Biology subjects

Ni, L.

Publications and source records attributed to Ni, L..

At least 19 recordsLinked to original sources

bioRxiv2026

Structural variants from donor-specific assemblies affect recurrent chromatin contact divergence in humans

Structural variants (SVs) are a major source of human genetic diversity, yet their contribution to three-dimensional (3D) genome organization remains difficult to resolve using a standard reference genome. Here, we integrate haplotype-resolved chromatin interaction maps across 354 human and 12 nonhuman ape haplotypes with matched genome assemblies and long-read transcriptomes to determine how inherited SVs influence chromatin organization. We observe significant improvements in contact mapping, with 13.2% of cis Hi-C contacts showing >25 kbp changes in inferred genomic separation and an additional 2.8% of valid contact pairs recovered when using donor-specific assemblies instead of standard references. We show that haplotype-specific chromatin differences are highly selective rather than pervasive, concentrating within 1,790 recurrent contact difference hotspots associated with a restricted subset of SVs. We identified 2,495 chromatin-structure-associated SVs that are enriched in regulatory genomic contexts and are linked to expression variation. Notably, more than 90% of these SVs are derived in the human lineage, consistent with recent remodeling of regulatory architecture at the population level. These findings highlight the importance of incorporating haplotype diversity from pangenomes into studies of chromatin organization and provide a framework for understanding how inherited genomic differences are linked to functional consequences across populations and evolution.

genomics↗

bioRxiv2026

No benefit of subsampling in ensemble coding

Our visual system compensates for its limited information processing capacity by creating summary representations of stimulus ensembles. A longstanding debate concerns whether summary statistics are computed by integrating information across the entire ensemble or by sampling only a subset of its items. Subsampling is intuitively appealing because 1) integrating over a small subset presumably reduces processing resource expenditure and 2) observer models employing this strategy can effectively reproduce ensemble coding performance. Here, we systematically evaluate both aspects. We first show that the apparent success of subsampling models depends on a problematic assumption: that the sensory encoding noise of each item remains constant as set size increases. This assumption entails that total coding resources, quantified as Fisher information, grow unconstrained with set size. Under the realistic assumption that total coding resources are limited, such that the encoding precision for each item decreases with increasing set size, we demonstrate that an ideal observer integrating the entire ensemble achieves the same accuracy with a strictly smaller total resource budget for every set size. We further show that this resource-constrained full-integration model provides a more parsimonious, yet equally good, account of ensemble coding behavior across multiple existing datasets as well as newly collected data. Our findings call into question the necessity of the subsampling hypothesis, as restricting integration to a subset of ensemble items confers neither a theoretical nor an explanatory benefit over resource-rational full integration.

neuroscience↗

bioRxiv2026

Duration judgments with conflicting audiovisual cues

Previous work showed that observers integrate audiovisual duration cues optimally when cue-conflict is small. Does causal inference lead to a breakdown of audiovisual integration when duration conflicts are large? We addressed this by testing a wide range of duration cue-conflicts. Participants compared the auditory durations of a test and a standard stimulus. Audiovisual durations were consistent in the test stimulus, but differed by seven conflict durations (up to 250 ms) in the standard. Two levels of auditory noise were tested. Auditory duration percepts shifted systematically toward the visual duration, especially with high auditory noise. The shift was proportional to cue-conflict magnitude, inconsistent with causal inference. We compared several models. A heuristic model in which the observer probabilistically switches between the visual and auditory cues was preferred for most participants, although performance differences across models were small. Within the tested conflict range, the forced fusion, causal inference, and probabilistic cue switching models produced overlapping, near-linear shifts as a function of cue-conflict. Model simulations further revealed that given the measured sensory noise, forced fusion and causal inference can be discriminated only with unreasonably large conflicts. Together, while our results suggest that observers do not rely on causal inference when judging auditory durations under our conditions, high sensory encoding noise in auditory duration limits the discriminability of competing computational models.

neuroscience↗

bioRxiv2026

Juvenile influenza can impair myelin development and adult behavior through chemokine signaling in mice

Brain development, especially developmental myelination, continues through young adulthood. Concordantly, children may be particularly vulnerable to neural-immune challenges. To investigate the consequences of major childhood immune challenges, juvenile mice were exposed to respiratory influenza (H1N1) infection. White matter-specific microglial reactivity accompanied by oligodendrocyte loss was evident until two months following infection. Mice exhibited hyperlocomotion and impaired attention, but not anxiety-like behavior, at one month following infection. Linking the oligodendroglial and behavioral deficits, genetic disruption of oligodendrocyte development at the same juvenile timepoint recapitulated this behavioral phenotype. Microglial reactivity and oligodendrocyte numbers normalized by young adulthood. However, myelin development was disrupted, with persistently decreased myelinated axon density and reduced myelin sheath thickness. Hyperlocomotion resolved, but anxiety-related behaviors emerged at two months after infection. At 6 months, anxiety resolved but cognitive deficits persisted. Elevated CSF chemokines and microglial chemokine expression prompted testing the role of the multi-chemokine receptor CCR3. CCR3 inhibition rescued these cellular and behavioral aberrations after juvenile H1N1 infection. Together, these findings underscore the potential for disruption of myelin development and lasting cognitive and neuropsychiatric sequelae following major immune challenges during the juvenile period and highlight chemokine signaling as an important therapeutic target.

neuroscience↗

bioRxiv2026

Population-scale Y chromosome assemblies reveal recurrent remodeling within constrained architectures

The human Y chromosome is among the most structurally dynamic chromosomes in the human genome, yet much of its diversity remains unresolved because of extensive palindromes, ampliconic gene families, satellite-rich heterochromatin and large segmental duplications. What remained unclear was how these diverse forms of variation fit together across the full chromosome, how often similar structures recur in different lineages, and which aspects of organization remain constrained despite rapid sequence turnover. Here, we generated and analyzed 142 nearly complete human Y chromosome assemblies from 17 major haplogroups spanning approximately 180,000 years of evolution, creating a population-scale resource for studying Y chromosome biology and diversity. These assemblies show that structural change on the Y chromosome is recurrent but constrained, even in its most repetitive regions. In the fertility-associated azoospermia factor c (AZFc) region, recurrent inversions, deletions, and complex rearrangements generate a limited repertoire of structural haplotypes. Multicopy ampliconic gene families follow distinct evolutionary paths: DAZ paralogues differ in structural constraint, RBMY evolves within a modular array, and TSPY copy number varies mainly through local expansion and contraction. The centromere and Yq12 heterochromatin vary greatly in size but retain a stable higher-order organization, including a single hypomethylated centromeric core and conserved Yq12 repeat composition and orientation. Methylation across palindromic and ampliconic regions is likewise structured by repeat class, copy order and local architecture. Together, these results provide a population-scale resource for the human Y chromosome and show that its rapid structural evolution is repeatedly funneled into a limited set of architectural outcomes.

genomics↗

bioRxiv2026

Comparative benchmarking of CRISPRi and CasRx in standardized pluripotent stem cell platforms reveals context-dependent knockdown performance

Advances in transcriptome profiling have revealed transcriptomic differences across different cellular states. However, functional interpretation requires precise perturbation tools and experimental frameworks. This study benchmarked two widely used modalities: CRISPR interference (CRISPRi) and Cas13d/CasRx. A standardized workflow was established to generate human pluripotent stem cells (PSCs) with inducible ZIM3-dCas9 or CasRx expression. The cell lines were subjected to flow cytometry, copy number, and immunocytochemical analyses. The knockdown performance was validated via robust OCT4 suppression and the expected downstream effects on pluripotency genes. Time-course measurements indicated that CRISPRi produced faster and stronger repression but slower recovery after inducer withdrawal. In contrast, CasRx yielded slower and typically weaker knockdown with rapid reversibility. Furthermore, a key limitation of CRISPRi was demonstrated using the ATF5-NUP62 locus, wherein CRISPRi could co-repress genes with overlapping promoter regions. In contrast, CasRx avoids these limitations and supports isoform-resolved targeting of circular and alternatively spliced transcripts, albeit with variable efficiency. These results provide practical guidance for selecting complementary knockdown tools to improve the interpretability of transcriptomic function studies. MOTIVATIONAdvances in transcriptome profiling have enabled the detection of subtle cell type-specific differences. However, mechanistic interpretation still depends on perturbation tools that can modulate transcripts with high precision and efficiency. Recent CRISPR-based modalities, CRISPRi and Cas13/CasRx, function as robust and orthogonal methods to achieve the knockdown of specific gene targets. However, a standardized approach for cell line preparation and comparative studies on their relative performances and limitations remains unclear. Consequently, this study presents a standardized workflow for generating cell lines that support high-efficiency knockdown using CRISPRi and CasRx. Moreover, it compares the trade-offs in potency, reversibility, and isoform resolution, along with a practical overview of method-specific pitfalls to guide tool selection and data interpretation in future studies. HIGHLIGHTSO_LIDoxycycline-inducible AAVS1 knock-in human PSC platforms for CRISPRi (ZIM3-dCas9) and CasRx (RfxCas13d) were generated to enable standardized RNA perturbation experiments. C_LIO_LIThe prepared cell lines demonstrated strong OCT4 knockdown, with expected downstream effects on the expression of another pluripotency gene, NANOG. C_LIO_LIA comparison of knockdown characteristics and their reversibility revealed rapid and sustained repression with CRISPRi, whereas slow but rapid recovery was observed with CasRx. C_LIO_LIA CRISPRi-specific off-target effect arising from TSS proximity/overlap (ATF5-NUP62) was identified, whereas CasRx achieved ATF5 knockdown without collateral repression of the neighboring NUP62 gene. C_LIO_LICasRx enables isoform-resolved knockdown of structural isoforms (circHIPK3 vs. linear HIPK3 mRNA) and splice isoforms (RAB6A-iso1 vs. RAB6A-iso2). C_LI

cell biology↗

bioRxiv2026

Empagliflozin alleviates doxorubicin-induced cardiotoxicity by suppressing oxidative stress via modulation of the JNK/Nrf2 signaling pathway

Doxorubicin (DOX) treatment increases the risk of myocardial dysfunction and heart failure, in which oxidative stress plays a central role. Empagliflozin (EMPA) has been shown to benefit heart failure patients, yet its underlying mechanism remains unclear. In this study, we showed that EMPA treatment improved cardiac function, ameliorated structural remodeling, and increased survival in DOX-treated mice. Furthermore, EMPA reduced DOX-induced reactive oxygen species (ROS) overproduction and myocardial injury. Through functional analysis overlapping DIC- and EMPA-regulated genes, we identified the involvement of JNK signaling in addition to redox pathways. Subsequent investigations demonstrated that EMPA restored redox homeostasis by inhibiting JNK activation, reactivating NRF2 and its downstream antioxidant proteins HO-1, NQO1, GPX4, and SOD2 both in vivo and in vitro. These protective effects were abolished by the Nrf2 inhibitor ML385 or the JNK activator anisomycin. Collectively, our findings indicate that EMPA protects against DOX-induced cardiotoxicity by modulating the JNK/Nrf2 signaling and attenuating oxidative stress. This study provides a rationale for further investigation of EMPA as a potential therapeutic strategy for chemotherapy-associated cardiac injury. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=135 SRC="FIGDIR/small/697595v1_ufig1.gif" ALT="Figure 1"> View larger version (24K): org.highwire.dtl.DTLVardef@16743d4org.highwire.dtl.DTLVardef@96495borg.highwire.dtl.DTLVardef@aa343dorg.highwire.dtl.DTLVardef@4ba18c_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

bioRxiv2025

Selective induction by statins of FAM134B-mediated sarcoplasmic reticulum (SR)-phagy degrades the SR calcium pump SERCA1 and contributes to myopathy

Statins, HMG-CoA reductase inhibitors, are the most prescribed medication for lowering low-density lipoprotein cholesterol. Although statin intolerance due to statin-associated muscle symptoms (SAMS) has been a clinically important issue for decades, the molecular mechanisms of statin myopathy remain incompletely understood. To seek to clarify how statins induce myopathy, here we perform transcriptome analysis and identify FAM134B short isoform (FAM134B-S), an endoplasmic reticulum (ER)-phagy receptor, as a statin-inducible gene. FAM134B-S expression is regulated by the mevalonate pathway and sterol regulatory element-binding proteins. We further show that FAM134B plays a critical role in the regulation of skeletal muscle integrity both in the steady-state and statin-treated conditions in human iPS cell-derived myocytes and mice. Mechanistically, FAM134B-S interacts with the sarcoplasmic reticulum (SR) calcium pump SERCA1 and promotes its autophagic degradation. Collectively, our work reveals a hitherto undisclosed mechanism of statin myopathy; blocking the mevalonate pathway induces SERCA1 degradation through FAM134B-mediated SR-phagy, exerting myotoxicity.

pharmacology and toxicology↗

bioRxiv2025

China Autism Brain Imaging Consortium: Charting Brain Growth in Chinese Children with Autism

Autism Spectrum Disorder (ASD) is a lifelong neurodevelopmental condition characterized by atypical brain growth. While advances in neuroimaging and openly sharing large-sample datasets such as the Autism Brain Imaging Data Exchange (ABIDE) have improved understanding of ASD, most studies focus on adolescents and adults, with early brain development-critical for diagnosis and intervention-remaining underexplored. Existing research predominantly involves Western samples, offering limited insight and generalizability into non-Caucasian populations. We introduce the China Autism Brain Imaging Consortium (CABIC) (https://php.bdnilab.com/resources/), a grassroots effort by researchers across the country to aggregate previously collected multi-site structural MRI datasets and phenotypic information from 1,451 autistic children and 1,119 typically developing children, covering an age range from early childhood to school age (1.0 - 12.92 years). Here, we present this resource and depict brain growth charts to push forward a more comprehensive understanding of the brain development in Chinese autism children. We constructed brain growth charts that reveal a developmental shift in autistic children, transitioning from early overgrowth to delayed maturation. Regional analyses identified distinct atypical trajectories across specific brain regions. Individual deviation scores quantified inter-subject variability, characterizing the heterogeneity of brain development in ASD. Comparative analyses between CABIC and ABIDE highlighted differences potentially attributable to ethnicity and culture, advancing our understanding of cross-population neurodevelopmental diversity. CABIC MRI datasets will be shared publicly to foster investigation of the potential neural mechanisms underlying ASD in non-Western populations and support efforts toward precision medicine for autistic individuals across diverse backgrounds.

neuroscience↗

bioRxiv2025

Fibroblast growth factor 21 regulates neuromuscular junctioninnervation through HDAC4 in denervation-induced skeletal muscle atrophy

Skeletal muscles undergo atrophy in response to denervation and neuromuscular diseases. Understanding the mechanisms by which denervation drives muscle atrophy is crucial for developing therapies against neurogenic muscle atrophy. Here, we identify muscle-secreted fibroblast growth factor 21 (FGF21) as a key inducer of atrophy following muscle denervation. In denervated skeletal muscles, FGF21 is uniquely upregulated among the FGF family members and acts in an autocrine/paracrine manner to promote muscle atrophy. Silencing FGF21 in muscle prevents denervation-induced muscle wasting by preserving neuromuscular junction (NMJ) innervation. Conversely, forced expression of FGF21 in muscle reduces NMJ innervation, leading to muscle atrophy. Mechanistically, TGFB1 released by denervated fibro-adipogenic progenitors (FAPs) upregulates FGF21 through the JNK/c-Jun axis, which in turn reduces the cytoplasmic level of histone deacetylase 4 (HDAC4), culminating in muscle atrophy. HDAC4 knockdown abolishes the atrophy-resistant effects observed in FGF21-deficient denervated muscles, resulting in muscle atrophy. Our findings reveal a novel role and heretofore unrecognized mechanism of FGF21 in skeletal muscle atrophy, suggesting that inhibiting muscular FGF21 could be a promising strategy for mitigating skeletal muscle atrophy.

biochemistry↗

bioRxiv2024

Dynamics of efficient ensemble coding

Ensemble coding creates compressed representations of a stimulus array. When discriminating the ensemble average against a reference, however, items in the ensemble with feature values closer to the reference are typically weighed stronger. We have recently shown that this "robust averaging" behavior can be explained as a form of efficient coding, where the sensory encoding precision is dynamically adapted to efficiently represent ensemble stimuli according to their overall distribution relative to a trial-by-trial varying reference. However, the specific mechanisms underlying such dynamic, efficient ensemble coding remain unknown. Here, we demonstrate that the relative timing between the presentation of the reference and the stimulus ensemble strongly affects efficient ensemble coding. We systematically probed participants decision behavior for varying time intervals between the presentation of the ensemble and the reference. We found that efficient ensemble coding was only clearly established when reference and ensemble were simultaneously presented. It was much weaker when the ensemble preceded the reference, and largely absent when the ensemble followed the reference. As captured by our model, reduced efficient ensemble coding thereby coincided with decreased decision accuracy in those asynchronous conditions. Our results indicate that any temporal offset between the ensemble and reference stimuli substantially disrupts the dynamic and efficient allocation of coding resource. This suggests that efficient ensemble coding is not the result of a preparatory attentional process nor due to evidence selection at the decision stage. Rather, it arises from a fast interaction between the simultaneously evoked, sensory representations of reference and ensemble stimuli.

neuroscience↗

bioRxiv2024

Feature-specific divisive normalization improves natural image encoding for depth perception

Vision science and visual neuroscience seek to understand how stimulus and sensor properties limit the precision with which behaviorally-relevant latent variables are encoded and decoded. In the primate visual system, binocular disparity--the canonical cue for stereo-depth perception--is initially encoded by a set of binocular receptive fields with a range of spatial frequency preferences. Here, with a stereo-image database having ground-truth disparity information at each pixel, we examine how response normalization and receptive field properties determine the fidelity with which binocular disparity is encoded in natural scenes. We quantify encoding fidelity by computing the Fisher information carried by the normalized receptive field responses. Several findings emerge from an analysis of the response statistics. First, broadband (or feature-unspecific) normalization yields Laplace-distributed receptive field responses, and narrowband (or feature-specific) normalization yields Gaussian-distributed receptive field responses. Second, the Fisher information in narrowband-normalized responses is larger than in broadband-normalized responses by a scale factor that grows with population size. Third, the most useful spatial frequency decreases with stimulus size and the range of spatial frequencies that is useful for encoding a given disparity decreases with disparity magnitude, consistent with neurophysiological findings. Fourth, the predicted patterns of psychophysical performance, and absolute detection threshold, match human performance with natural and artificial stimuli. The current computational efforts establish a new functional role for response normalization, and bring us closer to understanding the principles that should govern the design of neural systems that support perception in natural scenes.

neuroscience↗

bioRxiv2024

Modeling statin-induced myopathy with human iPSCs reveals that impaired proteostasis underlies the myotoxicity and is targetable for the prevention

Statins, HMG-CoA reductase inhibitors, have been widely prescribed to lower circulating low-density lipoprotein cholesterol levels and reduce the risk of cardiovascular disease. Although statins are well tolerated, statin-associated muscle symptoms (SAMS) are the major adverse effect and cause statin intolerance. Therefore, understanding the molecular mechanisms of SAMS and identifying effective strategies for its prevention are of significant clinical importance; however, both remain unclear. Here we establish a model of statin-induced myopathy (SIM) with human induced pluripotent stem cell (hiPSC)-derived myocytes (iPSC-MCs) and investigate the effect of statins on protein homeostasis (proteostasis) that affects skeletal muscle wasting and myotoxicity. We show that treating hiPSC-MCs with statins induces atrophic phenotype and myotoxicity, establishing a hiPSC-based SIM model. We then examine whether statins impair the balance between protein synthesis and degradation. The results show that statins not only suppress protein synthesis but also promote protein degradation by upregulating the expression of the muscle-specific E3 ubiquitin ligase Atrogin-1 in a mevalonate pathway-dependent manner. Mechanistically, blocking the mevalonate pathway inactivates the protein kinase Akt, leading to the inhibition of mTORC1 and GSK3{beta} but the activation of FOXO1. These changes explain the statin-induced impairment in proteostasis. Finally, we show that pharmacological blockage of FOXO1 prevents SIM in hiPSC-MCs, implicating FOXO1 as a key mediator of SIM. Taken together, this study suggests that the mevalonate pathway is critical for maintaining skeletal muscle proteostasis and identifies FOXO1 as a potential target for preventing SIM.

pharmacology and toxicology↗

bioRxiv2024

Pressorum Sensing: Growth-induced Compression Activates cAMP Signaling in Pseudomonas aeruginosa

Bacteria employ various strategies to coordinate population-level behaviors, with quorum sensing being a well-established mechanism. Here, we report a novel population-level regulatory mechanism in Pseudomonas aeruginosa, which we term pressorum sensing. This mechanism allows bacteria to modulate their collective behavior in response to growth-induced mechanical compression in confined spaces. Using a highly sensitive cAMP biosensor in combination with microfluidics, we demonstrate that when compressive forces reach approximately 30 nN, P. aeruginosa cells rapidly increases intracellular cAMP levels via the Pil-Chp chemosensory system. This response leads to up-regulation of the Type III Secretion System, a key virulence factor. Unlike quorum sensing, which relies on diffusible chemical signals, pressorum sensing utilizes mechanical cues to gauge population density and spatial confinement. In bacterial colonies, this mechanism generates striking spatial patterns of cAMP signaling, including traveling rings that coincide with step-like structures in colony morphology. Our findings reveal a previously unknown link between mechanical compression and bacterial virulence, providing new insights into how P. aeruginosa coordinates population-level responses in confined environments. This work also expands our knowledge of mechanogenetics and opens up new possibilities in synthetic biology and bioengineering applications.

microbiology↗

bioRxiv2024

The insulin / IGF axis is critically important controlling gene transcription in the podocyte.

Signalling to the podocyte via the structurally related insulin receptor (IR) or insulin-like growth factor 1 receptor (IGF1R) is important for podocyte function. This study sought to elucidate the compound role of the insulin/IGF1 axis in podocytes using transgenic mice and cell culture models deficient in both receptors. Podocyte specific IR/IGF1R knockdown mice developed a severe kidney phenotype with albuminuria, glomerulosclerosis and renal failure with death occurring in some mice between 4 and 24 weeks. Simultaneous knockdown of both receptors in cultured podocytes resulted in >50% cell death by 7 days. Proteomic analysis revealed a striking downregulation of spliceosome-related proteins in IR/IGF1R knockdown podocytes with long-read RNA sequence data indicating an increased fraction of transcripts with intron retention/premature termination codons in these cells. Furthermore, phospho-proteomic analysis revealed multiple insulin / IGF1 induced spliceosomal post-translational protein and kinase modifications suggesting dynamic control of this system. This study underlines the importance of podocyte insulin/IGF signalling demonstrating a novel role for this extrinsic hormonal signalling axis in regulating gene transcription in this cell type.

cell biology↗

bioRxiv2024

Immunotherapy-related cognitive impairment after CAR T cell therapy in mice

Persistent central nervous system (CNS) immune dysregulation and consequent dysfunction of multiple neural cell types is central to the neurobiological underpinnings of a cognitive impairment syndrome that can occur following traditional cancer therapies or certain infections. Immunotherapies have revolutionized cancer care for many tumor types, but the potential long-term cognitive sequelae are incompletely understood. Here, we demonstrate in mouse models that chimeric antigen receptor (CAR) T cell therapy for both CNS and non-CNS cancers can impair cognitive function and induce a persistent CNS immune response characterized by white matter microglial reactivity and elevated cerebrospinal fluid (CSF) cytokines and chemokines. Consequently, oligodendroglial homeostasis and hippocampal neurogenesis are disrupted. Microglial depletion rescues oligodendroglial deficits and cognitive performance in a behavioral test of attention and short-term memory function. Taken together, these findings illustrate similar mechanisms underlying immunotherapy-related cognitive impairment (IRCI) and cognitive impairment following traditional cancer therapies and other immune challenges.

neuroscience↗

bioRxiv2024

The Class III peroxidase OsPrx20 is a key regulator of stress response and growth in rice

In plants, reactive oxygen species maintain strictly low intracellular levels that is prerequisite for their function as second messengers. However, abiotic and biotic stresses are also long-term processes, requiring rapid scavenging of excess intracellular ROS. Plant Class III peroxidases, as multifunctional enzymes, are core enzymes in regulating intracellular ROS homeostasis and are key to regulating the complicated signaling network. Here, we found a rice Class III peroxidase OsPrx20 maintains intracellular ROS homeostasis in different conditions. OsPrx20 is a target of Ca2+/calmodulin-dependent protein kinase (OsDMI3) and phosphorylates its Thr-244 site by OsDMI3. Overexpression of OsPrx20 enhances osmotic stress tolerance but reduces blast resistance, while lack of OsPrx20 is opposite, suggesting OsPrx20 positively regulates osmotic stress tolerance but negatively regulates blast resistance in rice. Meanwhile, overexpression of OsPrx20 enlarges spike size and grain fullness, whereas lack of OsPrx20 leads to dwarfism and smaller spike. In ABA signaling, OsPrx20 Thr-244 phosphorylation is specifically dependent on OsDMI3 to reduce the sensitivity of ABA to seed germination and root growth and to enhance osmotic stress tolerance without affecting spike and grain development. Our study reveals an essential regulatory mechanism that directly activates OsPrx20 in ABA signaling, highlighting the multi-functionality of OsPrx20 in different biological processes.

plant biology↗

bioRxiv2024

Improved functions for non-linear sequence comparison using SEEKR

SEquence Evaluation through k-mer Representation (SEEKR) is a method of sequence comparison that utilizes sequence substrings called k-mers to quantify non-linear similarity between nucleic acid species. We describe the development of new functions within SEEKR that enable end-users to estimate p-values that ascribe statistical significance to SEEKR-derived similarities as well as visualize different aspects of k-mer similarity. We apply the new functions to identify chromatin-enriched long noncoding RNAs (lncRNAs) that harbor XIST-like sequence fragments and show that several of these fragments are bound by XIST-associated proteins. We also highlight the best practice of using RNA-Seq data to evaluate support for lncRNA annotations prior to their in-depth study in cell types of interest.

molecular biology↗