Biology subjects

Ma, K.

Publications and source records attributed to Ma, K..

At least 73 records · Page 4Linked to original sources

bioRxiv2023

Optimisation of asymmetric field pulses for transcranial magnetic stimulation

Transcranial magnetic stimulation (TMS) is a widely-used noninvasive brain stimulation technique through electromagnetic induction. Nowadays commercial TMS devices routinely use conventional biphasic pulses for repetitive TMS protocols and monophasic pulses for single-pulse stimulation. They respectively generate underdamped or damped cosinusoidal electric field pulses that have been proven to be power-inefficient. Recently, symmetric field pulses with near-rectangular electric fields show great potential in terms of energy loss and coil heating, but only limited studies have investigated asymmetric field pulses with different asymmetry levels for the induced electric field waveforms. Thus, this paper optimises and searches a wide range of potential current waveforms with the goal of minimising energy loss and coil heating. The optimised results demonstrated that asymmetric field pulses with near-rectangular electric fields have significantly lower power consumption than conventional ones. These optimised waveforms commonly consist of an initial falling phase followed by rapidly rising and falling phases, trailed by a slow decay to zero. Interestingly, the initial phase has a decay time constant around 260 {micro}s and introduces a pulse-duration-dependent negative bias for the current baseline to minimise the energy loss and coil heating. Thus, it is possible to directly design asymmetric field pulses with various asymmetry ratios by using several prediction equations rather than running optimisation. These results also suggest that introducing such an initial current phase could likely significantly reduce the coil heating of most TMS pulse shapes to improve their power efficiencies.

neuroscience↗

bioRxiv2023

PanGraphViewer: A Versatile Tool to Visualize Pangenome Graphs

Pangenome graphs provide a powerful way to present both sequence and structural features in a given genome relative to the typical features of a population. There are different methods of building pangenome graphs, but few tools are available to visualize them. To address this problem, we developed PanGraphViewer, which is written in Python 3 and runs on all major operating systems. The PanGraphViewer package contains two separate versions: a desktop-based application and a web-based application. Compared to other graph viewers that are initially designed to visualize individual genome graphs, PanGraphViewer targets pangenome graphs and allows the viewing of pangenome graphs built from multiple genomes in either the (reference) graphical fragment assembly format or the variant call format (VCF). Apart from visualization of different types of structural variations (SV), PanGraphViewer also integrates genome annotations with graph nodes to analyze insertions or deletions in a particular gene model. The graph node shapes in PanGraphViewer can represent different types of genomic variations when a VCF file is used. Notably, PanGraphViewer displays subgraphs from a chromosome or sequence segment based on any given coordinates. This function is absent from most genome graph viewers. PanGraphViewer is freely available at https://github.com/TF-Chan-Lab/panGraphViewer to facilitate pangenome analysis.

bioinformatics↗

bioRxiv2023

The clock-modulatory activity of Nobiletin suppresses adipogenesis via Wnt signaling

The circadian clock machinery exerts transcriptional control to modulate adipogenesis and its disruption leads to the development of obesity. Here we report that Nobiletin, a clock amplitude-enhancing molecule, displays anti-adipogenic properties via activating a clock-controlled Wnt signaling pathway that suppresses adipocyte differentiation. Nobiletin augmented clock oscillation with period length shortening in the adipogenic mesenchymal precursor cells and preadipocytes, accompanied by an induction of Bmal1 and core clock components. Consistent with its circadian clock-modulatory activity, Nobiletin inhibited the lineage commitment and terminal differentiation of adipogenic progenitors. Mechanistically, we show that Nobiletin induced the re-activation of Wnt signaling during adipogenic differentiation via transcriptional up-regulation of key components of this pathway. Furthermore, Nobiletin administration in mice markedly reduced adipocyte hypertrophy, leading to a significant loss of fat mass and body weight reduction. Lastly, Nobiletin inhibited the maturation of primary preadipocytes and this effect was dependent on a functional clock regulation. Collectively, our findings uncover a novel activity of Nobiletin in suppressing adipocyte development, implicating its potential therapeutic application in countering obesity and its associated metabolic consequences.

cell biology↗

bioRxiv2022

The more synthetic polymer types pollute the soil, the stronger the growth suppression of invasive alien and native plants

Although most studies on the ecological effects of microplastic pollution focus on a single type of synthetic polymer and a single species, most organisms will be exposed to multiple polymer types simultaneously and the effects may vary among species. To test the effects of polymer diversity on plants, we grew single plants of eight invasive and eight native species in pots with substrate polluted by 0, 1, 3 and 6 types of micro-sized synthetic polymers. We found that the growth suppression by microplastic pollution became stronger with the number of polymer types the plants were exposed to. This tended to be particularly the case for invasive species, whose biomass advantage over natives diminished with the number of polymer types. Our study thus shows that the negative effects of microplastic pollution on plant growth increase with the number of polymer types, and that these effects differ between invasive and native species.

ecology↗

bioRxiv2022

Small-molecule ketone esters treat brain network abnormalities in an Alzheimer's disease mouse model

Altered brain network activity and the resulting hypersynchrony are important for the pathogenesis of cognitive decline in Alzheimers disease (AD) mouse models. Treatments that reduce epileptiform discharges (EDs) or network hyperactivity improve cognition in AD models and humans. We first show that ketogenic diet, but not fasting, rapidly and persistently reduced EDs in the hAPPJ20 Alzheimers mouse model over timescales of hours to months. Then, to identify the specific mechanism of the pleiotropic ketogenic diet, we developed small molecule ketone esters to deliver ketone bodies pharmacologically. Two ketone esters recapitulate ED suppression without other dietary manipulation, over time scales of minutes to one week. This small molecule rescue was associated with reduced low-frequency oscillatory activity similar to the recently reported mechanism of an NMDA receptor modulator molecule in this model. Long-term KD resulted in cognitive improvement and in a sex-stratified analysis also improved survival in the more severely affected hAPPJ20 males. Agents that deliver ketone bodies via small molecules or act on downstream targets may hold therapeutic promise in AD through the mechanism of improved network function and reduced epileptiform activity.

neuroscience↗

bioRxiv2022

Neuronal SNAP-23 scales hippocampal synaptic plasticity and memory

Soluble NSF Attachment protein REceptor (SNARE)-mediated membrane fusion plays a crucial role not only in presynaptic vesicle exocytosis but also in postsynaptic receptor delivery. The latter is considered particularly important for long-term synaptic plasticity and learning and memory, yet underlying mechanisms including the identity of the key SNARE proteins remain elusive. Here, we investigate the role of neuronal Synaptosomal-Associated Protein-23 (SNAP-23) by analyzing pyramidal-neuron specific SNAP-23 conditional knockout (cKO) mice. SNAP-23 immunostaining in postsynaptic spines was effectively decreased in the SNAP-23 cKO hippocampus. Electrophysiological analysis of SNAP-23 deficient neurons using acute hippocampal slices showed normal basal neurotransmission in CA3-CA1 synapses with unchanged AMPA and NMDA currents. Nevertheless, we found theta-burst stimulation induced long-term potentiation (LTP) was vastly diminished in SNAP-23 cKO. Moreover, unlike syntaxin-4 cKO mice in which both basal neurotransmission and LTP decrease manifested changes in a broad set of behavioral tasks, deficits of SNAP-23 cKO is more limited to spatial memory. Our data reveal that neuronal SNAP-23 is selectively crucial for synaptic plasticity and spatial memory without affecting basal glutamate receptor function.

neuroscience↗

bioRxiv2022

Diversity and biogeography of plant leaf bacteria along a latitudinal gradient

Plant-associated microbes are essential for promoting plant well-being, maintaining biodiversity, and supporting ecosystem function. However, little is known about the geographic distribution of plant-microbe symbioses and how they are formed and change along latitudinal gradients. Here we identified leaf bacteria for 328 plant species sampled from 10 forests along a tropical to temperate gradient in China. We analyzed the diversity and composition of plant leaf-associated bacteria and quantified the contributions of hosts, habitats, and neighborhood plants to the plant-bacterial symbiosis. We found a strong latitudinal gradient in leaf bacterial diversity and composition. Bacterial assemblages on leaves were most strongly selected by host plants, and the selection pressure increased with latitude. In contrast, at low latitudes and at large geographical scales multiple factors were found to jointly regulate bacterial community composition. Our result also showed that plant-bacteria symbiotic networks were structured by network hub bacteria taxa with high co-occurrence network centrality, and the abundance of temperate hub taxa was more influenced by host plants than that in tropical forests. For the first time, we documented a previously unrecognized latitudinal gradient in plant-bacterial symbioses that was regulated by a joint effect of multiple factors at low latitudes but mostly by host selection at high latitudes, implying that leaf microbiomes are likely to respond differently to global change along the latitudinal gradient.

ecology↗

bioRxiv2022

Novel tumorigenic FOXM1-PTAFR-PTAF axis revealed by multi-omic profiling in TP53/CDKN2A-double knockout human gastroesophageal junction organoid model

Inactivation of the tumor suppressor genes TP53 and CDKN2A occurs early during gastroesophageal junction (GEJ) tumorigenesis. However, due to a paucity of GEJ-specific disease models, cancer-promoting consequences of TP53 and CDKN2A inactivation at the GEJ have been incompletely characterized. Here we report the development of the first wild-type primary human GEJ organoid model, as well as a CRISPR-edited transformed GEJ organoid model. CRISPR/Cas9 engineering to inactivate TP53 and CDKN2A (TP53/CDKN2AKO) in GEJ organoids induced morphologic dysplasia as well as pro-neoplastic features in vitro and tumor formation in vivo. Notably, lipidomic profiling identified several Platelet-Activating Factors (PTAFs) among the most upregulated lipids in CRISPR-edited organoids; and importantly, PTAF/PTAFR abrogation by siRNA knockdown or a pharmacologic inhibitor (WEB2086) significantly blocked proliferation and other pro-neoplastic features of TP53/CDKN2AKO GEJ organoids in vitro and tumor formation in vivo. In addition, murine xenografts derived from Eso26, an established esophageal adenocarcinoma (EAC) cell line, were suppressed by WEB2086. Mechanistically, TP53/CDKN2A dual inactivation disrupted both the transcriptome and the DNA methylome, likely mediated by key transcription factors, particularly Forkhead Box M1 (FOXM1). Importantly, FOXM1 activated PTAFR transcription by binding to the PTAFR promoter, further amplifying the PTAF-PTAFR pathway. In summary, we established a robust model system for investigating early GEJ neoplastic events, identified crucial metabolic and epigenomic changes occurring during GEJ model tumorigenesis, and discovered a potential cancer-therapeutic strategy, while providing insights into pro-neoplastic mechanisms associated with TP53/CDKN2A inactivation in early GEJ neoplasia. One Sentence SummaryNovel tumorigenic FOXM1-PTAFR-PTAF axis revealed by multi-omic profiling in TP53/CDKN2A-double knockout human gastroesophageal junction organoid model. Graphic Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=172 SRC="FIGDIR/small/491356v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@18dcb8dorg.highwire.dtl.DTLVardef@2ec0d6org.highwire.dtl.DTLVardef@17622b8org.highwire.dtl.DTLVardef@e184bc_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

bioRxiv2022

Actin cytoskeleton signaling via MRTF/SRF entrains circadian clock

The circadian clock is entrained to daily environmental cues. Integrin-linked intracellular signaling via actin cytoskeleton dynamics transduces extracellular matrix interactions to Myocardin-related Transcription Factor (MRTF)/Serum Response Factor (SRF)-mediated transcription. Actin cytoskeleton organization in liver displays diurnal oscillations and SRF-MRTF activity exert transcriptional control to entrain clock. By interrogating disparate upstream events involved in actin cytoskeleton-MRTF-A/SRF signaling cascade, here we show that this signaling cascade transduce cellular niche cues to modulate circadian clock function. Pharmacological inhibitions of MRTF-A/SRF, by disrupting actin polymerization or blocking ROCK kinase, induced period lengthening with augmented clock amplitude, and genetic loss-of-functions of Srf or Mrtf-a mimic that of actin-depolymerizing agents. In contrast, actin-polymerization induced by Jasplakinolide shortened period with attenuated amplitude. In addition, interfering with cell-matrix interaction through blockade of integrin, inhibition of focal adhesion kinase or attenuating matrix rigidity led to reduced period length while enhancing amplitude. Mechanistically, we identify that core clock repressors, Per2, Nr1d1, and Nfil3, are direct transcriptional targets of MRTF-A/SRF in mediating actin dynamic-induced clock response. Collectively, our findings defined an integrin-actin cytoskeleton-MRTF/SRF pathway in linking clock entrainment with extracellular microenvironment that may facilitate cellular adaptation to its physical niche. Summary statementOur study revealed the role of actin cytoskeleton-MRTF/SRF signaling in entraining circadian clock to its extracellular physical niche environment.

cell biology↗

bioRxiv2022

A revised calcium-dependent model of theta-burst transcranial magnetic stimulation

Calcium dependency is presently an essential assumption in modelling the neuromodulatory effects of transcranial magnetic stimulation (TMS). Among the various neuromodulatory TMS protocols, theta-burst stimulation (TBS) at present is the fastest intervention to generate strong effects. A decade ago, Y.Z. Huang et al. developed a first neuromodulation model to explain the bidirectional effects of TBS based on postsynaptic intracellular calcium concentration elevation. We discover, however, that the published computer code is not consistent with the model formulations in the corresponding paper. Further analysis confirms that the computer model with an index confusion was used for fitting the experimental results, running the simulation, and plotting the corresponding figures in the original publication. This paper intends to fix the computer code and additionally create a non-convex optimisation solution for re-calibrating the model. After re-calibration, the revised model outperforms the initial model in accuracy describing the MEP amplitudes of TBS-induced after-effects under specific situations.

neuroscience↗

bioRxiv2022

Circadian clock control of MRTF-SRF signaling suppresses beige adipocyte thermogenic recruitment

The morphological transformation of adipogenic progenitors into mature adipocytes requires dissolution of cytoskeleton driven by progressive loss of MRTF-SRF activity. Circadian clock confers temporal control in adipogenic differentiation, and MRTF-SRF inhibits beige adipocyte development. Here we identify that key components of the actin cytoskeleton-MRTF/SRF signaling cascade are direct transcriptional targets of circadian clock, and a clock-MRTF/SRF regulatory axis suppresses beige adipocyte thermogenic recruitment. Genetic loss- or gain-of-functions of the core clock regulator, Brain and Muscle Arnt-like 1 (Bmal1), altered actin cytoskeleton organization, cell shape and SRF activity. Genes involved in actin dynamic-MRTF-SRF pathway display diurnal expression profiles in beige adipose tissue, with identification of Bmal1 direct transcriptional regulation. Using beige adipocyte-selective genetic models together with pharmacological approaches, we demonstrate that Bmal1 inhibits beige adipogenesis and thermogenic capacity via the MRTF-SRF pathway. Selective ablation of Bmal1 induced beigeing, whereas its targeted overexpression attenuated the beige thermogenic program resulting in obesity. Collectively, our findings define a novel circadian clock control in actin cytoskeleton-MRTF-SRF signaling that suppresses beige adipogenesis to maintain metabolic homeostasis.

cell biology↗

bioRxiv2022

Tree species and genetic diversity increase productivity via functional diversity and trophic feedbacks

Addressing global biodiversity loss requires an expanded focus on multiple dimensions of biodiversity. While most studies have focused on the consequences of plant interspecific diversity, our mechanistic understanding of how the diversity within a given plant species (genetic diversity) affects plant productivity remains limited. Here, we use a tree species x genetic diversity experiment to disentangle the effects of species diversity and genetic diversity, and how they are related to tree functional diversity and trophic feedbacks. Tree species as well as genetic diversity increased tree productivity via increased tree functional diversity, reduced soil fungal diversity and marginally reduced herbivory. The effect of tree genetic diversity on productivity was partly different between tree species monocultures and mixtures: the functional diversity effect resulting from tree genetic diversity was only found in tree species monocultures, but the trophic feedbacks via herbivory were similar in species monocultures and mixtures. Given the complexity of interactions between tree species and genetic diversity, tree functional diversity and trophic feedbacks on productivity, we suggest that both tree species and genetic diversity should be considered in reforestation.

ecology↗

bioRxiv2022

Global Spatial Transcriptome of Macaque Brain at Single-Cell Resolution

Global profile of gene expression at single-cell resolution remains to be determined for primates. Using a recently developed technology ("Stereo-seq"), we have obtained a comprehensive single-cell spatial transcriptome map at the whole-brain level for cynomolgus monkeys, with [~]600 genes per cell for 10 m-thick coronal sections (up to 15 cm2 in size). Large-scale single-nucleus RNA-seq analysis for [~]1 million cells helped to identify cell types corresponding to Stereo-seq gene expression profiles, providing a 3-D cell type atlas of the monkey brain. Quantitative analysis of Stereo-seq data revealed molecular fingerprints that mark distinct neocortical layers and subregions, as well as domains within subcortical structures including hippocampus, thalamus, striatum, cerebellum, hypothalamus and claustrum. Striking whole-brain topography and coordinated patterns were found in the expression of genes encoding receptors and transporters for neurotransmitters and neuromodulators. These results pave the way for cellular and molecular understanding of organizing principles of the primate brain.

cell biology↗

bioRxiv2021

Histone demethylase UTX regulates glioblastoma progression through affecting periostin expression

The histone H3K27 demethylase UTX participates in regulating multiple cancer types. However, less is known about the UTX function in glioblastoma (GBM). This study aims to define the effect of UTX on GBM. GEPIA2 database analysis showed that UTX expression was significantly increased in GBM and inversely correlated with survival. Knockdown UTX inhibited GBM cell proliferation, migration, and invasion while promoting apoptosis. Moreover, knockdown UTX also hampered tumor growth in the heterotopic xenograft model. RNA-seq combined with qRT-PCR and ChIP-qPCR were used to identify the target genes. The results showed that the UTX-mediated genes were strongly associated with tumor progression and the extracellular environment. Protein-protein interaction analysis suggested that periostin (POSTN) interacted with most of the other UTX-mediated genes. POSTN supplement abolished the effect of UTX knockdown in GBM cells. Furthermore, silencing UTX exhibited similar antitumor effect in patient-derived glioblastoma stem-like cells, while UTX functions were partially restored after exposing POSTN. Our findings may reveal a new insight into the onset of gliomagenesis and progression, providing a promising therapeutic strategy for GBM treatment. Bullet PointsUTX correlates with survival in glioblastoma. Silencing UTX decreased the levels of H3K27 methylation in the POSTN gene, thereby suppressing POSTN expression. UTX-mediated POSTN expression is crucial for glioblastoma cell growth and tumorigenesis. O_LIUTX expression is increased in GBM and negatively correlated with survival. C_LIO_LIUTX knockdown influences proliferation and apoptosis in both GBM cells and GSCs. C_LIO_LIThe antitumor effect of UTX knockdown is achieved by suppressing POSTN expression. C_LI

cancer biology↗

bioRxiv2021

Spatiotemporal transcriptome at single-cell resolution reveals key radial glial cell population in axolotl telencephalon development and regeneration

Brain regeneration requires a precise coordination of complex responses in a time- and region-specific manner. Identifying key cell types and molecules that direct brain regeneration would provide potential targets for the advance of regenerative medicine. However, progress in the field has been hampered largely due to limited regeneration capacity of the mammalian brain and understanding of the regeneration process at both cellular and molecular level. Here, using axolotl brain with extrodinary regeneration ability upon injury, and the SpaTial Enhanced REsolution Omics-sequencing (Stereo-seq), we reconstructed the first architecture of axolotl telencephalon with gene expression profiling at single-cell resolution, and fine cell dynamics maps throughout development and regeneration. Intriguingly, we discovered a marked heterogeneity of radial glial cell (RGC) types with distinct behaviors. Of note, one subtype of RGCs is activated since early regeneration stages and proliferates while other RGCs remain dormant. Such RGC subtype appears to be the major cell population involved in early wound healing response and gradually covers the injured area before presumably transformed into the lost neurons. Altogether, our work systematically decoded the complex cellular and molecular dynamics of axolotl telencephalon in development and regeneration, laying the foundation for studying the regulatory mechanism of brain regeneration in the future.

developmental biology↗

bioRxiv2021

Spatiotemporal mapping of gene expression landscapes and developmental trajectories during zebrafish embryogenesis

Vertebrate embryogenesis is a remarkably dynamic process during which numerous cell types of different lineages generate, change, or disappear within a short period of time. A major challenge in understanding this process is the lack of topographical transcriptomic information that can help correlate microenvironmental cues within the hierarchy of cell fate decisions. Here, we employed Stereo-seq, a high-definition spatially resolved transcriptomic technology, to dissect the spatiotemporal dynamics of gene expression and regulatory networks in the developing zebrafish embryos. We profiled 91 embryo sections covering six critical time points during the first 24 hours of development, obtaining a total of 139,391 spots at cellular size ([~]100 m2) with spatial coordinates. Meanwhile, we identified spatial modules and co-varying genes for specific tissue organizations. By performing the integrative analysis of the Stereo-seq and scRNA-seq data from each time point, we reconstructed the spatially resolved developmental trajectories of cell fate transitions and molecular changes during zebrafish embryogenesis. We further investigated the spatial distribution of ligand-receptor pairs for major signaling pathways and identified novel interactions that potentially crosstalk with the Notch signaling pathway during zebrafish development. Our study constitutes a fundamental reference for further studies aiming to understand vertebrate development.

developmental biology↗

bioRxiv2021

Integrin signaling via actin cytoskeleton activates MRTF/SRF to entrain circadian clock

The circadian clock is entrained to daily environmental cues. Integrin-linked intracellular signaling via actin cytoskeleton dynamics transduces cellular niche signals to induce Myocardin-related Transcription Factor (MRTF)/Serum Response Factor (SRF)-mediated transcription. So far, how the integrin-associated signaling cascade may transmit cellular physical cues to entrain circadian clock remains to be defined. Using combined pharmacological and genetic approaches, here we show that the transcription factors mediating integrin to actin cytoskeleton signaling, MRTF-A and SRF, exert direct transcriptional control of core clock components, and that this signaling cascade modulates key properties of clock circadian activity. Pharmacological inhibition of MRTF/SRF activity by disrupting actin polymerization significantly augmented clock amplitude with period shortening, whereas an actin polymerizing compound attenuated oscillation amplitude with period lengthening. Genetic loss-of-function of Srf or Mrtf mimics that of actin-depolymerizing agents, validating the role of actin dynamics in driving clock function. Furthermore, integrin-mediated focal adhesion with extracellular matrix and its downstream signaling modulates the circadian clock, as blockade of integrin, focal adhesion kinase or Rho-associated kinase (ROCK) increased clock amplitude and shortened period length. Mechanistically, we identify specific core clock transcription regulators, Per1, Per2 and Nr1d1, as direct target genes of MRTF-A/SRF. Collectively, our findings uncovered an integrin-actin cytoskeleton-MRTF/SRF signaling cascade in linking clock entrainment to its extracellular microenvironment, which may mediate cellular adaptation to its physical niche. Author SummaryThe circadian clock anticipates and adapts to environmental changes. Interestingly, serum, as a universal clock synchronizing signal, drives intracellular actin cytoskeleton reorganization through modulation of MRTF/SRF activity. However, mechanisms that may transduce extracellular niche signals to circadian clock remains to be defined. We hypothesize that integrin-mediated intracellular signaling to actin cytoskeleton links extracellular microenvironment with MRTF/SRF transcriptional regulation to control clock function. Using small molecules and genetic approaches targeting distinct steps of integrin-actin cytoskeleton-MRTF/SRF signaling cascade, we uncover the effects of this pathway in controlling circadian clock oscillation. We also identify specific core clock regulators as direct gene target genes of MRTF and SRF-mediated transcriptional control. Our study revealed how integrin-mediated cellular interaction with its physical environment influences its intrinsic clock properties through signaling transduction via actin cytoskeleton remodeling, and that this mechanism may facilitate circadian clock adaptation to cellular physical niche.

cell biology↗

bioRxiv2021

Abundant and rare bacterial taxa structuring differently in sediment and water in thermokarst lakes in the Yellow River Source area, Qinghai-Tibet Plateau

Thermokarst lakes are forming from permafrost thaw and severely affected by accelerating climate change. Sediment and water in these lakes are distinct habitats but closely connected. However, our understanding of the differences and linkages between sediment and water in thermokarst lakes remain largely unknow, especially from the perspective of community assembly mechanisms. Here, we examined bacterial communities in sediment and water in thermokarst lakes in the Yellow River Source area, Qinghai-Tibet Plateau. Bacterial taxa were divided to abundant and rare according to their relative abundance, and the Sorensen dissimilarity ({beta}sor) was partitioned into turnover ({beta}turn) and nestedness ({beta}nest). The whole bacterial communities as well as the abundant and rare subcommunities differed substantially between sediment and water, in terms of taxonomical composition, -diversity, and {beta}-diversity. Sediment had significantly lower -diversity indexes but higher {beta}-diversity than water. Abundant taxa had significantly higher relative abundances but lower -diversity and {beta}-diversity than rare taxa. Moreover, bacterial communities are predominantly governed by strong turnover processes ({beta}turn/{beta}sor ratio of 0.925). Abundant subcommunities were significantly lower in {beta}turn/{beta}sor ratio compared to rare subcommunities. Bacterial communities in sediment had a significantly higher {beta}turn/{beta}sor ratio than in water. The results suggest that the bacterial communities of thermokarst lakes, especially rare subcommunities or particularly in sediment, might be strongly structured by environmental filtering and geographical isolation, leading to compositional distinct. This integral study increased our current knowledge of thermokarst lakes, enhancing our understanding of the community assembly rules and ecosystem structures and processes of these rapid changing and vulnerable ecosystems.

microbiology↗