bioRxiv : the preprint server for biology最新文献

{"title":"Distinct Quaternary States, Intermediates, and Autoinhibition During Loading of the DnaB-Replicative Helicase by the Phage λP Helicase Loader.","authors":"Abhipsa Shatarupa, Dhanjai Brown, Paul Dominic B Olinares, Jillian Chase, Eta Isiorho, Brian T Chait, David Jeruzalmi","doi":"10.1101/2022.12.30.522210","DOIUrl":"10.1101/2022.12.30.522210","url":null,"abstract":"<p><p>Replicative helicases require loader proteins for assembly at the origins of DNA replication. Multiple copies of the bacteriophage λP (P) loader bind to and load the <i>E. coli</i> DnaB (B) replicative helicase on replication-origin-derived single-stranded DNA. We find that the <i>E. coli</i> DnaB•λP complex exists in two forms: B ₆ P ₅ and B ₆ P ₆ . In the 2.66 Å cryo-EM model of B ₆ P ₅ , five copies of the λP loader assemble into a crown-like shape that tightly grips DnaB. In this complex, closed planar DnaB is reconfigured into an open spiral with a sufficiently sized breach to permit ssDNA to enter an internal chamber. The transition to the open spiral involves λP-mediated changes to the Docking Helix (DH)-Linker Helix (LH) interface. The loader directly stabilizes the open spiral. Unexpectedly, one λP chain in B ₆ P ₅ is bound across the breach, precluding entry of replication-origin-derived ssDNA into DnaB's central chamber. We suggest that the B ₆ P ₆ complex is an early intermediate in the helicase activation pathway wherein neither the DnaB helicase nor the λP loader has attained its final form. DnaB in this complex adopts a partially open planar configuration, termed ajar planar. The partially ordered λP loader assembly features a much looser interaction with DnaB. The ssDNA and ATP sites in both complexes are in a configuration ill-suited for binding or hydrolysis. Our work specifies the conformational changes required for the intermediate B ₆ P ₆ to transition to B ₆ P ₅ on the pathway to recruitment by the initiator protein complex to the replication origin.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"76 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12157507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91535039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The striatal heterogeneous nuclear ribonucleoprotein H mRNA targetome associated with methamphetamine administration and behavior.","authors":"Qiu T Ruan, William B Lynch, Rebecca H Cole, Michael A Rieger, Britahny M Baskin, Sophia A Miracle, Jacob A Beierle, Emily J Yao, Jiayi W Cox, Amarpreet Kandola, Kayla T Richardson, Melanie M Chen, Julia C Kelliher, R Keith Babbs, Peter E A Ash, Benjamin Wolozin, Karen K Szumlinski, W Evan Johnson, Joseph D Dougherty, Camron D Bryant","doi":"10.1101/2021.07.06.451358","DOIUrl":"10.1101/2021.07.06.451358","url":null,"abstract":"<p><p>Methamphetamine addiction remains a major public health concern in the United States that has paralleled the opioid epidemic. Psychostimulant use disorders have a heritable genetic component that remains unexplained. Methamphetamine targets membrane and vesicular transporters to increase synaptic dopamine, norepinephrine, and serotonin. We previously identified <i>Hnrnph1</i> (heterogeneous nuclear ribonucleoprotein H1) as a quantitative trait gene underlying methamphetamine behavioral sensitivity. <i>Hnrnph1</i> encodes the RNA-binding protein hnRNP H1 that is ubiquitously expressed in neurons throughout the brain. Gene-edited mice with a heterozygous frameshift deletion in <i>Hnrnph1's</i> first coding exon of showed reduced methamphetamine-induced dopamine release and behaviors. To inform the mechanism linking hnRNP H with methamphetamine neurobehavioral effects, we surveyed the mRNA targetome of hnRNP H via cross-linking immunoprecipitation coupled with RNA-sequencing in striatal tissue at baseline and at 30 min post-methamphetamine in wild-type male and female C57BL/6J mice. Methamphetamine induced changes in RNA-binding targets of hnRNP H in mice, including differential binding to 3'UTR targets and multiple enriched mRNAs involved in synaptic plasticity. Targetome, transcriptome, and spliceome analyses triangulated on <i>Cacna2d2</i> as a suggestive target, with differences in hnRNP H binding, gene expression and splicing following methamphetamine treatment (2 mg/kg, i.p.). Furthermore, pre-treatment with pregabalin, an inhibitor of α2δ2 and α2δ1 voltage-gated calcium channel subunits, attenuated methamphetamine-induced locomotor activity in male and female mice, supporting a role for Cacna2d1/d2 in methamphetamine locomotor stimulant sensitivity. Our study identifies a dynamic hnRNP H RNA targetome that can rapidly and adaptively respond to methamphetamine to regulate gene expression and likely synaptic plasticity and behavior.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12154668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82387600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation.","authors":"Jie Wang, Jun Nishiyama, Paula Parra-Bueno, Elwy Okaz, Goksu Oz, Xiaodan Liu, Tetsuya Watabe, Irena Suponitsky-Kroyter, Timothy E McGraw, Erzsebet M Szatmari, Ryohei Yasuda","doi":"10.1101/2022.05.17.492345","DOIUrl":"10.1101/2022.05.17.492345","url":null,"abstract":"<p><p>Rab-dependent membrane trafficking is critical for changing the structure and function of dendritic spines during synaptic plasticity. Here, we developed highly sensitive sensors to monitor Rab protein activity in single dendritic spines undergoing structural long-term potentiation (sLTP) in rodent organotypic hippocampal slices. During sLTP, Rab10 was persistently inactivated (>30 min) in the stimulated spines, whereas Rab4 was transiently activated over ∼5 min. Inhibiting or deleting Rab10 enhanced sLTP, electrophysiological LTP and AMPA receptor (AMPAR) trafficking during sLTP. In contrast, disrupting Rab4 impaired sLTP only in the first few minutes, and decreased AMPAR trafficking during sLTP. Thus, our results suggest that Rab10 and Rab4 oppositely regulate AMPAR trafficking during sLTP, and inactivation of Rab10 signaling facilitates the induction of LTP and associated spine structural plasticity.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12154598/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79706128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging reduces the number and function of L-type calcium channels in the membrane of cardiac pacemaker cells.","authors":"Oscar Vivas, Matthias Baudot, Roxanne Madden, Sabrina Choi, Victor A Flores, L Fernando Santana, Claudia M Moreno","doi":"10.1101/2022.06.22.497267","DOIUrl":"10.1101/2022.06.22.497267","url":null,"abstract":"<p><p>Every heartbeat is initiated by a spontaneous electrical signal generated inside the cardiac pacemaker. The generation of this electrical signal depends on the coordinated opening and closing of different ion channels, where voltage-gated L-type calcium channels play a central role. Despite the reliability of the pacemaker, all mammals experience a linear slowdown of the pacemaker rate with age. In humans, this slowing can become pathological and constitutes the main cause for the requirement of the implantation of artificial pacemakers. However, the mechanisms behind the age-associated slowdown of the pacemaker are not well understood. Here, we show that age alters L-type calcium channels in pacemaker cells from mice. The age-associated alterations include: i) a reduction in the density of the channels at the plasma membrane, ii) a reduction in the clustering of the channels, and iii) a decrease in channel open probability. Altogether, these age-associated alterations result in a global reduction of the L-type calcium current density and in a slowdown of the pacemaker diastolic depolarization. Remarkably, increasing the open probability of L-type calcium channels pharmacologically was enough to restore pacemaker rate in old cells to the same levels observed in the young. Overall, our findings provide evidence that proper organization and function of L-type calcium channels is impaired by aging and that this dysfunction contributes to the slowdown of pacemaker cells in old animals.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"174 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12154664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80728210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacteria detect neutrophils via a system that responds to hypochlorous acid and flow.","authors":"Ilona P Foik, Runhang Shu, Serena Abbondante, Summer J Kasallis, Lauren A Urban, Andy P Huang, Leora Duong, Michaela E Marshall, Eric Pearlman, Timothy L Downing, Albert Siryaporn","doi":"10.1101/2022.02.01.478687","DOIUrl":"10.1101/2022.02.01.478687","url":null,"abstract":"<p><p>Neutrophils respond to the presence of bacteria by producing oxidative molecules that are lethal to bacteria, including hypochlorous acid (HOCl). However, the extent to which bacteria detect activated neutrophils or the HOCl that neutrophils produce, has not been understood. Here we report that the opportunistic bacterial pathogen <i>Pseudomonas aeruginosa</i> upregulates expression of its <i>fro</i> operon in response to stimulated neutrophils. This operon was previously shown to be activated by shear rate of fluid flow in the environment. We show that <i>fro</i> is specifically upregulated by HOCl, while other oxidative factors that neutrophils produce including H₂O₂, do not upregulate <i>fro</i>. The <i>fro</i>-dependent response to HOCl upregulates the expression of multiple methionine sulfoxide reductases, which relieve oxidative stress that would otherwise inhibit growth. Our findings suggest a model in which the detection of shear rate or HOCl activates the <i>fro</i> operon, which serves as an early and sensitive host-detection system for <i>P. aeruginosa</i> that improves its own survival against neutrophil-mediated host defenses. In support of this model, we found that the <i>fro</i> operon is activated in an infection model where flow and neutrophils are present. This response could promote the bacterium's pathogenicity, colonization of tissue, and persistence in infections.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82540699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mediator Kinase Module regulates cell cycle re-entry and transcriptional responses following DNA damage.","authors":"Gönen Memişoğlu, Stefan Bohn, Nevan J Krogan, James E Haber, Alexander J Ruthenburg","doi":"10.1101/2023.02.26.530133","DOIUrl":"10.1101/2023.02.26.530133","url":null,"abstract":"<p><p>The Cdk8 kinase module (CKM) is a non-obligate and dissociable subcomplex of Mediator of transcription, a key regulator of RNA polymerase II (RNAPII). Through a genetic screen in yeast, we discovered a surprising role for Mediator CKM in the DNA damage response (DDR) and mitotic re-entry. Remarkably, we find that a single DNA break is sufficient for CKM-dependent global transcriptional attenuation. Upon DDR activation, the kinase activity of CKM antagonizes RNAPII binding to core Mediator, thereby reducing the transcriptionally-engaged RNAPII pool. This transcriptional attenuation is essential for DDR inactivation and limits the spreading of γ-H2AX into gene bodies. Furthermore, CKM localizes to DNA breaks to impede RNAPII binding. Importantly, we demonstrate that the role of CKM on DDR and transcriptional attenuation is conserved from yeast to mammals, establishing a multifaceted and essential function for CKM in transcriptional regulation of DNA-damage response.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77839067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo CRISPR screening identifies SAGA complex members as key regulators of hematopoiesis.","authors":"Michael S Haney, Archana Shankar, Leonid Olender, Ian Hsu, Masashi Miyauchi, Róbert Pálovics, Grace A Meaker, Satoshi Kaito, Ola Rizq, Hwei Minn Khoo, Yavor Bozhilov, Kyomi J Igarashi, Joydeep Bhadury, Christy Munson, Paul K Mack, Tze-Kai Tan, Jan Rehwinkel, Atushi Iwama, Tony Wyss-Coray, Hiromitsu Nakauchi, Adam C Wilkinson","doi":"10.1101/2022.07.22.501030","DOIUrl":"10.1101/2022.07.22.501030","url":null,"abstract":"<p><p>The biological mechanisms that sustain the vast blood production required for healthy life remain incompletely understood. To search for novel regulators of hematopoiesis, we performed genome-wide in vivo hematopoietic stem cell (HSC)-based CRISPR knockout screens for regulators of hematopoiesis. We discovered SAGA complex members, including <i>Tada2b</i> and <i>Taf5l</i> , as key regulators of hematopoiesis. Loss of <i>Tada2b</i> or <i>Taf5l</i> strongly inhibited hematopoiesis <i>in vivo</i> , led to a buildup of immature hematopoietic cells in the bone marrow, and was associated with upregulation of interferon pathway genes. Loss of these factors also enhanced the cell outgrowth and the interferon pathway in an <i>in vivo</i> human myelodysplastic syndrome model, suggesting that loss of SAGA complex activity could contribute to hematological disease progression. In summary, this study has identified the SAGA complex as an important regulator of hematopoiesis.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"2018 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87799153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Information about task duration influences energetic cost during split-belt adaptation and retention of walking patterns post-adaptation.","authors":"S Jeffcoat, A Aragon, A Kuch, S Farrokhi, A Hooyman, R Johnson, N Sanchez","doi":"10.1101/2024.05.24.595558","DOIUrl":"10.1101/2024.05.24.595558","url":null,"abstract":"<p><p>Studies of locomotor adaptation have shown that adaptation can occur in short bouts and can continue for long bouts or across days. Information about task duration might influence the adaptation of gait features, given that task duration influences the time available to explore and adapt the aspects of gait that reduce energy cost. We hypothesized that information about task duration influences adaptation to split-belt walking based on two competing mechanisms: individuals anticipating a prolonged adaptation period may either (1) extend exploration of energetically suboptimal gait patterns, or (2) adapt toward a more energy-efficient pattern earlier to maintain an energetic reserve to sustain the task longer. We tested three groups: N=19 participants received minute-by-minute updates during a 10-minute adaptation duration (True group), N=19 participants received no updates during a 10-minute adaptation duration and were misled to expect a prolonged 30-minute adaptation duration (False group), and N=14 participants received one update halfway through a 10-minute adaptation duration (Control group). We measured step length asymmetry, leg work, and metabolic cost. Our results partially supported our hypothesis but did not confirm the underlying mechanisms. While step length asymmetry did not differ significantly between groups during adaptation, the True group generated a more effortful gait pattern with a greater increase in metabolic cost (p=0.002) and higher work with the leg on the slow belt (p=0.012). Additionally, the True group showed no association between step length asymmetry and metabolic cost (p=0.203), contrary to the Control (r=-0.55, p=0.043) and False groups (r=-0.51, p=0.027). Finally, we observed that the False group showed greater retention of the split-belt aftereffects than the Control and False groups (p<0.001). Thus, adapted locomotor and energetic patterns are influenced by information about task duration, indicating that Information about task duration should be controlled for, or can be manipulated to elicit different efforts during adaptation.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11142228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141201453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conserved developmental rewiring of the TCR signalosome drives tolerance in innate-like lymphocytes.","authors":"Amanpreet Singh Chawla, Harriet J Watt, Stefan A Schattgen, Neema Skariah, Irene Saha, Kathrynne A Warrick, Masahito Ogawa, Jessica Strid, Frederic Lamoliatte, Alastair Copland, Sara Pryde, Elena Knatko, Kasper D Rasmussen, Kazu Kikuchi, Paul G Thomas, Chandrashekar Pasare, David Bending, Mahima Swamy","doi":"10.1101/2023.09.01.555859","DOIUrl":"10.1101/2023.09.01.555859","url":null,"abstract":"<p><p>Natural intraepithelial T lymphocytes (T-IELs) are innate-like, intestine-resident T cells essential for gut homeostasis. These cells express self-reactive T cell antigen receptors (TCRs) due to thymic agonist selection, but they do not cause autoimmunity. The mechanism underlying natural T-IELs tolerance in the gut is unclear. Using TCR reporter mouse models and phosphoproteomics, we demonstrate that TCR signaling is intrinsically suppressed in natural T-IELs. We discover that this suppression occurs post-selection in the thymus through altered expression of TCR signalosome components, a mechanism we term RePrESS (Rewiring of Proximal Elements of TCR Signalosome for Suppression). RePrESS is evolutionarily conserved and also found in autoreactive innate-like T cells from skin, breast and prostate. In coeliac disease, tolerance breakdown is associated with loss of RePrESS in natural T-IELs. Our findings reveal a distinct, conserved mechanism of tolerance involving TCR signaling rewiring, with implications for understanding barrier tissue homeostasis and autoimmune disease.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"45 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12132402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82567093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A framework for analyzing <i>C. elegans</i> neural activity using multi-dimensional hyperbolic embedding.","authors":"Iulia Rusu, Zachary T Cecere, Javier J How, Kathleen T Quach, Eviatar Yemini, Tatyana O Sharpee, Sreekanth H Chalasani","doi":"10.1101/2021.04.09.439242","DOIUrl":"10.1101/2021.04.09.439242","url":null,"abstract":"<p><p>Neurons represent changes in external and internal environments by altering their activity patterns. While coherent brain-wide patterns of neural activity have been observed in neuronal populations, very little is known about their dimensionality, geometry, and how they are correlated with sensory inputs. Here, we recorded the activity of most head neurons in <i>Caenorhabditis elegans</i> experiencing changes in bacterial or control buffer stimuli around their nose. We first classified active neurons into six functional clusters: two sensory neuron clusters (ON and OFF responding to addition and removal of stimuli, respectively) and four motor/command neuron clusters (AVA, RME, SMDD and SMDV). Next, we estimated stimulus selectivity for each cluster and found that while sensory neurons exhibit their maximal responses within 15 seconds, changes in bacterial stimuli drive maximal responses in command and motor neuron clusters after tens of seconds. Furthermore, we show that bacterial stimuli induce neural dynamics that are best described by a hyperbolic, not Euclidean, space, of dimensionality eight. The hyperbolic space provided a better description of neural activity than the standard Euclidean space. This space can be separated into three components - one sensory, and two motor directions (forward-backward and dorsal-ventral). Collectively, we show that <i>C. elegans</i> neural activity can be effectively represented in low-dimensional hyperbolic space to describe a sensorimotor transformation.</p>","PeriodicalId":72407,"journal":{"name":"bioRxiv : the preprint server for biology","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12132397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88626297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}