Biology subjects

Morgan, A.

Publications and source records attributed to Morgan, A..

At least 19 recordsLinked to original sources

bioRxiv2026

Reconstruction of FACS-partitioned Adaptive Immune Receptor Repertoires from FACS-partitioned B and T Cell Subsets

Adaptive immune-receptor repertoire sequencing (AIRRseq) is crucial for understanding immune system diversity and its relationship to disease dynamics. Partitioning of total B and T cells into their major subsets with distinct immunological functions - IgM+ vs. class-switched B cells (IgG+ > IgA+) and CD4+ vs. CD8+ T cells, respectively - allows for AIRRseq-based analysis of the unique contributions of each compartment to the overall immune response, a major advantage over traditional bulk sequencing workflows. However, data from these subsets is not directly comparable with the vast majority of publicly available AIRRseq data, which comes from unfractionated B and T cells, an important incompatibility. Here we investigate computational methods for reconstructing complete AIRRseq repertoires from partitioned B and T cell subsets in diverse individuals. Peripheral blood mononuclear cells (PBMCs) were partitioned via positive selection of IgM+ B-cell subsets and CD4+ T cells using immunomagnetic beads; genomic DNA was then extracted and B- and T-cell receptors were sequenced. Four reconstruction methods are introduced and evaluated for concordance with matching unpartitioned repertoires to assess preservation of key repertoire characteristics. Results show that these methods enable accurate estimates of overall immune-repertoire diversity from B- and T-cell subsets in a way that simply pooling the sequence data from sub-repertoires cannot.

immunology↗

bioRxiv2026

Nociceptor-enriched CAPS1 isoform couples to CaV2.2 channels and underlies inflammatory pain hypersensitivity

How broadly expressed presynaptic proteins acquire the cell-type specificity needed to couple to CaV2 channels in defined neurons, and whether this specialization contributes to behavior, remains poorly understood. We show that alternative splicing of Cadps, encoding the vesicle-priming factor CAPS1, generates nociceptor-selective CaV2.2 regulation and underlies inflammatory pain hypersensitivity. Although Cadps is comparably expressed across dorsal root ganglion neurons, exon-resolution analysis identified exon 16a, a conserved 23-amino-acid cassette, as selectively enriched in nociceptors. The e16a-containing CAPS1 isoform, but not CAPS1 lacking e16a, enhanced recombinant CaV2.2 currents, whereas disruption of the e16a-encoded sequence blocked this effect and reduced endogenous CaV2.2 currents in nociceptors. Conditional Cadps deletion in Trpv1-lineage nociceptors similarly reduced CaV2.2 currents and attenuated capsaicin-evoked inflammatory hypersensitivity while sparing baseline sensitivity, an effect replicated by intrathecal delivery of an exon 16a-derived peptide. Alternative splicing of a presynaptic partner protein thus confers cell-type-specific CaV2.2 coupling and underlies inflammatory pain hypersensitivity.

neuroscience↗

bioRxiv2026

Addiction-Like Severity Predicts Prolonged Oxycodone Withdrawal-Induced Allodynia in Genetically Diverse Rats

Opioid withdrawal is associated with heightened pain sensitivity, including allodynia. Although opioid-induced allodynia is well-documented in humans and animal models, the relationship between the severity of opioid withdrawal-induced allodynia and individual addiction-like behaviors remains poorly understood. To address this gap, Heterogeneous Stock rats underwent long access (12 hours/day) intravenous oxycodone self-administration, followed by measurement of mechanical sensitivity at six timepoints across three weeks of abstinence. Rats were stratified by an Addiction Index derived from individual differences in the escalation of oxycodone intake, motivation to consume oxycodone, tolerance to oxycodones analgesic effects, and acute withdrawal-induced mechanical pain sensitivity. Here, we show that oxycodone withdrawal induces significant and prolonged allodynia for up to three weeks, with High Addiction Index rats exhibiting greater intensity and longer duration of pain sensitivity than Low Addiction Index rats. Results remained consistent even when excluding allodynia from the Addiction Index, highlighting the robustness of the association between addiction-like severity and protracted allodynia. Linear regression associations revealed that self-administration behaviors, particularly oxycodone intake escalation and motivation to seek oxycodone, predicted subsequent withdrawal-induced allodynia severity. These findings demonstrate that greater addiction-like severity is associated with more intense and prolonged withdrawal-induced pain, supporting mechanical allodynia as a marker of addiction severity. These results motivate future work to define the mechanisms linking addiction severity to protracted opioid withdrawal-induced pain, with the goal of informing targeted clinical interventions for individuals most susceptible to severe abstinence-related allodynia.

pharmacology and toxicology↗

bioRxiv2026

Gene model for the ortholog of Lst8 in Drosophila yakuba

Gene model for the ortholog of Lst8 (Lst8) in the May 2011 (WUGSC dyak_caf1/DyakCAF1) Genome Assembly (GenBank Accession: GCA_000005975.1) of Drosophila yakuba. This ortholog was characterized as part of a developing dataset to study the evolution of the Insulin/insulin-like growth factor signaling pathway (IIS) across the genus Drosophila using the Genomics Education Partnership gene annotation protocol for Course-based Undergraduate Research Experiences.

genomics↗

bioRxiv2025

Cell-based calcification assays - magnesium overrules calcium phosphate saturation in overall outcome

Soft tissue calcification, a common cause of cardiovascular mortality in conditions like chronic kidney disease (CKD), is influenced by magnesium (Mg). However, the exact mechanism, whether extracellular chemistry-mediated or cell-mediated, remains unclear. Here we focused on the extracellular milieu. Using fluorescence-labelled fetuin-A and a live imaging platform, we found that Mg reduced spontaneous mineral precipitation by stabilizing calcium and phosphate as colloidal protein-mineral particles (CPP) in calcification media containing up to 10 mM calcium and phosphate. Addition of 1.25-5 mM Mg progressively stabilized the protein-mineral particles in the fluid phase, increasing calcification. Dynamic light scattering revealed smaller and more numerous CPP at up to 4 mM Mg. At 10 mM Mg, no calcification occurred even with 10 mM added calcium and phosphate. This suggested a critical Mg concentration range in supersaturated calcification media, where Mg paradoxically enhanced calcification by stabilizing mineral precursors and increasing their availability. These findings demonstrate Mgs dual role: an inhibitor of protein-mineral complex aggregation at high concentrations and a facilitator of mineral availability from colloidal protein-mineral phases at concentrations up to about 5 mM Mg. This highlights the role of Mg in providing highly dynamic, mineral-rich, stable protein-mineral complexes driving matrix calcification, yet preventing mineral precipitation.

pathology↗

bioRxiv2025

Miniaturized Device for Assessing Calcification Propensity of Biohybrid Implants Under Continuous Flow

Biohybrid implants are a promising development for cardiovascular disease treatment but suffer from problems like thrombogenesis and calcification. However, testing and validating biohybrid implants can be difficult and expensive due to material handling, fabrication methods and specialty medium components. The devices used to test potential samples can be large and expensive, requiring significant amounts of cell culture medium to operate. Additional, conventional static cell culture conditions do not accurately represent the vascular environment as shear and mechanical forces play key roles in the development of calcification. To address these challenges, a miniaturized, dual-channel flow chamber was designed and validated that allowed for real-time visualization of biohybrid calcification in a physiological environment. Computational Fluid Dynamics simulations were performed to determine the flow characteristics that generated physiological shear stress homogeneously across the sample surface. Micro particle tracking velocimetry measurements validated the simulated shear stresses near the sample surface. Two implant materials used for biohybrid construction, bovine pericardium and polycarbonate urethane, were inserted in the device and exposed to a flowing calcification medium for 14 days. Fluorescent fetuin-A was introduced into the calcification medium for real-time calcification monitoring. The two materials were compared with matched samples calcified in a large fatigue tester for 14 days. Our results showed similar material calcification for bovine pericardium and no calcification for polycarbonate urethane in the large fatigue tester and in our newly developed device. Biohybrid textile-reinforced fibrin-based scaffold populated with vascular smooth muscle cells started to calcify over 7 days in calcification medium. We conclude that this platform will provide novel insights into the origin and progression of pathological calcification and its potentially harmful health effects, which can occur as a result of tissue or metabolic abnormalities, disease, or implantation of certain biomaterials, by providing the ability to monitor the progression of calcification in biohybrid implants in real time, while also minimizing the cost and size of samples and reagents required for testing.

bioengineering↗

bioRxiv2025

HuBIE: The Human Blood Immunome Encyclopedia Of TCRs and BCRs in Bloodstream Infections and Cancer

T and B cells are central to adaptive immunity, where they identify and neutralize foreign antigens and cancer neo-antigens. Large-scale elucidation of T- and B-cell receptors (TCRs and BCRs) through immune-repertoire sequencing promises novel diagnostics, prognostic markers, and therapeutic strategies. However, progress is hampered by small cohort sizes, a lack of real-world patient diversity, and heterogeneous sample processing, impeding cross-study comparability. To overcome these limitations, here we introduce the Human Blood Immunome Encyclopedia (HuBIE), comprising immune-repertoire data from 2,614 samples collected from 1,941 participants. The cohort includes a range of bloodstream infections, several cancer types, and control participants, with many individuals providing longitudinal samples. We employed Roches immune receptor Primer Extension Target Enrichment (immunoPETE) platform to perform simultaneous targeted sequencing of T-cell receptor {beta} chains (TRB), T-cell receptor {delta} chains (TRD), and immunoglobulin heavy chains (IGH), thereby profiling TCRs and BCRs in all participants. We provide a comprehensive description of immune-repertoire diversity in cancer and bloodstream infections and examine variations across demographic variables such as age and race. We find significant differences in TRB and IGH composition across ethnic groups, and show that the fall in repertoire diversity with age follows distinct patterns for TRB, TRD, and IGH and is accompanied by age-related differences in VJ gene usage. Finally we demonstrate that greater immunological diversity is associated with improved survival but only for elderly participants. HuBIE thus constitutes a valuable resource for the immune-repertoire community, enabling large-scale mapping of the human immunome to accelerate development of diagnostics, prognostic biomarkers, and innovative therapeutic strategies.

immunology↗

bioRxiv2025

Incentive Salience, not Psychomotor Sensitization or Tolerance, Drives Escalation of Cocaine Self-Administration in Heterogeneous Stock Rats

Sensitization and tolerance are two phenomena often studied independently despite overlapping neurobiological substrates. Each has extensive research showing their influence on the development and maintenance of addiction, but the degree to which they drive escalation in cocaine self-administration is poorly understood. Using self-administration, intravenous noncontingent infusions, and pose-estimation machine vision, we find that incentive salience, not psychomotor sensitization or tolerance, drives the escalation of cocaine self-administration in heterogenous stock rats. Individual differences in psychomotor sensitization or tolerance were found to have no effect on cocaine intake. Incentive salience as measured by locomotion and active lever entrances per meter traveled occurring before the self-administration session began (pre-lever activity measures) during Short Access (2-hours) was found to predict intake during Long Access (6-hours). Both pre-lever locomotion and active lever entrances per meter were found to increase during Long Access and after two-to-three days of abstinence. Critically, rats with low pre-lever activity during Short Access escalated both their intake and pre-lever measures by the end of Long Access to levels comparable with high pre-lever activity rats who maintained their elevated responding. These findings support the notion that incentive salience during Short Access is a catalyst to escalated use and an early marker of addiction vulnerability. Moreover, they suggest that individuals initially resistant to incentive salience can, with sufficient exposure, become sensitized and escalate cocaine use to the same level as more susceptible individuals. Analysis of pre-lever activity offers a novel longitudinal behavioral marker to predict vulnerability and provides a framework for understanding individual trajectories of addiction.

neuroscience↗

bioRxiv2025

Alternate Splicing Directs PMCA2 to Lysosomes and is Linked to Neurodegeneration

Plasma membrane calcium ATPases (PMCAs) are believed to function exclusively at the plasma membrane where they expel calcium from the cytosol. We have unexpectedly identified a splice variant-dependent localisation of the PMCA isoform PMCA2 to the lysosome, where it forms an evolutionarily conserved complex with NPC1, the lysosomal membrane protein defective in the rare lysosomal storage disease Niemann-Pick disease type C (NPC). This interaction is required for lysosomal Ca2+ homeostasis and implicates PMCA2 as a mediator of Ca2+ uptake into lysosomes. Disruption of the NPC1-PMCA2 complex contributes to the pathophysiology of both Niemann-Pick disease type C and Parkinsons disease, revealing an unrecognised intracellular function for PMCA2 and a shared mechanism linking lysosomal Ca2+ and lipid regulation in neurodegeneration.

cell biology↗

bioRxiv2025

Gene model for the ortholog of Akt in Drosophila elegans

Gene model for the ortholog of Akt kinase (Akt) in the April 2013 (BCM-HGSC/Dele_2.0) Genome Assembly (GenBank Accession: GCA_000224195.2) of Drosophila elegans. This ortholog was characterized as part of a developing dataset to study the evolution of the Insulin/insulin-like growth factor signaling pathway (IIS) across the genus Drosophila using the Genomics Education Partnership gene annotation protocol for Course-based Undergraduate Research Experiences.

genomics↗

bioRxiv2025

Genome-wide association study of cocaine self-administration behavior in Heterogeneous Stock rats

BackgroundCocaine use disorder (CUD) is a major public health crisis with detrimental individual and societal effects. The specific genes mediating CUD remain largely unknown. MethodsWe conducted a genome-wide association study (GWAS) using outbred N/NIH Heterogeneous Stock (HS; n = 836, female = 415, male = 421) rats. We examined multiple CUD-related phenotypes that captured acquisition of self-administration, escalation of intake, and compulsive-like responding. ResultsConsistent with the existing literature, these traits were phenotypically and genetically correlated and exhibited modest heritability (h2 = 0.07 - 0.16). We identified six genome-wide significant associations. One locus on chromosome 19 was associated with the variable time between cocaine infusions (post infusion interval) and contains several carboxylesterase genes that are orthologous to the human CES1 gene; notably, carboxylesterases metabolize cocaine. Three non-synonymous coding variants in the genes Ces1c and Ces1d were in perfect linkage disequilibrium with this locus, suggesting that one or more of them might be the causal SNP. The other 5 loci also contained promising coding and expression variants, including Trak2, a gene previously associated with CUD in human GWAS and Slc10a7, Plcl1, and Satb2 which have been associated with alcohol and tobacco use disorder. ConclusionsThis is the largest genetic study of cocaine self-administration ever conducted in any species. Our results replicate previous loci associated with CUD in humans and provide several novel biological insights including the potential of pharmacological strategies targeting carboxylesterases for the treatment of CUD.

genetics↗

bioRxiv2025

Remote sensing of endogenous pigmentation by inducible synthetic circuits in grasses

Plant synthetic biology holds great promise for engineering plants to meet future demands. Genetic circuits are being designed, built, and tested in plants to demonstrate proof of concept. However, developing these components in monocots, which the world relies on for grain, lags behind dicot models, such as Arabidopsis thaliana and Nicotiana benthamiana. Here, we show the successful adaptation of a ligand-inducible sensor to activate an endogenous anthocyanin pathway in the C4 monocot model Setaria viridis. We identify two transcription factors sufficient to induce endogenous anthocyanin production in S. viridis protoplasts and whole plants in a constitutive or ligand-inducible manner. We also test multiple ligands to overcome physical barriers to ligand uptake, identifying triamcinolone acetonide (TA) as a highly potent inducer of this system. Using hyperspectral imaging and a discriminative target characterization method in a near-remote configuration, we can non-destructively detect anthocyanin production in leaves in response to ligands. This work demonstrates the use of inducible expression systems in monocots to manipulate endogenous pathways, stimulating plants to overproduce secondary metabolites with value to human health. Applying inducible pigmentation coupled with sensitive detection algorithms could enable crop plants to report on the status of field contamination or detect undesirable chemicals impacting agriculture, ushering in an era of agriculture-based sensor systems. SummaryO_ST_ABSSynbio tools for C4 grass modelC_ST_ABS[bullet] Advantage of synthetic switches as tools for biopharming and functional genomics [bullet]Our workflow to optimize the gene circuits from a transient system to a stable transgenic [bullet]Testing and taming golden gate elements in monocot system, S. viridis

plant biology↗

bioRxiv2025

Perinatal Fentanyl Exposure Drives Enduring Addiction Risk and Central Amygdala Gene Dysregulation

The use of fentanyl and other opioids during pregnancy is a pressing public health issue due to its association with Neonatal Opioid Withdrawal Syndrome (NOWS) and long-term neurobehavioral deficits. Human epidemiologic studies are confounded by both genetic and environmental factors that differ between exposed and unexposed children. We developed a novel rat model of perinatal fentanyl exposure to characterize NOWS symptoms and investigate enduring behavioral and molecular outcomes. Offspring born to fentanyl-exposed dams exhibited reduced survival, lower body weight, spontaneous withdrawal symptoms, and mechanical hypersensitivity. In adolescence, these rats displayed negative affect, while in adulthood, they showed increased fentanyl self-administration, heightened drug-seeking during reinstatement, and elevated corticosterone levels during withdrawal. To explore the molecular underpinnings of these physiological and behavioral outcomes, we conducted RNA-seq in the central amygdala of adult rats, revealing dysregulated pathways related to GPCR signaling, adaptive immune response and neurodevelopmental processes. These transcriptional changes provide insights into the mechanisms driving addiction vulnerability and stress-related behaviors following early fentanyl exposure. Our findings highlight the lasting impact of perinatal opioid exposure in an experimental system that avoids many of the confounds that plague studies in humans, underscoring the need for preclinical models to study NOWS and its long-term consequences. This model offers translational relevance for developing therapeutic strategies to mitigate NOWS and reduce neuropsychiatric risks associated with prenatal opioid exposure.

animal behavior and cognition↗

bioRxiv2025

Pnrc2 promotes rapid mRNA decay and coordinately supports early development with P-body factors Ddx6 and Ddx61

Somitogenesis is controlled by the segmentation clock, a molecular oscillator that controls periodic gene expression in unsegmented mesoderm and is regulated by a negative feedback loop driven by Hes/Her transcriptional repressors. In zebrafish, Pnrc2 is required for decay of her1 transcript and additional oscillatory gene transcripts. Despite accumulation of numerous mRNAs including those encoding developmental regulators, overt embryonic phenotypes are absent in pnrc2 mutants. Our previous work suggested that accumulated mRNAs are not translated in pnrc2 mutants, though the underlying mechanism(s) was unknown. We show here that many overexpressed transcripts in pnrc2 mutants have shortened poly(A) tails and are disengaged from ribosomes, and that deadenylation inhibition leads to somite defects in pnrc2 mutants. Transcripts encoding the P-body-associated protein, Ddx61, are overexpressed and engaged with ribosomes in pnrc2 mutants, leading to an increase in Ddx61 protein that may compensate against the negative effects of transcript accumulation. Co-depletion of Ddx61 and Ddx6 in pnrc2 mutants increases her1 accumulation and leads to pleiotropic defects. Together, our results show that multiple post-transcriptional mechanisms ensure proper translation when mRNA decay is inhibited.

developmental biology↗

bioRxiv2025

Fis1 is required for the development of the dendritic mitochondrial network in pyramidal cortical neurons

Mitochondrial ATP production and calcium buffering are critical for metabolic regulation and neurotransmission making the formation and maintenance of the mitochondrial network a critical component of neuronal health. Cortical pyramidal neurons contain compartment-specific mitochondrial morphologies that result from distinct axonal and dendritic mitochondrial fission and fusion profiles. We previously showed that axonal mitochondria are maintained at a small size as a result of high axonal mitochondrial fission factor (Mff) activity. However, loss of Mff activity had little effect on cortical dendritic mitochondria, raising the question of how fission/fusion balance is controlled in the dendrites. Thus, we sought to investigate the role of another fission factor, fission 1 (Fis1), on mitochondrial morphology, dynamics and function in cortical neurons. We knocked down Fis1 in cortical neurons both in primary culture and in vivo, and unexpectedly found that Fis1 depletion decreased mitochondrial length in the dendrites, without affecting mitochondrial size in the axon. Further, loss of Fis1 activity resulted in both increased mitochondrial motility and dynamics in the dendrites. These results argue Fis1 exhibits dendrite selectivity and plays a more complex role in neuronal mitochondrial dynamics than previously reported. Functionally, Fis1 loss resulted in reduced mitochondrial membrane potential, increased sensitivity to complex III blockade, and decreased mitochondrial calcium uptake during neuronal activity. The altered mitochondrial network culminated in elevated resting calcium levels that increased dendritic branching but reduced spine density. We conclude that Fis1 regulates morphological and functional mitochondrial characteristics that influence dendritic tree arborization and connectivity.

cell biology↗

bioRxiv2024

A selective GSK3β inhibitor, tideglusib, decreases intermittent access and binge ethanol self-administration in C57BL/6J mice

Over 10% of the US population over 12 years old meets criteria for Alcohol Use Disorder (AUD), yet few effective, long-term treatments are currently available. Glycogen synthase kinase 3 beta (GSK3{beta}) has been implicated in ethanol behaviors and poses as a potential therapeutic target in the treatment of AUD. Here we investigate the role of tideglusib, a selective GSK3{beta} inhibitor, in ethanol consumption and other behaviors. We have shown tideglusib decreases ethanol consumption in both a model of daily, progressive ethanol intake (two-bottle choice, intermittent ethanol access) and binge-like drinking behavior (drinking-in-the-dark) without effecting water intake. Further, we have shown tideglusib to have no effect on ethanol pharmacokinetics, taste preference, or anxiety-like behavior, though there was a transient increase in total locomotion following treatment. Additionally, we assessed liver health following treatment via serum levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase and showed no effect on aminotransferase levels though there was a decrease in alkaline phosphatase. RNA sequencing studies revealed a role of GSK3{beta} inhibition via tideglusib on the canonical Wnt signaling pathway, suggesting tideglusib may carry out its effects on ethanol consumption through effects on {beta}-catenin binding to the transcription factors TCF3 and LEF1. The data presented here further implicate GSK3{beta} in alcohol consumption and support the use of tideglusib as a potential therapeutic in the treatment of AUD.

pharmacology and toxicology↗

bioRxiv2023

Contrasting Effects of SARS-CoV-2 Vaccination vs. Infection on Antibody and TCR Repertoires

Antibodies and helper T cells play important roles in SARS-CoV-2 infection and vaccination. We sequenced B- and T-cell receptor repertoires (BCR/TCR) from the blood of 251 infectees, vaccinees, and controls to investigate whether features of these repertoires could predict subjects SARS-CoV-2 neutralizing antibody titer (NAbs), as measured by enzyme-linked immunosorbent assay (ELISA). We sequenced recombined immunoglobulin heavy-chain (IGH), TCR{beta} (TRB), and TCR{delta} (TRD) genes in parallel from all subjects, including select B- and T-cell subsets in most cases, with a focus on their hypervariable CDR3 regions, and correlated this AIRRseq data with demographics and clinical findings from subjects electronic health records. We found that age affected NAb levels in vaccinees but not infectees. Intriguingly, we found that vaccination and infection have an effect on non-productively recombined IGHs, suggesting an effect that precedes clonal selection. We found that repertoires binding capacity to known SARS-CoV-2-specific CD4+ TRBs performs as well as the best hand-tuned approximate or "fuzzy" matching at predicting a protective level of NAbs, while also being more robust to repertoire sample size and not requiring hand-tuning. The overall conclusion from this large, unbiased, clinically well annotated dataset is that B- and T-cell adaptive responses to SARS-CoV-2 infection and vaccination are surprising, subtle, and diffuse. We discuss methodological and statistical challenges faced in attempting to define and quantify such strong-but-diffuse repertoire signatures and present tools and strategies for addressing these challenges.

immunology↗

bioRxiv2023

Activity-dependent subcellular compartmentalization of dendritic mitochondria structure in CA1 pyramidal neurons

Neuronal mitochondria play important roles beyond ATP generation, including Ca2+ uptake, and therefore have instructive roles in synaptic function and neuronal response properties. Mitochondrial morphology differs significantly in the axon and dendrites of a given neuronal subtype, but in CA1 pyramidal neurons (PNs) of the hippocampus, mitochondria within the dendritic arbor also display a remarkable degree of subcellular, layer- specific compartmentalization. In the dendrites of these neurons, mitochondria morphology ranges from highly fused and elongated in the apical tuft, to more fragmented in the apical oblique and basal dendritic compartments, and thus occupy a smaller fraction of dendritic volume than in the apical tuft. However, the molecular mechanisms underlying this striking degree of subcellular compartmentalization of mitochondria morphology are unknown, precluding the assessment of its impact on neuronal function. Here, we demonstrate that this compartment-specific morphology of dendritic mitochondria requires activity-dependent, Camkk2- dependent activation of AMPK and its ability to phosphorylate two direct effectors: the pro-fission Drp1 receptor Mff and the recently identified anti-fusion, Opa1-inhibiting protein, Mtfr1l. Our study uncovers a new activity- dependent molecular mechanism underlying the extreme subcellular compartmentalization of mitochondrial morphology in dendrites of neurons in vivo through spatially precise regulation of mitochondria fission/fusion balance.

cell biology↗