Biology subjects

Komaki, S.

Publications and source records attributed to Komaki, S..

17 recordsLinked to original sources

bioRxiv2025

Genome-wide mapping of sex-associated autosomal DNA methylation in major blood cell types

Sex differences shape human physiology and disease risk, yet their autosomal epigenetic basis remains incompletely understood. Using whole genome bisulfite sequencing data from iMETHYL database ([~]100 adults) across three purified blood cell types (CD4 T cells, monocytes, neutrophils), we performed comprehensive mapping of cell-type specific sex-associated DNA methylation. Using genome-wide Z-test and confidence-interval method, we identified thousands of autosomal differentially methylated sites (DMSs), the majority of which were cell type-specific. We found that neutrophils exhibited pronounced female-biased hypermethylation, whereas CD4 T cells and monocytes showed more balanced patterns. DMSs were enriched within gene bodies and annotated to neuronal and adhesion functions, with T-cell activation uniquely associated in CD4 T cells. Transcription factor binding site enrichment indicated hematopoietic regulators, suggesting that sex-associated methylation is tightly linked to early developmental processes within blood lineages. Differentially methylated regions overlapped genome-wide association study loci for lifetime smoking, multiple sclerosis, and psoriasis, indicating convergence between sex-associated epigenetic states and genetic susceptibility. Evolutionary analysis revealed limited conservation but identified a conserved intronic CpG within FIGN. This study provides the first genome-wide, cell type-resolved map of autosomal sex-associated DNA methylation in human blood and establishes a foundation for mechanistic and translational studies in sex-informed biology and medicine. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=79 SRC="FIGDIR/small/682299v1_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@18524c0org.highwire.dtl.DTLVardef@2fd8cdorg.highwire.dtl.DTLVardef@142b445org.highwire.dtl.DTLVardef@4949be_HPS_FORMAT_FIGEXP M_FIG C_FIG

genetics↗

bioRxiv2025

Molecular characterization of capulet2 reveals the importance of ANAPHASE PROMOTING COMPLEX 6 maternal expression in endosperm development

Flowering plants are characterized by a double fertilization event, and the fertilized female gametes develop into the endosperm and embryo. Genomic imprinting promotes parental allele-specific gene expression in the endosperm by epigenetic modifications such as DNA methylation. Similarly, gametophyte maternal effects influence gene function in the female gametophyte that affects development of the endosperm and embryo post-fertilization. While most imprinted genes do not display a seed phenotype upon mutation, gametophyte maternal effect mutants are characterized by distorted seed development upon maternal transmission of the mutant allele. Here, we have investigated the gametophyte maternal effect mutant capulet2 (cap2). We have established CAP2 to be encoded by ANAPHASE PROMOTING COMPLEX 6 (APC6), a subunit of the anaphase promoting complex/cyclosome (APC/C). Investigation of further cap2/apc6 alleles revealed female gametophyte maternal effects both in mutant segregation and seed phenotype, and both cap2 and apc6 phenotypes were rescued by an APC6 transgene. Furthermore, we demonstrate that APC6 is a maternally expressed imprinted gene, in line with the observed female gametophyte maternal effect phenotype. To this end, we observed irregular nuclear division of the endosperm coenocyte in cap2/apc6 mutants, suggesting a role for the APC/C in early endosperm development. We further demonstrate that similar endosperm defects are also produced by mutation of APC1, another subunit of the APC/C. Similar to cap2/apc6, APC1 is imprinted and only expressed from the maternal allele, suggesting a maternal bias in the control of APC/C in the developing endosperm.

developmental biology↗

bioRxiv2025

Changes over a 10-year Period in the Distribution Ranges and Genetic Hybridization of Three Pelophylax Pond Frogs in Central Japan

In this study, we focused on interspecial interactions in Central Japan where three closely related pond frog species, Pelophylax nigromaculatus, Pelophylax porosus porosus and Pelophylax porosus brevipodus (two species and two subspecies) are distributed and are in contact and/or overlap. The presence or absence of hybridization between these species was evaluated by comparing the sequences of the mitochondrial DNA Cyt-b (586-bp) and the nuclear gene Tyrosinase (747-bp) regions of each specimen collected. By comparing interspecific hybridization in the same area in both 2010 (119 specimens) and 2020 (152 specimens), we clarified population distributions and corresponding genetic dynamics over a 10-year period; there was no major change in the degree of interspecific hybridization between P. nigromaculatus and P. p. brevipodus in the Ina Basin, but it was revealed that the proportion of "pure"-bred Pelophylax p. brevipodus remained low. On the other hand, in the Matsumoto Basin, interspecific hybridization between P. nigromaculatus and P. p. porosus was evaluated to have progressed slightly. The proportion of "pure"-bred Pelophylax p. porosus declined to less than half, while the proportion of hybrid individuals showed a tendency to increase. Moreover, the dispersal of P. nigromaculatus was confirmed in areas along the Sai River, where only the pure-bred P. p. porosus was previously known to inhabit. Since the three frogs targeted in this study are all "Red List" species that are endangered, continuous monitoring of population structures and genetic dynamics is required.

ecology↗

bioRxiv2025

Studies on Gene Enhancer with KSHV mini-chromatin

Kaposis sarcoma-associated herpesvirus (KSHV) genome contains a terminal repeats (TR) sequence. Previous studies demonstrated that KSHV TR functions as a gene enhancer for inducible lytic gene promoters. Gene enhancers anchor bromodomain-containing protein 4 (BRD4) at specific genomic region, where BRD4 interacts flexibly with transcription-related proteins through its intrinsically disordered domain and exerts transcription regulatory function. Here, we generated recombinant KSHV with reduced TR copy numbers and studied BRD4 recruitment and its contributions to the inducible promoter activation. Reducing the TR copy numbers from 21 (TR21) to 5 (TR5) strongly attenuated viral gene expression during de novo infection and impaired reactivation. The EF1 promoter encoded in the KSHV BAC backbone also showed reduced promoter activity, suggesting a global attenuation of transcription activity within TR5 latent episomes. Isolation of reactivating cells confirmed that the reduced inducible gene transcription from TR-shortened DNA template and is mediated by decreased efficacies of BRD4 recruitment to viral gene promoters. Separating the reactivating iSLK cell population from non-responders showed that reactivatable iSLK cells harbored larger LANA nuclear bodies (NBs) compared to non-responders. The cells with larger LANA NBs, either due to prior transcription activation or TR copy number, supported KSHV reactivation more efficiently than those with smaller LANA NBs. With auxin-inducible LANA degradation, we confirmed that LANA is responsible for BRD4 occupancies on latent chromatin. Finally, with purified fluorescence-tagged proteins, we demonstrated that BRD4 is required for LANA to form liquid-liquid phase-separated dots. The inclusion of TR DNA fragments further facilitated the formation of larger BRD4-containing LLPS in the presence of LANA, similar to the "cellular enhancer dot" formed by transcription factor-DNA bindings. These results suggest that LANA binding to TR establishes an enhancer domain for infected KSHV episomes. The strength of this enhancer, regulated by TR length or transcription memory, determines the outcome of KSHV replication. ImportanceGene enhancers are genomic domains that regulate frequency and duration of transcription burst at gene promoters, with BRD4 playing a critical role in their enhancer functions. KSHV latent mini-chromosome also contains an enhancer domain made with multiple copies of 801 bp identical repeat DNA fragments, terminal repeats. Here, we utilized manipulable mini-scale chromatins with convenient inducible KSHV reactivation to systematically examine the association between enhancer strength and the outcome of inducible promoter activation. This study illustrated the amount of BRD4 recruitment at the enhancer associated with frequencies of BRD4 distribution to the inducible promoters during KSHV reactivation and, therefore, KSHV lytic replication. Recruitment of BRD4 to the TR is specifically regulated by KSHV latent protein, LANA. KSHV evolves clever enhancer elements designed to be regulated by the KSHV own latent protein, LANA.

microbiology↗

bioRxiv2025

Design, development, and evaluation of gene therapeutics specific to KSHV-associated diseases

Kaposis sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposis sarcoma (KS) and two human lymphoproliferative diseases: primary effusion lymphoma and AIDS-related multicentric Castlemans disease. KSHV-encoded latency-associated nuclear antigen (LANA) is expressed in KSHV-infected cancer cells and is responsible for maintaining viral genomes in infected cells. Thus, LANA is an attractive target for therapeutic intervention for KSHV-associated diseases. Here, we devised a cancer gene therapy vector using the adeno-associated virus (AAV), which capitalizes the LANAs function to maintain terminal repeat (TR) containing circular genome in latently infected cells and the TRs enhancer function for KSHV inducible gene promoters. By including two TR copies with a lytic inducible gene promoter (TR2-OriP), we prepared an AAV vector, which expresses an engineered thymidine kinase (TK) selectively in KSHV-infected cells. Ganciclovir (GCV), an anti-herpesvirus drug, effectively eradicated multiple KSHV-infected cells that include iPSC-derived epithelial colony-forming cells, but not non-KSHV-infected counterparts in the presence of AAV8-TR2-OriP-TK. In addition, AAV8-TR2-OriP-TK prevents KSHV virion production from reactivated cells, spreading KSHV infections from reactivated cells. Anti-cancer drugs, known to reactivate KSHV, stimulated TK expression from the vector and, therefore, synergized with AAV8 TR2-OriP-TK to induce KSHV-infected cancer cell death. Finally, the AAV8-TR2-OriP-TK with GCV completely diminished KSHV-infected cancer cells in the xenograft tumor model. The new cancer gene therapeutics should augment the current clinical protocol for KS.

microbiology↗

bioRxiv2024

Functional framework of the kinetochore and spindle assembly checkpoint in Arabidopsis thaliana

The kinetochore, critical for accurate chromosome segregation and genome stability in eukaryotes, comprises the Constitutive Centromere Associated Network (CCAN) and the KMN network. In animals, the CCAN associates with centromeric nucleosomes throughout the cell cycle, while the KMN network assembles at kinetochores during M phase, binding spindle microtubules and serving as a platform for the spindle assembly checkpoint (SAC) complex. Despite conserved functions, kinetochore components vary across organisms. This study investigates the subcellular localization and interaction maps of core kinetochore components in Arabidopsis thaliana, finding that only CENP-C of the four conserved CCAN components localizes to kinetochores, while all KMN components consistently localize to the kinetochore throughout the cell cycle. Immunoprecipitation assays revealed interactions between core kinetochore proteins and regulators involved in DNA replication, histone modification, and chromatin remodeling, suggesting that the kinetochore may also function outside of M phase. Examining interactions between kinetochore and SAC components elucidates plant-specific SAC localization mechanisms providing a functional framework for understanding plant kinetochores and offering new insights into SAC regulation in plants.

cell biology↗

bioRxiv2023

Dimension reduction of microbiome data linked Bifidobacterium to allergic rhinitis

Dimension reduction has been used to visualise the distribution of multidimensional microbiome data, but the composite variables calculated by the dimension reduction methods have not been widely used to investigate the relationship of the human gut microbiome with lifestyle and disease. In the present study, we applied several dimension reduction methods, including principal component analysis (PCA), principal coordinate analysis (PCoA), non-metric multidimensional scaling (NMDS), and non-negative matrix factorization (NMF), to a microbiome dataset from 186 subjects with symptoms of AR and 106 controls. All the dimension reduction methods supported that the enterotype clusters were overlapped in the dimension reduction plots, and that the distribution of microbial data points appeared to be continuous rather than discrete. Comparison of the composite variables calculated from the different dimension reduction methods showed that the characteristics of the composite variables differed between the dimension reduction methods. The second composite variable calculated from PCoA was significantly associated with the intake of several nutrients, including omega-3 polyunsaturated fatty acids, and the risk of AR. The composite variable was also correlated with the relative abundance of Bifidobacterium, and thus, Bifidobacterium was related to the risk of AR and intake of several nutrients through dimension reduction. Our results highlight the usefulness of the dimension reduction methods for investigating the association of microbial composition with lifestyle and disease in clinical research.

microbiology↗

bioRxiv2023

Prolonged Kaposi's Sarcoma-associated Herpesvirus vIL-6 Exposure Enhances Inflammatory Responses by Epigenetic Reprogramming

Kaposi sarcoma-associated herpesvirus (KSHV) inflammatory cytokine syndrome (KICS) is a newly described chronic inflammatory disease condition caused by KSHV infection and is characterized by high KSHV viral load and sustained elevations of serum KSHV-encoded IL-6 (vIL-6) and human IL-6 (hIL-6). KICS has significant immortality and possesses greater risks of having other complications, which include malignancies. Although prolonged inflammatory vIL-6 exposure by persistent KSHV infection is expected to have key roles in subsequent disease development, the biological effects of prolonged vIL-6 exposure remain elusive. Using thiol-Linked Alkylation for the Metabolic Sequencing and Cleavage Under Target & Release Using Nuclease analysis, we studied the effect of prolonged vIL-6 exposure in chromatin landscape and resulting cytokine production. The studies showed that prolonged vIL-6 exposure increased Bromodomain containing 4 (BRD4) and histone H3 lysine 27 acetylation co-occupancies on chromatin, and the recruitment sites were frequently co-localized with poised RNAPII with associated enzymes. Increased BRD4 recruitment on promoters was associated with increased and prolonged NF-KB p65 binding after the lipopolysaccharide stimulation. The p65 binding resulted in quicker and sustained transcription bursts from the promoters; this mechanism increased total amounts of hIL-6 and IL-10 in tissue culture. Pretreatment with the BRD4 inhibitor, OTX015, eliminated the enhanced inflammatory cytokine production. These findings suggest that persistent vIL-6 exposure may establish a chromatin landscape favorable for the reactivation of inflammatory responses in monocytes. This epigenetic memory may explain the greater risk of chronic inflammatory disease development in KSHV-infected individuals. Author summaryCombined and continuous cytokine stimulation triggers transcription reprogramming and is often used for specific tissue development. Continuous vIL-6 exposure occurs in KSHV-infected patients and leads to inflammatory cytokine storm with high mortality. However, possible epigenetic reprogramming by the vIL-6 and its association with pathogenesis remain unclear. Here we demonstrate the establishment of a new chromatin landscape mediated by BRD4 through prolonged vIL-6 exposure which contributes to more robust and rapid transcription and increased cytokines production. Inhibition of BRD4 suppressed this inflammatory response. Our results indicate that targeting the epigenetic effect of viral cytokines may lead to novel therapies for KSHV-induced inflammatory cytokine storms.

microbiology↗

bioRxiv2023

A cytological and functional framework of the meiotic spindle assembly checkpoint in Arabidopsis thaliana

The spindle assembly checkpoint (SAC) is a surveillance mechanism active during metaphase to prevent aneuploidy. The SAC is especially important during meiosis to maintain genome stability over generations and sustain fertility. However, despite its crucial role for reproduction and breeding, little is known about the plant meiotic SAC. Here, we present a cytological and functional framework of the SAC in male meiocytes of Arabidopsis thaliana. Using live-cell imaging, we have dissected the temporal association of SAC components with the kinetochore and have identified the three conserved kinases BMF1, MPS1 and AURORA as crucial regulators of the loading of BMF3 to kinetochores. Functionally characterizing core SAC components, we found that BUB3.3 has a predominant and previously not recognized role in chromosome congression. We suggest that BUB3.3 is involved in efficient kinetochore-microtubule interactions. Furthermore, the meiotic SAC is only active for a limited time under severe microtubule destabilizing conditions leading to the hypothesis that the relaxed nature of the meiotic SAC is a gateway to polyploidization and hence might contribute to genome evolution in plants.

cell biology↗

bioRxiv2022

The cohesin subunit RAD21.2 functions as a recombination silencer of ribosomal DNA arrays

Introductory ParagraphIn many species, including Arabidopsis, heterochromatin often comprises repetitive DNA elements, such as arrays of ribosomal DNA (rDNA). Repetitive regions pose a risk in meiosis since recombination between them can lead to gross genomic rearrangements. However, meiotic recombination at rDNA arrays and other heterochromatic repeat regions is blocked by not well understood mechanisms. Here, we have identified RAD21.2, an -kleisin subunit of cohesin, as a repressor of meiotic recombination at the rDNA regions in Arabidopsis. We show that RAD21.2 co-localizes with heterochromatic factors and is specifically enriched at rDNA repeats, which are devoid of the meiosis specific -kleisin REC8, needed for recombination. Knocking down RAD21.2, we find that REC8 moves into the nucleolus organizing regions (NORs), where we see an increase of RAD51 recombinase foci numbers. Concomitantly, we find extensive rearrangements of the NORs and the offspring of these plants have large variation in rDNA copy numbers demonstrating that RAD21.2 is necessary for transgenerational genome stability. One-Sentence SummaryThe cohesin component RAD21.2 represses meiotic recombination and by that contributes to genome stability over generations.

cell biology↗

bioRxiv2022

Molecular convergence by differential domain acquisition is a hallmark of chromosomal passenger complex evolution

The chromosomal passenger complex (CPC) is a heterotetrameric regulator of eukaryotic cell division, consisting of an Aurora-type kinase and a scaffold built of INCENP, Borealin and Survivin. While most CPC components are conserved across eukaryotes, orthologs of the chromatin reader Survivin have previously only been found in animals and fungi, raising the question of how its essential role is carried out in other eukaryotes. By characterizing proteins that bind to the Arabidopsis Borealin ortholog, we identified BOREALIN RELATED INTERACTOR 1 and 2 (BORI1 and BORI2) as redundant Survivin-like proteins in the context of the CPC in plants. Loss of BORI function is lethal and a reduced expression of BORIs causes severe developmental defects. Similar to Survivin, we find that the BORIs bind to phosphorylated histone H3, relevant for correct CPC association with chromatin. However, this interaction is not mediated by a BIR domain as in previously recognized Survivin orthologs, but by an FHA domain, a widely conserved phosphate-binding module. We propose that the unifying criterion of Survivin-type proteins is a helix that facilitates complex formation with the other two scaffold components, and that the addition of a phosphate-binding domain, necessary for concentration at the inner centromere, evolved in parallel in different eukaryotic groups. Using sensitive similarity searches, we indeed find conservation of this helical domain between animals and plants, and identify the missing CPC component in most eukaryotic supergroups. Interestingly, we also detect Survivin orthologs without a defined phosphate-binding domain, possibly reflecting the situation in the last eukaryotic common ancestor. Significance StatementThe identification of two SURVIVIN-type genes in the model plant Arabidopsis unfolded the evolutionary trajectories of this central chromosomal passenger complex component and led to the identification of SURVIVIN orthologs in almost the entire eukaryotic kingdom. Our work indicates that the central most aspect of the SURVIVIN gene family is a helix to make contact with two other core chromosomal passenger complex members whereas the addition of a phosphate-binding domain shown to bind to chromatin in animals and plants evolved in parallel at least 3 times in different eukaryotic branches.

cell biology↗

bioRxiv2021

Resistance to chemical carcinogenesis induction via a dampened inflammatory response in naked mole-rats

Naked mole-rats (NMRs) have a very low spontaneous carcinogenesis rate, which has prompted scientists to study their cancer resistance mechanisms in order to provide clues for human cancer prevention. Although cancer resistance in NMRs has been intensively investigated at the cellular level, it is still unknown how strongly resistant NMR individuals are to carcinogenesis and how NMR tissues respond to experimental carcinogenesis induction. Here, we show that NMRs exhibit extraordinary resistance against potent chemical carcinogenesis induction through a dampened inflammatory response. Although carcinogenic insults damaged skin cells of both NMRs and mice, NMR skin showed markedly lower immune cell infiltration and reduced induction of inflammatory genes. NMRs harbor loss-of-function mutations in receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like (MLKL) genes, which are essential for necroptosis, a type of necrotic cell death that activates strong inflammation. A necroptosis-inducing stimulus did not increase death of NMR cells. After carcinogenic insults, leakage of the HMGB1, a marker of necrotic cell death, was not increased in NMR skin. In mice, inhibition or knockout of RIPK3 reduced immune cell infiltration and delayed the onset of chemical carcinogenesis. Therefore, necroptosis deficiency may serve as a cancer resistance mechanism via attenuating the inflammatory response in NMRs. Our study sheds light on the importance of a dampened inflammatory response as a non-cell-autonomous cancer resistance mechanism in NMRs. Further in vivo study of the unusual tissue immune system and carcinogenesis resistance of NMRs may lead to the development of new strategies to prevent carcinogenesis in humans. Significance StatementIn contrast with intensive studies of cancer resistance mechanisms in naked mole-rats (NMRs) at the cellular level, little is known about how NMR individuals respond to carcinogenesis induction, despite the fact that cell-to-cell interactions in tissues regulate carcinogenesis in vivo. Here, we demonstrate that NMRs are remarkably resistant to chemical carcinogenesis induction and characteristically have attenuated tissue inflammatory responses to carcinogenic insults. NMRs have loss-of-function mutations in RIPK3 and MLKL genes and thus cannot activate necroptosis, a type of inflammation-inducing cell death. RIPK3 inhibition in mice reduced immune cell infiltration in response to carcinogenic insults and delayed the onset of chemical-induced carcinogenesis. Our results highlight the importance of studies on dampened tissue inflammatory responses to understand cancer resistance of NMRs.

cancer biology↗

bioRxiv2021

B1-type cyclins control microtubule organization during cell division in Arabidopsis

Flowering plants contain a large number of cyclin families, each containing multiple members, most of which have not been characterized to date. Here, we analyzed the role of the B1 subclass of mitotic cyclins in cell cycle control during Arabidopsis development. While we reveal CYCB1;5 to be a pseudogene, the remaining four members were found to be expressed in dividing cells. Mutant analyses showed a complex pattern of overlapping, development-specific requirements of B1-type cyclins with CYCB1;2 playing a central role. The double mutant cycb1;1 cycb1;2 is severely compromised in growth, yet viable beyond the seedling stage, hence representing a unique opportunity to study the function of B1-type cyclin activity at the organismic level. Immunolocalization of microtubules in cycb1;1 cycb1;2 and treating mutants with the microtubule drug oryzalin revealed a key role of B1-type cyclins in orchestrating mitotic microtubule networks. Subsequently, we identified the GAMMA-TUBULIN COMPLEX PROTEIN 3-INTERACING PROTEIN 1 (GIP1/MOZART) as an in vitro substrate of B1-type cyclin complexes and further genetic analyses support an important role in the regulation of GIP1 by CYCB1s.

cell biology↗

bioRxiv2020

Functional analysis of the chromosomal passenger complex in Arabidopsis

A key regulator of cell division in all eukaryotes is the kinase Aurora B, which is encoded by the Aurora 3 (AUR3) gene in Arabidopsis. Aurora B has at least two central functions during cell division. On the one hand, it is essential for the correct, i.e. balanced, segregation of chromosomes in mitosis and meiosis by controlling kinetochore function. On the other hand, Aurora B acts at the division plane, where it is necessary to complete cytokinesis. To accomplish these two spatially distinct functions, Aurora B in animals is guided to its sites of action by Borealin, INCENP, and Survivin that build together with Aurora B the chromosome passenger complex (CPC). However, besides Aurora homologs, only a candidate gene with restricted homology to INCENP has so far been described in Arabidopsis raising the question whether there exists a full complement of the CPC in plants and how Aurora homologs are targeted subcellularly. Here, we have identified and functionally characterized a Borealin homolog, BOREALIN RELATED (BORR), in Arabidopsis. This, together with detailed localization studies including the putative Arabidopsis INCENP homolog, supports the existence of a CPC in plants.

cell biology↗

bioRxiv2019

Patronus is the elusive plant securin, preventing chromosome separation by antagonizing separase

Chromosome distribution at anaphase of mitosis and meiosis is triggered by separase, an evolutionarily conserved protease. Separase must be tightly regulated to prevent the untimely release of chromatid cohesion and disastrous chromosome distribution defects. Securin is the key inhibitor of separase in animals and fungi, but has not been identified in other eukaryotic lineages. Here, we identified PATRONUS1 and PATRONUS2 (PANS1 and PANS2) as the Arabidopsis homologues of securin. Disruption of PANS1 is known to lead to the premature separation of chromosomes at meiosis, and the simultaneous disruption of PANS1 and PANS2 is lethal. Here, we show that PANS1 targeting by the anaphase-promoting-complex is required to trigger chromosome separation, mirroring the regulation of securin. We showed that PANS1 acts independently from Shugosins. In a genetic screen for pans1 suppressors, we identified SEPARASE mutants, showing that PANS1 and SEPARASE have antagonistic functions in vivo. Finally, we showed that the PANS1 and PANS2 proteins interact directly with SEPARASE. Altogether, our results show that PANS1 and PANS2 act as a plant securin. Remote sequence similarity was identified between the plant patronus family and animal securins, suggesting that they indeed derive from a common ancestor. Identification of patronus as the elusive plant securin illustrates the extreme sequence divergence of this central regulator of mitosis and meiosis.

cell biology↗

bioRxiv2018

Live cell imaging of meiosis in Arabidopsis thaliana - a landmark system

Meiosis is essential for sexual reproduction and key to the generation of genetic diversity. To reveal the robustness of meiocyte differentiation and progression through meiosis, we have here established a live cell imaging setup to follow the dynamics of individual male meiocytes in Arabidopsis. Our method is based on the concomitant visualization of microtubules and a meiotic cohesion subunit that allowed following five cellular parameters: cell shape, nucleus position, nucleolus position, chromatin condensation and microtubule array. We find that the states of these parameters are not randomly associated and identify 11 states, referred to as landmarks, that occur much more frequently than closely related states, indicating that they are convergent points of meiotic progression. With this, the here-presented landmark system represents a novel method to analyze meiosis not only allowing a high-temporal dissection but also providing new criteria to evaluate mutants or environmental effects on meiosis.

cell biology↗

bioRxiv2017

The widespread misconception about the Japanese major biogeographic boundary, the Watase line (Tokara gap), revealed by bibliographic and beta diversity analyses

The biota of the Japanese Archipelago is divided into the Palearctic and Oriental realms by the Watase line (Tokara gap), a major biogeographic boundary of Japan. This boundary is generally placed between Akusekijima and Kodakarajima Islands of the Tokara Archipelago, and has been the subject of many biogeographic debates. However, despite being widely accepted, the position of the boundary is doubtful because of a lack of clear evidence. Here, to verify the definition and existence of the biogeographic boundary, we performed a documentary search and beta diversity analysis of multiple taxa. Our documentary search suggested that the Watase line (Tokara gap) should be put between Yakushima/Tanegashima and Amamioshima Islands, but recent references to it clearly deviate from its original definition, and that the placement of the boundary line between Akusekijima and Kodakarajima Islands is based on limited and biased evidence. Our beta diversity analyses found no common biogeographic boundary dividing the Tokara Archipelago into two realms, and showed that the beta diversity pattern of this region is explained by the areas and geographic distances of the islands in agreement with the general principles of island biogeography. The widespread misunderstanding of biogeography in this region could have been perpetuated by preconception and the citation of references without verification. Our study proposes that revision of the biogeography in the Tokara Archipelago, a gap region between the Palearctic and Oriental realms, is necessary and demonstrates the negative influence of preconception in biogeographic debate.

ecology↗