Biology subjects

Ou, J.

Publications and source records attributed to Ou, J..

At least 19 recordsLinked to original sources

bioRxiv2026

Long-read MitoScope reveals tissue-resolved somatic mitochondrial variation and landscape of nuclear-embedded mitochondrial sequences

The mitochondrial genome (mtDNA), rich in repeats and prone to nuclear mitochondrial DNA segments (NUMTs), drives somatic mosaicism implicated in cancer, metabolic syndromes, and neurodegeneration, yet short-read sequencing yields incomplete catalogs, mapping artifacts, and false heteroplasmies. Here, we introduce MitoScope, a scalable long-read workflow to assemble mtDNA, perform high-fidelity variant calling, resolve heteroplasmy, and characterize NUMTs in benchmarking tissues from the Somatic Mosaicism Across Human Tissues (SMaHT) Network. MitoScope shows high sensitivity and precision, determines copy number, and uncovers low-frequency variants. We define an age- and tissue-dependent landscape of mtDNA mosaicism, including low-frequency pathogenic heteroplasmies, a bimodal heteroplasmy spectrum shaped by purifying selection, and age-accumulating deletions enriched for microhomology. Parallel profiling of NUMTs identifies high-confidence events with >2-fold more NUMTs than short-read surveys--with evidence of nonrandom trinucleotide contexts at breakpoints. These findings expose pervasive, tissue-resolved somatic mtDNA and NUMT instability with direct relevance for variant interpretation, aging, and human disease.

genomics↗

bioRxiv2026

Donor-specific assemblies enhance somatic structural variant detection in complex genomic regions

Structural variants (SVs) contribute substantially to genomic variation and disease, but detecting somatic SVs (sSVs) remains difficult due to reference bias, mosaicism, and enrichment in repetitive regions. Linear reference genomes, like GRCh38 and CHM13, do not fully capture individual genomic structure, which can obscure true somatic variation. Donor-specific assemblies (DSAs) generated from the same genome where sSVs are being assayed provide a personalized alternative, yet their performance for sSV detection has not been systematically assessed. As part of the Somatic Mosaicism across Human Tissues (SMaHT) Network, we benchmark a DSA for sSV discovery in the COLO829 melanoma cell line with a matched normal sample from the same individual. We compare sSV detection across GRCh38, CHM13, and the COLO829BL_DSA using three different sSV callers (Delly, Severus, and Sniffles2) and sequence data from multiple long-read platforms. The COLO829BL_DSA identifies 1.8-fold more manually validated sSVs than linear references, in regions both shared with GRCh38 and CHM13 and unique to the COLO829BL_DSA. Variants detected only with the COLO829BL_DSA are often found in satellite and other repeat-rich regions that are difficult to resolve using standard references. In addition, several COLO829BL_DSA-specific sSVs are located in genes, some of which are associated with cancer. Overall, these results underscore the utility of DSAs in improving sSV detection.

genomics↗

bioRxiv2025

Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors

Limb loss remains a significant clinical challenge, but regenerative medicine approaches such as gene therapy offer a promising strategy to trigger endogenous regeneration programs. Optimal vector configurations and molecular targets for appendicular skeletal repair are not well defined. Here, we leveraged insights from species with a high endogenous capacity for appendage regeneration to design an enhancer-directed gene delivery platform that functions during mouse digit regeneration, a well characterized model for partial limb regeneration in mammals. Single-cell RNA sequencing of zebrafish caudal fin regeneration, combined with expression data in regenerating salamander limbs and mouse digit tips, implicated the SP family of transcription factors as conserved, epidermally-expressed mediators of appendage regrowth. Null mutants of Sp8 demonstrated impaired limb regeneration in salamanders, while conditional knockout of Sp6 and/or Sp8 in the mouse basal epidermis resulted in defective bony digit tip regeneration, involving an IL-17 mediated osteoclastogenic program. Spatiotemporally focused expression of FGF8, a known target of SP factors, using a zebrafish-derived tissue regeneration enhancer element via adeno-associated viral vectors, could partially rescue digit tip regeneration in SP knockout mice and accelerate digit regeneration in wildtype mice. Our results demonstrate a contextual gene therapy approach to address limb loss based on genes like SP transcription factors conserved across multiple contexts of appendage regeneration. Significance StatementInstructing regeneration of complex structures in mammals remains an unsolved problem. Gene therapy offers a compelling approach to foster endogenous regeneration by delivering therapeutic gene products to specific cells post injury. We identified a conserved regeneration-linked epidermal transcriptional program in mouse digit regeneration centered on the SP6 and SP8 transcription factors, involving inflammatory responses from osteoclasts. We engineered AAVs harboring a zebrafish tissue regeneration enhancer to direct FGF8 expression in the epidermis after amputation. This enhancer directed delivery partially rescued impaired digit regeneration in Sp6 and Sp8 conditional knockout mice and accelerated regrowth in wildtype digits. Our work links developmental signaling to adult regeneration and establishes a modular, injury site specific gene therapy framework that enables new interventions for limb healing.

genetics↗

bioRxiv2025

Live visualization of extracellular matrix dynamics during development and regeneration in zebrafish

Extracellular matrix (ECM) plays fundamental roles in animal development, regeneration, and disease. The difficulty of tagging endogenous matrix proteins in vertebrates has limited the understanding of ECM composition and dynamics in complex tissues. To visualize vertebrate ECM components, we tagged zebrafish Laminin, gamma 1 (Lamc1), Collagen, type I, alpha 2 (Col1a2), and Transforming growth factor, beta-induced (Tgfbi) using C-terminus in-fusion genome editing. Analysis of these knock-in lines revealed distinct expression of each protein in various tissues during development and regeneration. Fluorescent recover after photobleaching (FRAP) analysis further indicated that Lamc1 is stable in fin fold matrix but more dynamic in myoseptal matrix of developing zebrafish, while Col1a2 and Tgfbi are stable matrix components in myosepta. Strikingly, we found that Col1a2-mScarlet protein accumulates at the amputation plane during tailfin regeneration, where it remains concentrated for several days and distant from the regeneration blastema. This "foundation" region also displayed a distinct transcriptome suggesting active and dedicated events at the base of the regenerating appendage. Our resource enables live capture of ECM dynamics that can identify new events in developing and regenerating zebrafish. Summary statementExtracellular matrix resources for zebrafish development and tissue regeneration.

developmental biology↗

bioRxiv2025

Comprehensive benchmarking of somatic single-nucleotide variant and indel detection at ultra-low allele fractions using short- and long-read data

Mosaic mutations in normal tissues occur at low variant allele fractions (VAFs), complicating detection. To benchmark strategies, the SMaHT Network created a cell-line mixture (1:49) and produced ultra-deep whole-genome sequencing using short and long reads (five centers, 180-500x each). We assembled a reference of 44,008 mosaic SNVs and 2,059 Indels, cross-validation between platforms to expose limits of short-read analysis. We also partitioned the genome by mappability to examine the impact of genomic context, added a negative reference set, and accounted for culture-derived mutations. When seven institutions applied eleven algorithms to mixture data, call sets were largely discordant across tools and replicates, partly reflecting stochastic presence of low-VAF mutations in biological replicants. For >2% VAF SNVs, sensitivity and precision approached [~]80% at [≥]300x, with little gain from additional sequencing. This work provides a comprehensive framework for reliable detection of low-VAF mutations in non-cancer tissues and a valuable resource for the community.

bioinformatics↗

bioRxiv2025

A telomere-to-telomere map of somatic mutation burden and functional impact in cancer

Oncogenesis involves widespread genetic and epigenetic alterations, yet the full spectrum of somatic variation genome-wide remains unresolved. We generated a near-telomere-to-telomere (T2T) diploid assembly of a donor paired with deep short- and long-read sequencing of their melanoma. This revealed that 16% of somatic variants occur in sequences absent from GRCh38, with satellite repeats acting as hotspots for UV-induced damage due to sequence-intrinsic mutability and inefficient repair. Centromere kinetochore domains emerged as focal sites of structural, genetic, and epigenetic variation, leading to remodeling of centromere kinetochore binding domains during tumor evolution. Single-molecule telomere reconstructions uncovered cycles of attrition, deletion, and telomerase-mediated extension that shape cancer telomeres. Finally, diploid chromatin maps exposed that copy number alterations and epimutations, rather than point mutations, predominate in rewiring cancer regulatory programs. These findings define the full landscape of a cancers somatic variation and their functional impact, establishing a blueprint for T2T studies of mosaicism.

genomics↗

bioRxiv2025

Development of Replay-DMN Coordination Predicts Entorhinal Grid Codes

Neural replay, the reactivation of experience-related activity patterns during offline periods, has been implicated in organising memories into cognitive maps. However, how replay processes mature through childhood and adolescence remains unclear. Here we studied 106 participants aged 8-25 who learned a hidden two-dimensional (2D) associative structure and then underwent magnetoencephalography (MEG) during a map-based inference task and post-task rest to detect spontaneous replay. We found that during post-task rest, younger individuals relied primarily on replay alone to represent the 2D relationships, whereas older individuals showed increasingly precise timing alignment between replay events and activity in the default mode network (DMN), particularly when replay occurred at the trough of a DMN theta oscillation. Such replay-DMN coupling predicted the strength of a grid-cell-like code in the entorhinal cortex identified in this cohort with fMRI. Furthermore, resting-state fMRI revealed that DMN functional connectivity strengthened with age, in parallel with reduced reliance on replay and more efficient inference performance. These results reveal a developmental progression in which replay shifts from an isolated process in youth to a coordinated DMN mechanism by adulthood. This transition predicts the maturation of grid-like schema representations, shedding light on how children gradually build internal knowledge structures to support flexible inference.

neuroscience↗

bioRxiv2025

Decaying and expanding Erk gradients process memory of skeletal size during zebrafish fin regeneration

Regeneration of an amputated salamander limb or fish fin restores pre-injury size and structure, illustrating the phenomenon of positional memory. Although appreciated for centuries, the identity of position-dependent cues and how they control tissue growth are not resolved. Here, we quantify Erk signaling events in whole populations of osteoblasts during zebrafish fin regeneration. We find that osteoblast Erk activity is dependent on Fgf receptor signaling and organized into millimeter-long gradients that extend from the distal tip to the amputation site. Erk activity scales with the amount of tissue amputated, predicts the likelihood of osteoblast cycling, and predicts the size of regenerated skeletal structures. Mathematical modeling suggests gradients are established by the transient deposition of long-lived ligands that are transported by tissue growth. This concept is supported by the observed scaling of expression of the essential epidermal ligand fgf20a with extents of amputation. Our work provides evidence that localized, scaled expression of pro-regenerative ligands instructs long-range signaling and cycling to control skeletal size in regenerating appendages.

developmental biology↗

bioRxiv2025

Replay builds an efficient cognitive map offline to avoid computation online

How do humans integrate fragmented experiences into a coherent structure that supports novel inferences? Addressing this question requires tracking learning from the very first encounters. Using magnetoencephalography, we recorded human neural activity throughout the full process - from initial learning to inference. Participants first learned one-dimensional, pairwise rank relationships that collectively formed a two-dimensional (2D) conceptual map, and then inferred unobserved relationships. During rest, offline replay integrated piecemeal memories into a coherent 2D representation, predicting the emergence of a grid-cell-like code that reflected a generalizable task schema. This schema reduced the need for effortful computations during subsequent inference. During inference, two types of on-task replay emerged: a fast replay, resembling offline replay and representing the full map, and a slow replay, focused on trial-specific details. Notably, slow replay negatively correlated with both grid-like coding and inference performance. Together, these results suggest that replay builds an efficient cognitive map offline, thereby reducing reliance on deliberate computation online.

neuroscience↗

bioRxiv2025

Human hippocampal ripples predict the alignment of experience to a grid-like schema

Humans create internal cognitive maps that allow us to make inferences beyond direct experience. These maps often rely on hexagonal grid-cell-like neural codes, serving as a schema for two-dimensional (2D) spaces. Yet it remains unclear how new experiences become aligned with this schema, especially in non-spatial contexts. Here, we show that hippocampal ripples - brief bursts of neuronal activity during rest - predict the emergence of grid-like codes in a novel 2D inference task. We recorded intracranial neuronal activity in 42 epilepsy patients as they learned rank relationships among feature objects (for example, objects differing in "magic" or "speed"). After learning, these objects were combined to form "compounds" occupying a 2D conceptual space defined by two feature dimensions. During learning, hippocampal ripple activity increased during pauses between trials, suggesting that ripples integrated newly acquired information offline. Subsequently, ripple activity during post-learning rest predicted the later emergence of grid-like codes in the entorhinal cortex (EC) and medial prefrontal cortex (mPFC), a core region of the default mode network (DMN), when participants inferred unseen relationships among the compounds. Critically, coordination during rest between hippocampal ripples and DMN activity in the mPFC predicted participants ability to infer complex relationships beyond direct memory retrieval. These findings provide the first direct evidence that hippocampal ripples, working with the DMN, align new experiences with a grid-like schema offline, transforming discrete learning events into structured knowledge that supports flexible and adaptive reasoning in human cognition.

neuroscience↗

bioRxiv2024

Development of Non-Spatial Grid-Like Neural Codes Predicts Inference and Intelligence

Piagets theory posits that children develop structured knowledge schemas for inferring and assimilating new information, yet the underlying neural mechanisms remain unclear. In 203 participants aged 8-25 years, we investigated how maturation of a two-dimensional (2D) knowledge map underpins inferential reasoning and knowledge assimilation. Grid-cell-like codes in the entorhinal cortex (EC) strengthened with age, reflecting schema representations in non-spatial conceptual spaces, and were directly linked to improved inferential reasoning. These grid-like codes also supported the medial prefrontal cortex (mPFC) in encoding distance relationships between objects on the 2D map. As participants assimilated new information, they integrated it into existing grid patterns in the EC. Moreover, the maturation of these neural codes predicted real-world intelligence measures, particularly in reasoning abilities. Our findings demonstrate that the development of non-spatial grid-like neural codes offers a mechanistic account of cognitive development, bridging psychological theory with a fundamental cellular representation of cognitive map.

neuroscience↗

bioRxiv2024

Genome-wide CRISPRi-seq identified ferredoxin-NADP reductase FprB as a synergistic target for gallium therapy in Pseudomonas aeruginosa

With the rise of antibiotic-resistant bacteria, non-antibiotic therapies like gallium are increasingly gaining attention. Gallium ions exhibit potent activity against multidrug-resistant bacteria and intravenous gallium nitrite is under phase 2 clinical trials to treat chronic Pseudomonas aeruginosa infections in cystic fibrosis patients. However, its clinical efficacy is constrained by the achievable peak concentration in human tissue. To address this limitation, we applied a genome-wide CRISPR interference approach (CRISPRi-seq), to identify potential synergistic targets with gallium. Through the systemic screening, we classified the essential genes by response time and growth reduction, pinpointing the most vulnerable therapeutic targets in this species. In addition, we identified a highly conserved gene fprB, encoding a ferredoxin-NADP+ reductase, the downregulation of which dramatically sensitized the cells to gallium. Using a null mutant, we confirmed the loss of fprB lowers the minimum inhibitory concentration of gallium from 320 {micro}M to 10 {micro}M and shifted galliums mode of action from bacteriostatic to bactericidal. Further investigation revealed that FprB plays a critical role in modulating oxidative stress induced by gallium, via control of the iron homeostasis and reactive oxygen species accumulation. Deleting fprB also enhanced galliums efficacy against biofilms formation and improved outcomes in murine lung infection model of P. aeruginosa, suggesting FprB as a promising drug target in combination with gallium. Overall, our data showed CRISPRi-seq as a powerful tool for systematic genetic analysis of P. aeruginosa, advancing identification of novel therapeutic targets.

microbiology↗

bioRxiv2023

Disease-specific selective vulnerability and neuroimmune pathways in dementia revealed by single cellgenomics

Summary/AbstractThe development of successful therapeutics for dementias requires an understanding of their shared and distinct molecular features in the human brain. We performed single-nuclear RNAseq and ATACseq in Alzheimer disease (AD), Frontotemporal degeneration (FTD), and Progressive Supranuclear Palsy (PSP), analyzing 40 participants, yielding over 1.4M cells from three brain regions ranging in vulnerability and pathological burden. We identify 35 shared disease-associated cell types and 14 that are disease-specific, replicating those previously identified in AD. Disease-specific cell states represent molecular features of disease-specific glial-immune mechanisms and neuronal vulnerability in each disorder, layer 4/5 intra-telencephalic neurons in AD, layer 2/3 intra-telencephalic neurons in FTD, and layer 5/6 near-projection neurons in PSP. We infer intrinsic disease-associated gene regulatory networks, which we empirically validate by chromatin footprinting. We find that causal genetic risk acts in specific neuronal and glial cells that differ across disorders, primarily non-neuronal cells in AD and specific neuronal subtypes in FTD and PSP. These data illustrate the heterogeneous spectrum of glial and neuronal composition and gene expression alterations in different dementias and identify new therapeutic targets by revealing shared and disease-specific cell states.

neuroscience↗

bioRxiv2023

A muscle hypertrophy-derived myokine reprograms the stromal vascular fractions differentiation towards thermogenic adipocytes in subcutaneous adipose tissue

Skeletal muscle plays a significant role in both local and systemic energy metabolism; however, the cross-talk between skeletal muscle and adipose tissue remains largely unexplored. In this study, we identify the HIF2-Bambi-Thbs4 axis as a critical driver of muscle hypertrophy and metabolic improvement. Deletion of Bambi induces muscle hypertrophy and oxidative switching, thereby enhancing local and systemic metabolism under conditions of rodent chow and high-fat diets (HFD). Other than the metabolic regulation of skeletal muscle hypertrophy, we hypothesize that a portion of this improvement may be attributed to the metabolic reprogramming of the stromal vascular fraction (SVFs) of iWAT, promoting the development of beige adipocytes. Leveraging multi-omics approaches, we establish Thbs4 as a newly identified, muscle hypertrophy-derived myokine that serves as an essential regulator of this metabolic reprogramming. Thbs4 is upregulated in skeletal muscle during hypertrophy and aerobic exercise, localizes to the iWAT membrane, and facilitates the transformation of white adipocytes into beige adipocytes under conditions such as cold exposure, muscle hypertrophy, or aerobic exercise. Moreover, overexpression of Thbs4 elevates its plasma levels and leads to the transformation of white to beige adipocytes, therefore offering long-term protection against HFD-induced metabolic disorders. Conversely, Thbs4 knockout (Thbs4-KO) disrupts the metabolic reprogramming of SVFs and exacerbates metabolic syndromes induced by an HFD, mirroring the observed decline in Thbs4 levels in aged mice. Therefore, our findings underscore Thbs4s potential as both a long-term metabolic protective factor and a therapeutic target for the treatment of metabolic disorders. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=197 HEIGHT=200 SRC="FIGDIR/small/558627v1_ufig1.gif" ALT="Figure 1"> View larger version (63K): org.highwire.dtl.DTLVardef@1178e6org.highwire.dtl.DTLVardef@1184d4eorg.highwire.dtl.DTLVardef@7b592aorg.highwire.dtl.DTLVardef@1b0b03_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIBambi, a direct target gene of HIF2 in skeletal muscle, when deleted, triggers muscle hypertrophy and the transformation of white into beige adipocytes, improving systemic energy metabolism. C_LIO_LIThe metabolic reprogramming of stromal vascular fractions (SVFs) contributes to the observed improvements in energy metabolism and adipocyte hyperplasia. C_LIO_LIThbs4, a novel myokine produced in skeletal muscle during hypertrophy and aerobic exercise, plays a key role in the transformation of white into beige adipocytes. C_LIO_LIOverexpression of Thbs4 provides enduring protection against high-fat diet (HFD)-induced metabolic disorders, demonstrating its potential as a therapeutic target. C_LIO_LIThbs4 deletion abrogates the beneficial metabolic reprogramming of SVFs and exacerbates HFD-induced metabolic syndromes, further underlining its crucial role in metabolic regulation. C_LI

physiology↗

bioRxiv2023

Reduced Reverse Replay in Anxious Individuals Impairs Reward Prediction

Understanding how we learn about the value and structure of our environment is central to neurocognitive theories of many psychiatric and neurological disorders. Learning processes have been extensively studied during performance of behavioural tasks (online learning) but less so in relation to "resting" (offline) states. A candidate mechanism for such offline learning is "replay," the sequential neural reactivation of past experiences. Notably, value-based learning is especially tied to replay unfolding in reverse order relative to the original experience ("backward replay"). Here, we demonstrate the utility of EEG-based neural decoding for investigating offline learning, and relate it to trait anxiety. Participants were first required to infer sequential relationships among task objects by using a learned rule to reorganise their visual experiences into distinct sequences. Afterwards, they observed that the final object in one of the sequences was associated with a monetary reward and then entered a post-value resting state. During this rest, we found evidence of backward replay for reward-linked object sequences. The strength of such replay was negatively associated with trait anxiety and positively predicted an increased behavioural preference for reward-predictive stimuli. We also found that high-trait-anxiety individuals showed inefficient credit assignment irrespective of reward magnitude, indicating that this effect does not merely reflect reduced reward sensitivity. Together, these findings suggest a potential aberrant replay mechanism during offline learning in individuals with high trait anxiety. More broadly, our approach illustrates the potential of EEG for measuring structured neural representations in vivo, with implications for studying cognition across a range of neuropsychiatric and neurological disorders.

neuroscience↗

bioRxiv2023

LCP1 Regulates Cell Motility in Chondrosarcoma and Correlates with Metastatic Potential and Poor Patient Outcomes

Chondrosarcoma (CSA) is the second most common primary malignancy of bone, whose aggressive potential and chemo-resistant nature result in extremely poor outcomes in patients with advanced disease. Grading and prognostication of these tumors remain a significant challenge for pathologists, and medical oncologists have no effective therapies to prevent or treat metastatic disease. In the present study, we sought to explore the pathogenesis and aggressive progression of chondrosarcoma by comparing gene expression differences from metastasizing and non-metastasizing CSA tumors. We hypothesized that metastasizing tumors have inherent differences that may be attributed to the dysregulation of specific oncogenic cell signaling pathways. RNA-Seq analysis from patient-derived low-passage cell lines of metastasizing and non-metastasizing tumors pinpointed the gene LCP1 (lymphocyte cytosolic protein 1) as upregulated in CSA cells from metastasizing tumors. Analysis of a large clinical cohort of CSA demonstrated that increased expression of LCP1 correlated with poor patient survival. In vitro analyses confirmed the ability of LCP1 to promote migration and invasion of CSA cells. These data support the key role of LCP1 on metastatic potential and poor prognosis in CSA. In conclusion, we confirm the ability of LCP1 to drive metastatic behavior and correlate with poor outcomes in patients.

cancer biology↗

bioRxiv2022

FOXC2 marks and maintains the primitive spermatogonial stem cells subpopulation in the adult testis

In adult mammals, spermatogenesis embodies the complex developmental process from spermatogonial stem cells (SSCs) to spermatozoa. At the top of this developmental hierarchy lie a series of SSC subpopulations. Their individual identities as well as the relationships with each other, however, remain largely elusive. Using single-cell analysis and lineage tracing, we discovered both in mice and humans the quiescent adult SSC subpopulation marked specifically by forkhead box protein C2 (FOXC2). All spermatogenic progenies can be derived from FOXC2+ SSCs and the ablation of FOXC2+ SSCs led to the depletion of the undifferentiated spermatogonia pool. During germline regeneration, FOXC2+ SSCs were activated and able to completely restore the process. Germ cell specific Foxc2 knockout resulted in an accelerated exhaustion of SSCs and eventually led to male infertility. Furthermore, FOXC2 prompts the expressions of negative regulators of cell cycle thereby ensures the SSCs reside in quiescence. Thus, this work proposes that the quiescent FOXC2+ SSCs are essential for maintaining the homeostasis and regeneration of spermatogenesis in adult mammals.

developmental biology↗

bioRxiv2022

Bacterial mobility and motility in porous media mimicked by microspheres

Bacterial motion in porous media are essential for their survival, proper functioning, and various applications. Here we investigated the motion of Escherichia coli bacteria in microsphere-mimicked porous media. We observed reduced bacterial velocity and enhanced directional changes of bacteria as the density of microspheres increased, while such changes happened mostly around the microspheres and due to the collisions with the microspheres. More importantly, we established and quantified the correlation between the bacterial trapping in porous media and the geometric confinement imposed by the microspheres. In addition, numerical simulations showed that the active Brownian motion model in the presence of microspheres resulted in bacterial motion that are consistent with the experimental observations. Our study suggested that it is important to distinguish the ability of bacteria to move easily - bacterial mobility - from the ability of bacteria to move independently - bacteria motility. Our results showed that bacterial motility remains similar in porous media, but bacterial mobility was significantly affected by the pore-scale confinement.

biophysics↗