoplasmic streaming with a velocity of 70 m s-1 occurs in Chara cells. However, a myosin with that velocity has not yet been identified. In this work, we succeeded in cloning a myosin XI with a velocity of 73 m s-1, the fastest myosin so far measured. We also successfully crystallized myosin XI for the first time. Structural analyses and mutation experiments suggest that the central regions that define the fast movement of Chara myosin XI are the actin-binding sites.

cell biology↗

Timing of fruiting rather than topography determines the direction of vertical seed dispersal by mammals and birds

Vertical seed dispersal toward higher or lower altitudes has been recognized as one of the critical processes for plants to escape from climate change. Studies exploring vertical seed dispersal are scarce, preventing the prediction of future vegetation dynamics. In the present study, we show that the timing of fruiting, rather than topography, determines the direction of vertical seed dispersal by mammals and birds across mountains in central Japan. We found strong uphill seed dispersal of summer fruiting cherry and weak downhill seed dispersal of summer-to-autumn fruiting cherry, irrespective of mountains and animals. The ascent or descent of animals, following the altitudinal gradients in food plant phenology in the temperate zone, was considered to be a driver of the biased seed dispersal. We found that megafauna (i.e., bears) intensively dispersed seeds vertically. The results suggest that the timing of fruiting and megafauna strongly affect whether animal-dispersed temperate plants can maintain their populations under climate change.

ecology↗

Turning and twisting motion of chromosomes as an accelerating force to align homologous chromosomes during meiosis

Homologous sets of parental chromosomes must pair during meiosis to produce recombined sets of chromosomes for their progeny. This is accompanied by nuclear oscillatory movements. This study aimed to elucidate the significance of these movements with a model, wherein external force was applied to the oscillating nucleus and via hydrodynamic interactions within the nucleus. Simulations revealed that a major force for aligning homologous chromosomes is length-dependent sorting during chromosomal torsional turning, which occur when the nucleus reverses the direction of its movement.

biophysics↗