Biology subjects

Amin, R.

Publications and source records attributed to Amin, R..

At least 19 recordsLinked to original sources

bioRxiv2026

Microglia sculpt dopamine receptor-mediated adolescent behaviors in a social experience dependent manner

Adverse childhood experiences like social isolation (SI) contribute to long term negative health outcomes and the development of severe psychiatric disorder. Adolescence is a unique period of coordinated social and motivational system development driven by dopamine (DA) signaling. Microglia, immune cells of the brain, may play a unique role in regulating SI-induced DA system changes and associated behavioral dysfunction. Male microglia refine dopamine D1 receptors (D1rs) in the nucleus accumbens (NAc) of adolescent male rats shaping play behavior. Here we characterized the molecular developmental impacts of postweaning SI from P21-P38, with a resocialization period to P54. We tested the role of microglial engulfment of D1rs in mediating behavioral consequences of SI using neutrophil inhibitory factor (NIF) to block complement-mediated engulfment required for D1r pruning. We found sex specific impacts of SI on brain development and the DA system. In SI males, microglia engulf more NAc D1rs than group housed (GH) controls. Within GH animals, NAc D1r density is positively correlated to play and allogrooming. In SI animals, NAc D1r density is negatively correlated to biting behavior, and is not correlated to play or allogrooming. Pharmacologically inhibiting microglial engulfment of D1r via bilateral NAc NIF injection prevents observed D1r:behavior correlations in GH and SI animals. NIF treatment interacts with SI, exaggerating aggressive-like behavior, showing a role for microglia in regulating aggressive-like behavior via complement pruning in adolescence. Microglia may play a unique role in regulating behavior that drive negative health outcomes in the face of developmental stress, including SI.

neuroscience↗

bioRxiv2026

Mind the gap between functional groups and surface of magnetic nanoparticles for highly specific magnetic-based protein assays in biological medium

Magnetic readout-based assays are compatible with unprocessed biological samples as unbound background molecules do not interfere with magnetic signal. Yet, a true challenge is their poor specificity and susceptibility of magnetic nanoparticles (MNPs) to clusters in complex biological media, hampering their true advancement. Here, we demonstrate that the spatial organization of functional groups at the external periphery of custom magnetic nanoparticles by harnessing ultra-dense double-stranded DNA results in an efficient antibody conjugation with good accessibility toward antigen. By labeling our MNPs with anti-S protein neutralizing IgG antibody, we showcase the detection of S1 subunit of SARS-CoV-2 Spike protein in a wash-free fashion in less than five minutes in nM regime using magnetic particle spectrometer. By mixing our IgG-labelled MNPs with DMEM cell culture (10-20% FBS serum), we sense the S1 proteins in a one-pot fashion with high specificity. Our results show that by having the ultra-dense dsDNA shell on MNPs, the entropic cost of an irreversible protein binding to particle surface is high, thus allowing the formation of dynamic protein corona on the DNA shell that can be replaced with S1 protein with high affinity. When the azide moieties are placed at the close proximity of MNPs by using non-functional dsDNA, antibody conjugation becomes inefficient, to a level not sufficient for S1 protein detection. Our study highlights the importance of spatial organization of functional moieties on the nanoscale on magnetic nanoparticles for highly specific assays in biologically complex media.

biochemistry↗

bioRxiv2026

Protein design to broadly reprogram engineered T cell function

The efficacy of engineered T cell therapies in solid tumors remains limited by T cell dysfunction, driven by complex processes that cannot be easily manipulated via genetic knockouts or overexpression of individual genes. Protein design can create new biological functions that can rewire these consequential cell fate decisions. Here, we introduce OUTLAST Regulators, designed proteins that reprogram critical T cell signaling pathways to enhance functional persistence. These proteins are capable of regulating diverse groups of proteins such as the NR4A family of pro-exhaustion transcription factors, E3 ligases Cbl-b and c-Cbl, and SOCS family proteins. Our designs markedly improve CAR-T and TCR-T performance in vitro and in vivo in stringent solid tumor preclinical models. OUTLAST Regulators are implemented as compact genetic modules compatible with standard viral vectors and cell therapy manufacturing processes, creating a powerful platform for programming new functions into enhanced cell and gene therapies.

synthetic biology↗

bioRxiv2026

The metastasis susceptibility gene RRP1B is a stress-responsive regulator of nuclear RNA processing and splicing in breast cancer

The tumor microenvironment exposes cancer cells to mechanical, thermal, hypoxic, and acidic stresses, yet how cells integrate these signals to remodel RNA processing remains poorly understood. Here, we show that ribosomal RNA Processing 1B (RRP1B), previously characterized as a nucleolar ribosome biogenesis factor and metastasis modifier, functions as a broad-spectrum stress sensor that dynamically repositions among the nuclear envelope, nucleolus, and nuclear speckles (NS). Relocalization is governed by multi-site phosphorylation within intrinsically disordered regions (IDRs): phosphomimetic substitutions promote NS-proximal condensate formation in an RNA-dependent manner, while unphosphorylatable substitutions confine RRP1B to the nucleolus. Under stress, the RRP1B interactome shifts globally, with ribosomal processing partners replaced by pre-mRNA splicing components enriched for NS-resident proteins. RNA immunoprecipitation sequencing (RIP-seq) demonstrates that under basal conditions RRP1B associates with long, intron-rich, nuclear periphery-proximal transcripts, whereas heat shock redirects binding toward shorter, exon-dense transcripts enriched for motifs of serine/arginine-rich (SR) proteins near the NS. RRP1B overexpression nearly abolishes cytoplasmic retained intron accumulation and drives preferential export of specific transcript isoforms in a compartment- and temperature-dependent manner, establishing RRP1B as a regulator of RNA localization fidelity rather than transcriptional output. An RRP1B overexpression signature is most highly activated in basal-like and claudin-low breast tumors, and the RRP1B-associated retained intron splicing program correlates with reduced survival in a tumor-grade-dependent manner. These findings reframe RRP1B as a microenvironmentally sensitive regulator of nuclear RNA processing with direct implications for aggressive breast cancer biology.

Cancer Biology↗

bioRxiv2026

Magnetic DNA Origami Nanorotors

Self-assembled DNA nanostructures show great promise as functional devices, highly configurable materials, and in nanorobotics. Magnetic control can provide a powerful actuation mechanism in a broad range of contexts, since it affords a high-level of external control, it is biocompatible, and orthogonal to chemical or electrical stimuli. Here we demonstrate magnetic molecular nanoactuators by leveraging the unique site-specificity of DNA origami to assemble highly anisotropic magnetic nanocubes on high-aspect ratio DNA origami bundles. We traced and controlled 100s of our DNA origami nanorotors at the single-rotor level and demonstrated their programmable magnetic clamping and controlled rotation under uniform and rotating magnetic fields. By varying the population and inter-particle spacing of the nanocubes, magnetic torque values in the order of 10-100 pN nm are achieved at field strengths < 10 mT. Monte Carlo simulations reveal that assembly of nanocubes on DNA origami rotors leads to collective magnetic properties, with numerically estimated torque values in good agreement with the experiments. Our magnetic nanorotors offer a foundation for biocompatible nanorobotics, as well as high-throughput magnetic force and torque tweezers.

biophysics↗

bioRxiv2026

Distribution-Aware Federated Learning for Diabetes Prediction Using Tabular Clinical Data Under Non-IID and Class-Imbalanced Settings

Federated learning (FL) enables collaborative clinical model training without centralized data sharing, yet its deployment is hindered by statistical heterogeneity (non-IID data) and inherent class imbalance across healthcare institutions. Conventional aggregation strategies such as FedAvg and FedProx weight client updates solely by dataset size, ignoring class distributions and thereby biasing the global model toward the majority class. To address this, we propose Distribution-Aware Federated Learning (DA-FL), which introduces a minority-class amplification factor{phi} k computed as the ratio of a clients local positive class rate to the global positive class rate. Combined with class-weighted cross-entropy loss at the client level, DA-FL forms a two-level correction mechanism that mitigates imbalance without additional data sharing. Experiments on the CDC BRFSS 2021 diabetes dataset (236,378 records across five simulated clients under three non-IID levels) show that DA-FL improves F1-Macro by 18.2% and G-Mean by 26.7% over FedAvg under moderate non-IID conditions, while achieving 31-fold greater F1-Macro stability across 30 communication rounds. These findings demonstrate that DA-FL is an effective and practically deployable solution for federated clinical prediction under realistic non-IID and class-imbalanced settings.

developmental biology↗

bioRxiv2026

The relationship between changes in psychosocial domains with a virtual salsa class and personality, perceived performance and enjoyment

This pre-post-test study investigated 1) pre-post changes in psychosocial domains with a single virtual salsa class; 2) effect sizes relative to an in-person class, and 3) individual factors, including personality, perceived performance, and enjoyment. An experimental group (n=33) of novice dancers 18-30 years old, participated in a single virtual salsa class. Positive and Negative Affect Scale (PAS, NAS), Perceived Stress Scale (PSS), and the Inclusion in Community and Self-Scale (ICS) were administered before and after class. Participants completed the Big Five Inventory-10 (BFI-10) before, and rated their performance and enjoyment (ordinal scale 1-5) after class. Effect sizes were calculated, and pre-post changes were analyzed with Wilcoxon signed-rank tests. Relationships between pre-post changes and individual factors were analyzed with Spearmans rank correlations. PAS, NAS, PSS, and ICS significantly improved and effect sizes were larger than those for an in-person salsa class except for ICS. Change in NAS was negatively correlated with neuroticism. These results suggest that a virtual salsa class may improve mood, stress, and social connection similar to in-person classes and change in mood may be influenced by personality traits such as neuroticism. Understanding the psychosocial effects of virtual dance and the influence of individual factors will facilitate implementation of dance as an accessible rehabilitation intervention to improve psychosocial well-being.

neuroscience↗

bioRxiv2025

Predictors of extinction risk in large tropical forest mammals: from global to local

Studies can only guide conservation if their findings are informative at the scales at which practitioners and policymakers operate. Yet, it is rarely tested whether large-scale studies reach similar conclusions to the smaller-scale studies on which conservation traditionally relies. We examine whether predictors of extinction risk are consistent across global, regional, and local scales, for 210 tropical forest mammal species ([≥] 1 kg) that existed during the last 130,000 years, in 64 tropical forests, across three biogeographical realms. We found consistent predictors of extinction risk (body mass, generation length, diet, brain volume and scansoriality) when analyses differed only in their spatial resolution. However, predictors differed when analyses also varied in their temporal extent. Macroecological findings about extinction risk can, thus, inform conservation at smaller scales, but they risk misidentifying threatened species if differences in temporal extent are not recognised.

ecology↗

bioRxiv2025

GOALS: Gene Ontology Analysis with Layered Shells for Enhanced Functional Insight and Visualization

Gene Ontologies (GOs) are standardized descriptions of gene functions in terms of biological processes, molecular functions, and cellular components, capturing their Parent-Child relationships in a structured framework and advancing cancer biological modeling to provide consistent and meaningful insights into functional genomics analysis. The conventional GO hierarchical structure is defined by human curation experts, with levels determined by the shortest path to the root term. However, grouping GOs poses challenges due to the uneven distribution of gene members within GO terms and inconsistencies in the level of detail across terms at the same GO level. In this work, we introduce Gene Ontology Analysis using Layered Shells (GOALS), a novel tool that discretizes GOAs into optimal layers. GOALS creates scalable GO layers while maintaining a balanced number of genes across GOs in each layer. Unlike existing tools, the GOALS framework organizes GO terms using a bottom-up approach based on their co-membership network, discretizing GOs to achieve an exponential fit with GOs gene member size. Meanwhile, GOALS reveals clusters or supersets reflecting biological relevance by unsupervised clustering of GOs latent projections. In a case study on mouse natural killer (NK) cell development, GOALS identified distinct GO functional clusters with multi-GO layers to reveal multiple levels of detail from specific to abstract contexts to maximize signal discovery and uncover those signals associations with trajectory divergence. More importantly, GOALS enhances enrichment analysis by introducing additional GO stratification and latent GO map that enables more accurate classification of functional differences. GOALS offers a robust and innovative framework for exploring disordered GO clusters, mining GO activities, and analyzing potential GO-GO interplays. By addressing critical challenges in functional genomics, GOALS provides a powerful tool for advancing our understanding of cell heterogeneity and potentially uncovering actionable insights for therapeutic development.

bioinformatics↗

bioRxiv2025

A Single Mutation in TRPC6 Protects Mice from Acute Lung Injury by Regenerating Endothelium

Regenerating vascular endothelium under sepsis, trauma, and viral infections is vital for promoting the resolution of inflammatory diseases such as acute lung injury (ALI). Transient receptor potential canonical (TRPC) channels mediated Ca2+ entry compromises organ functions and survival from lung injury. Through decoding the domain in TRPC6 responsible for vascular injury, we unveiled the intricate molecular mechanisms underlying vascular regeneration in injured tissue. We found that the substitution of isoleucine111 within the Ist ankyrin domain of TRPC6 for its isomer 111leucine (I111L-TRPC6) altered channel localization at the membrane, blocked TRPC6-mediated Ca2+ entry and cation currents without affecting TRPC6 protein expression. Next, we delivered WT-TRPC6 and I111L-TRPC6 to the endothelial cells (ECs) of TRPC6 knockout mice using liposomes and found that while WT-TRPC6 induced lung vascular inflammatory injury and EC death these responses were blocked in lungs expressing I111L-TRPC6 mutant. Instead, the I111L-TRPC6 mutant promoted lung EC proliferation and prevented vascular injury. These responses were recapitulated in a preclinical mouse model of ALI after injection of engineered TRPC6-blocking peptide, suggesting a novel strategy for regenerating anti-inflammatory vascular niche and preventing ALI therapeutically.

cell biology↗

bioRxiv2025

Orally Delivered Milk-Derived Nanovesicles Loaded with Connexin 43 Peptides forTargeted Cardiac Ischemia-Reperfusion Therapy

Extracellular vesicles have emerged as promising nanocarriers for targeted drug delivery, but their therapeutic potential is limited by challenges related to administration route, loading, targeted delivery and production at scale. Here, we report an innovative approach for targeted delivery of therapeutic peptides to injured tissues using milk-derived small extracellular vesicles (mEVs) as an abundant, safe, orally administrable nanoplatform. We demonstrate that a sub-population of mEVs naturally contain Connexin 43 (Cx43) and its Carboxyl-Terminal (CT) polypeptides, which have been shown to play crucial roles in wound healing and tissue repair. Leveraging this intrinsic property, we developed an esterification method to efficiently and uniformly load mEVs with enhanced levels of an exogenous Cx43 CT peptide (CT11 - RPRPDDLEI), as assessed by flow cytometry-based vesicle quantification and mass spectrometry. These engineered mEVs exhibited remarkable injury targeting capabilities, with > 30-fold increases in uptake by injured cells compared to non-wounded cells in vitro and preferential accumulation in wounded tissues in vivo. Notably, CT11-loaded mEVs orally administered after myocardial infarction reduced infarct size by >60% and preserved heart function in a mouse model of ischemia-reperfusion injury. This study represents a significant advance in nanomedicine, demonstrating the utilization of naturally occurring milk-derived extracellular vesicles as an oral delivery system for therapeutic peptides, achieving unprecedented targeting efficiency and efficacy in the treatment of myocardial ischemia-reperfusion injury.

bioengineering↗

bioRxiv2024

eIF4ET regulates meiotic proteome levels to enable oocyte formation and storage

Animals store oocytes in a dormant state for weeks to decades before ovulation. The homeostatic programs oocytes use to endure long-term storage are poorly understood. Using female nematodes as a short-lived model, we found that oocyte formation and storage required IFET-1, the conserved eIF4E-Transporter protein (eIF4ET). IFET-1 co-assembled with CAR-1 (Lsm14) to form micron-scale condensates in stored oocytes, which dissipated after oocyte activation. Depletion of IFET-1 destabilized the stored oocyte proteome, leading to lower translation, a decline in microtubule maintenance proteins, and errors in microtubule organization and meiotic spindle assembly. Deleting individual domains within IFET-1 impaired oocyte storage without affecting oocyte formation. Thus, in addition to establishing a healthy oocyte reserve in young mothers, IFET-1 ensures that correct levels of cytoskeletal proteins are maintained as oocytes age. Human eIF4ET also localized to micron-scale puncta in dormant oocytes in a reproductively healthy patient. Our results clarify the role for eIF4ET in maintaining the oocyte reserve and further support eIF4ET dysfunction as an upstream cause of embryonic aneuploidy and age-related infertility.

developmental biology↗

bioRxiv2024

Loss of NAT10 disrupts enhancer organization via p300 mislocalization and suppresses transcription of genes necessary for metastasis progression.

Acetylation of protein and RNA represent a critical event for development and cancer progression. NAT10 is the only known RNA acetylase that catalyzes the N4-actylcytidine (ac4C) modification of RNAs. Here, we show that the loss of NAT10 significantly decreases lung metastasis in allograft and genetically engineered mouse models of breast cancer. NAT10 interacts with a mechanosensitive, metastasis susceptibility protein complex at the nuclear pore. In addition to its canonical role in RNA acetylation, we find that NAT10 interacts with p300 at gene enhancers. NAT10 loss is associated with p300 mislocalization into heterochromatin regions. NAT10 depletion disrupts enhancer organization, leading to alteration of gene transcription necessary for metastatic progression, including reduced myeloid cell-recruiting chemokines that results in a less metastasis-prone tumor microenvironment. Our study uncovers a distinct role of NAT10 in enhancer organization of metastatic tumor cells and suggests its involvement in the tumor-immune crosstalk dictating metastatic outcomes.

cancer biology↗

bioRxiv2023

Increased spontaneous Ca2+ activity in Cardiac Purkinje cells after myocardial infarction; A consequence of a dramatic shift of SERCA isoforms as potential adaptation to acute ischemia?

BackgroundStudies of Purkinje cells (Pcells) from canine hearts have suggested an increase of Ca2+-release by the sarcoplasmic reticulum (SR) but also reported a potential augmentation of SR-Ca2+-uptake after MI. Abnormal increase of SR-Ca2+-uptake in heart cells is novel and contrasts with the reduction of this function in cells of failing heart. Our study examined the origin of this increased SR-Ca2+-uptake by considering a change in SR-Ca2+ pump (SERCA2) expression in Purkinje fibers (PFs) post MI. MethodsPcells were isolated from canine hearts 48Hrs post MI. Intracellular Ca2+-activity was captured by confocal microscopy. Purkinje-typical Ca2+ events were analyzed to probe the regional Ca2+-dynamics within Pcells. A Purkinje-specific numerical model assisted in the interpretation of Ca2+-anomalies detected in Pcells Ca2+-transients. SR-Ca2+-uptake system was studied by immunofluorescence in Pcells from canine, ovine and human hearts post MI. SERCA protein and gene expressions in PFs and myocardium were measured by Western Blots and RT-qPCR in a classical porcine model of MI. Results48Hrs after MI, Pcells showed 60% increase in spark-rate and 37% acceleration of Ca2+ wave decay. In the model of normal wave, 35% increase of Ca2+-uptake rate reproduced the actual post-MI wave alterations. In apparent contrast with increased Ca2+-uptake rate, SERCA2 protein expression was reduced in canine, sheep, and human Pcells after MI. In pig MI model, the protein level of cardiac-specific SERCA2-splicing variant SERCA2a was reduced by 52% in the whole infarcted ventricle whereas the "non-cardiac" SERCA2b level was increased by 120%. In the infarcted regions, PFs showed 30% downregulation of SERCA2a gene expression and 630% upregulation of SERCA2b. ConclusionOur results confirm that elevated spontaneous Ca2+-activity in post-MI PFs is due to increased SR-Ca2+-uptake within Pcells. Data suggest that a replacement of "cardiac" SERCA2a by the "non-cardiac" SERCA2b sub-isoform in cardiac cells in response to ischemia is implicated in this alteration.

cell biology↗

bioRxiv2023

RGS2 is an innate immune checkpoint for TLR4 and Gαq-mediated IFNγ generation and lung injury

IFN{gamma}, a type II interferon secreted by immune cells, augments tissue responses to injury following pathogenic infections leading to lethal acute lung injury (ALI). Alveolar macrophages (AM) abundantly express Toll-like receptor-4 and represent the primary cell type of the innate immune system in the lungs. A fundamental question remains whether AM generation of IFNg leads to uncontrolled innate response and perpetuated lung injury. LPS induced a sustained increase in IFNg levels and unresolvable inflammatory lung injury in the mice lacking RGS2 but not in RGS2 null chimeric mice receiving WT bone marrow or receiving the RGS2 gene in AM. Thus, indicating RGS2 serves as a gatekeeper of IFNg levels in AM and thereby lungs innate immune response. RGS2 functioned by forming a complex with TLR4 shielding Gaq from inducing IFNg generation and AM inflammatory signaling. Thus, inhibition of Gaq blocked IFNg generation and subverted AM transcriptome from being inflammatory to reparative type in RGS2 null mice, resolving lung injury. HighlightsO_LIRGS2 levels are inversely correlated with IFN{gamma} in ARDS patients AM. C_LIO_LIRGS2 in alveolar macrophages regulate the inflammatory lung injury. C_LIO_LIDuring pathogenic insult RGS2 functioned by forming a complex with TLR4 shielding Gq from inducing IFN{gamma} generation and AM inflammatory signaling. C_LI eToc BlurbAuthors demonstrate an essential role of RGS2 in macrophages in airspace to promoting anti-inflammatory function of alveolar macrophages in lung injury. The authors provided new insight into the dynamic control of innate immune response by Gq and RGS2 axis to prevent ALI.

immunology↗

bioRxiv2021

Population size, density, and ranging behaviour in a key leopard population in the Western Cape, South Africa

Globally, leopards are the most widespread large felid. However, mounting anthropogenic threats are rapidly reducing viable leopard populations and their range. Despite the clear pressures facing this species, there is a dearth of robust and reliable population and density estimates for leopards across their range, which is particularly important in landscapes that consist of protected and non-protected areas. We conducted a camera trapping survey between 2017 and 2018 in the Western Cape, South Africa to estimate the occupancy, density, and population size of a leopard population. Leopards were recorded at 95% of camera trapping sites, which resulted in a high occupancy that showed no significant variation between seasons, habitat types, or along an altitudinal gradient. Our results indicated a low leopard density in the study area, with an estimated 1.53 leopards/100 km2 in summer and 1.62 leopards/100 km2 in winter. Mean leopard population size was therefore estimated at 107 and 113 individuals in the winter and summer respectively. Leopard activity centres for female ranges were centred in the core study area and could be predicted with good certainty, while males appeared to move out of the study area during winter which resulted in a higher uncertainty in locations of activity centres. Interestingly, livestock depredation events in the surrounding farmlands were significantly higher in winter, which coincides with male leopards moving outside the core protected area into the surrounding farmlands. To reduce livestock losses and retaliatory leopard killings, we suggest that human-carnivore conflict mitigation measures be intensely monitored during the winter months in the study area. We also suggest that future leopard conservation efforts should focus on privately-owned land as these non-protected areas contain the majority of the remaining suitable leopard habitat and may provide important dispersal corridors and buffer zones on which the long-term sustainability of leopard populations depends.

ecology↗

bioRxiv2020

A comprehensive logic-based model of the human immune system to study the dynamics responses to mono- and coinfections

The immune system is a complex and dynamic network, crucial for combating infections and maintaining health. Developing a comprehensive digital twin of the immune system requires incorporating essential cellular components and their interactions. This study presents the first blueprint for an immune system digital twin, consisting of a comprehensive and simulatable mechanistic model. It integrates 51 innate and adaptive immune cells, 37 secretory factors, and 11 disease conditions, providing the foundation for developing a multi-scale model. The cellular-level model demonstrates its potential in characterizing immune responses to various single and combinatorial disease conditions. By making the model available in easy-to-use formats directly in the Cell Collective platform, the community can easily and further expand it. This blueprint represents a significant step towards developing general-purpose immune digital twins, with far-reaching implications for the future of digital twin technology in life sciences and healthcare, advancing patient care, and accelerating precision medicine.

systems biology↗

bioRxiv2020

C. elegans nuclear RNAi factor SET-32 deposits the transgenerational heritable histone modification, H3K23me3

Nuclear RNAi provides a highly tractable system to study RNA-mediated chromatin changes and epigenetic inheritance. Recent studies have indicated that the regulation and function of nuclear RNAi-mediated heterochromatin are highly complex. Our knowledge of histone modifications and the corresponding histone modifying enzymes involved in the system remains limited. In this study, we show that the heterochromatin mark, H3K23me3, is induced by nuclear RNAi at both exogenous and endogenous targets in C. elegans. In addition, dsRNA-induced H3K23me3 can be inherited for four generations. We demonstrate that the histone methyltransferase SET-32, methylates H3K23 in vitro. Both set-32 and the germline nuclear RNAi Argonaute, hrde-1, are required for nuclear RNAi-induced H3K23me3 in vivo. Our data poise H3K23me3 as an additional chromatin modification in the nuclear RNAi pathway and provides the field with a new target for uncovering the role of heterochromatin in transgenerational epigenetic silencing.

molecular biology↗