Genes & development最新文献

{"title":"Pediatric sarcomas: challenges and opportunities.","authors":"Yuan Gao, Kelly M Bailey, Samuel C Blackman, John H Bushweller, Shasha Chong, Kevin DeHond, Jolanta Grembecka, Mark E Hatley, Cigall Kadoch, Angela N Koehler, Corinne M Linardic, Phil Renna, Frederic J Reu, Miguel N Rivera, Elizabeth A Stewart, Bruce Stillman, E Alejandro Sweet-Cordero, Kimberly Stegmaier, Christopher R Vakoc, Lillian M Guenther","doi":"10.1101/gad.353549.125","DOIUrl":"10.1101/gad.353549.125","url":null,"abstract":"<p><p>Pediatric sarcomas are a heterogeneous group of rare mesodermal malignancies. These cancers, which affect children from infancy through adolescence and young adulthood, are in general challenging to treat with currently available therapies. Biologically, many are characterized by quiet genomes, fusion oncoproteins, immune \"cold\" microenvironments, and vast epigenetic deregulation that contributes to diverse and complex mechanistic drivers. Multifaceted advancements in research strategies, including high-throughput screening, new model systems, surfaceome profiling, and study of oncogenic fusion condensates have led to new opportunities for understanding the biology of pediatric sarcomas. To continue to make progress for these difficult to treat cancers, it will be critical to continue to improve access to bioinformatic data, approach patient care using innovative clinical trial frameworks, and foster interdisciplinary partnerships among medicinal chemists, scientists, clinicians, advocates, and industry partners.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1370-1381"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13532659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic identification of germ granule proteins reveals specialized roles in RNAi and small RNA inheritance.","authors":"Shihui Chen, Lucas H Prescott, Craig C Mello, Carolyn M Phillips","doi":"10.1101/gad.353482.125","DOIUrl":"10.1101/gad.353482.125","url":null,"abstract":"<p><p>Biomolecular condensates, such as germ granules, organize RNAi pathways critical for fertility and genome regulation. However, the protein composition and functional contributions of these condensates remain poorly defined. Here, we applied TurboID proximity labeling to the <i>Caenorhabditis elegans</i> germ granule protein SIMR-1, integrating mass spectrometry with genetic screening, CRISPR-based tagging, and small RNA sequencing. This systematic approach identified several previously uncharacterized germ granule proteins that contribute to fertility, germline immortality, exogenous RNAi, and transgenerational inheritance. Small RNA sequencing of 21 mutants revealed broad and class-specific defects in siRNA and miRNA biogenesis, with distinct factors associated with defects in WAGO-class 22G-RNAs, CSR-class 22G-RNAs, or histone-directed small RNAs. Among these, we identified PINT-1, a highly disordered protein that directly interacts with and is recruited to germ granules by the PIWI Argonaute PRG-1. PINT-1 is required for piRNA-dependent and -independent secondary siRNA biogenesis and germline development. Comparative genomics revealed that PINT-1 has coevolved with PRG-1 across clade V nematodes, with a conserved structured N terminus and a rapidly diverging repeat-rich intrinsically disordered region. Together, our findings expand the germ granule proteome and reveal how distinct condensate components contribute to specialized functions within the small RNA pathways, while highlighting an evolutionarily coadapted PIWI interactor critical for siRNA biogenesis.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1484-1507"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13599730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148648510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNK1 is a targetable JAK-independent driver of STAT signaling and inflammation.","authors":"Tania P López-Palacios, Deshan Madhusanka, Samuel M Scott, Alec J Vaughan, Christina M Egbert, Tsz-Yin Chan, Yaphet Bustos, Spencer W Ashworth, Jacob M Truman, Angela Per Moreno, Tsz-Ming Tsang, Dasun N Jayatunge, Jingshu Yang, Paige Nelson, Fatima Al-Sudani, Madelyn Tarara, Emmalee Kohler, Nelson E Pereira Mendiola, Erik J Soderblom, Chris J Stubben, Paul A Stewart, Reza Kolasangiani, Kasidy K Dobish, Beate Knobel, Shannon M Buckley, Tamara C Bidone, Rory L Smoot, Amiko M Uchida, Mareen Morawe, Milena Armacki, Joshua L Andersen","doi":"10.1101/gad.353368.125","DOIUrl":"10.1101/gad.353368.125","url":null,"abstract":"<p><p>Deregulated inflammatory signaling via STAT family transcription factors, particularly STAT1, underlies a variety of immune-related diseases, including inflammatory bowel disease. Whereas activation of STATs by JAKs via canonical receptor-driven JAK-STAT signaling is well understood, little is known about JAK-independent mechanisms of STAT activation. Here, we identify the understudied nonreceptor tyrosine kinase TNK1 as a therapeutically targetable, JAK-independent activator of STAT signaling. Using a multiomics approach, we mapped a network of TNK1 substrates associated with protein condensates and proinflammatory signaling, including STAT1. We found that TNK1, but not its sister kinase ACK1, directly phosphorylates STATs at well described STAT-activating JAK sites. In cells, TNK1-mediated STAT1 phosphorylation and activation occurs independently of JAKs. Imaging and interactomics data suggest that TNK1 interacts with STAT1 in cytosolic condensates, which likely compartmentalize TNK1-substrate interactions. We show that an intrinsically disordered proline-rich region in TNK1, which includes a 14-3-3 docking phosphorylation site, is required for the formation of kinase-active TNK1 condensates and STAT1 phosphorylation. Mutations within the proline-rich region that eliminate 14-3-3 binding increase formation of TNK1 condensates, suggesting a model in which 14-3-3 acts as a clamp that constrains the flexible PRR to inhibit condensate formation and STAT1 activation. Finally, we show that TNK1 is a targetable driver of STAT1-mediated inflammation in the gut as inhibition of TNK1 reduces active STAT1 in the colon and ameliorates colitis symptoms in mice.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1408-1428"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MRE11 suppresses germline mutagenesis at meiotic double-strand breaks in mice.","authors":"Agnieszka Lukaszewicz, Thomas E Wilson, Soonjoung Kim, Scott Keeney, Maria Jasin","doi":"10.1101/gad.353693.126","DOIUrl":"10.1101/gad.353693.126","url":null,"abstract":"<p><p>SPO11 forms hundreds of double-strand breaks (DSBs) to initiate meiotic recombination that is normally error-free. However, SPO11 activity can be mutagenic when one chromatid incurs closely spaced DSBs (double cuts), especially when DSBs are dysregulated by loss of the ATM kinase. De novo indels and structural variants can arise via end joining at double cuts within a single hotspot (microdeletions) or at adjacent hotspots separated by at least 30 kb, as we now show, sometimes accompanied by ectopic insertions of double-cut fragments. Here, we investigate how meiotic DSB end processing influences end joining. In MRE11-deficient mouse spermatocytes, which do not resect their DSBs, deletions at double cuts occur readily, with end-joining breakpoint profiles closely matching SPO11 DSB profiles. Microdeletions suggest that two DSBs can be as close as ∼21 bp. The tyrosyl-DNA phosphodiesterase TDP2 contributes to both deletion formation and ectopic insertion of double-cut fragments, presumably by removing SPO11 from DNA ends prior to joining. Finally, observations suggest a cooperative role for MRE11 and ATM in locally regulating DSB distributions. Our findings provide insight into the mechanism of de novo mutation origin, emphasizing the role of meiotic DSBs in shaping genome evolution.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1466-1483"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13532658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148648452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting <i>EZH2</i> oncogenic splicing: decoding the regulatory network and antisense correction.","authors":"Md Rafikul Islam, Preeti Nagar, Naomi McNaughton, Shabiha Afroj Heeamoni, Md Mahbub Hasan, Shila Kandel, Israt Jahan Mukta, Panagiotis Tsakiroglou, William Brian Dalton, Omar Abdel-Wahab, Adrian R Krainer, Mohammad Alinoor Rahman","doi":"10.1101/gad.353628.126","DOIUrl":"10.1101/gad.353628.126","url":null,"abstract":"<p><p>Recurrent mutations in splicing factors (SFs) have been established as crucial drivers of tumorigenesis in several types of blood cancer and are also common in a variety of solid tumors. Mutations change the RNA-binding preferences of SFs, promote global splicing alterations, and often generate erroneous mRNAs that are then degraded by nonsense-mediated mRNA decay (NMD). Consequently, several critical genes linked to hematopoiesis are dysregulated, leading to blood cancer. Although the field has progressed considerably in identifying aberrant genes and affected pathways, effective therapies have not yet emerged. To address this key gap, we instigated a gene-specific targeted strategy by unlocking the regulatory network. As a proof of concept, we scrutinized a tumor suppressor gene, <i>EZH2</i>, which is a bona fide target in SRSF2 mutated cancer. We precisely defined splicing <i>cis</i>-elements in <i>EZH2</i> transcripts and illustrated the dynamic choreography of regulatory proteins in the entire splicing and NMD catalytic pathways. We then designed antisense oligonucleotides (ASOs) targeting important regulatory sites. Our lead ASO successfully corrects aberrant splicing and NMD, restores the expression and function of EZH2, and partially rescues hematopoietic defects and cellular properties. Our study demonstrates that ASO pharmacology is an actionable strategy for clinical development, challenging the existing paradigms in SF mutated cancers.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1508-1522"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13474417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Architectural logic of the 3D genome: mechanisms of dysregulation and emerging cancer therapeutics.","authors":"Rebecca G Smith, Hannah M Wilson, Kathleen L Schiela, Yu Liu","doi":"10.1101/gad.353831.126","DOIUrl":"10.1101/gad.353831.126","url":null,"abstract":"<p><p>The three-dimensional (3D) genome provides an essential layer of organization that shapes genome function in space and time. Chromatin compartments and topologically associating domains (TADs) arise from the interplay between intrinsic properties of chromatin and architectural factors, including cohesin and CTCF. Despite substantial progress in defining these structural features, whether 3D genome architecture plays a causal role in regulating processes such as transcription, DNA replication, and DNA repair, or instead reflects underlying regulatory activity, remains unresolved. Here, we use the distinction between chromatin-intrinsic features and architectural factors as a framework to evaluate evidence for causality in genome structure-function relationships. We extend this framework to cancer, where both intrinsic alterations (including noncoding mutations, structural variants, and changes in chromatin state) and architectural factor perturbations (such as mutations in architectural proteins and dysregulation of transcriptional machinery) disrupt genome organization and contribute to disease progression. These findings suggest that alterations in genome structure can, in some contexts, actively reshape oncogenic programs. A major limitation in applying 3D genome insights to cancer biology is the cost and complexity of omics assays. Recent advances in artificial intelligence (AI) and machine learning (ML) enable inference and prediction of 3D genome organization from sequence and epigenomic features, providing insight into the extent to which genome folding is encoded intrinsically versus dynamically regulated in architectural factors. This perspective provides a unified view of how genome structure is established, how it relates to function, and how its disruption contributes to tumorigenesis.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148827295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal small RNAs as gatekeepers of hybrid compatibility in plants and animals.","authors":"Katarzyna Dziasek, Claudia Köhler","doi":"10.1101/gad.353754.126","DOIUrl":"10.1101/gad.353754.126","url":null,"abstract":"<p><p>Hybridization between species can enable introgression of advantageous traits, yet hybrid offspring often show reduced fitness, sterility, or developmental arrest due to postzygotic hybrid incompatibility. Understanding the molecular bases of these barriers could help overcome reproductive limits and enable the creation of currently inaccessible hybrids. In this review, we compare two small RNA-associated routes through which parental genomes can become incompatible: maternally biased sirenRNAs in the endosperm of flowering plants and animal PIWI-interacting RNAs (piRNAs), with emphasis on <i>Drosophila</i> hybrid dysgenesis and mammalian pachytene piRNA biology. We highlight conceptual parallels, including sequence-specific recognition, dosage-sensitive regulation, transposon or repeat control, and parent-of-origin effects. We also emphasize important differences: sirenRNA-associated incompatibility in plants emerges postfertilization during endosperm development, whereas piRNA-mediated incompatibilities in animals primarily affect germline genome defense and reproductive fertility.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1382-1396"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A conserved Notch-Meis1-Pbx cascade specifies secretory progenitors into spatially diverse intestinal <i>best4</i> ⁺ cells.","authors":"Abhinav Sur, Ella X Segal, Michael P Nunneley, Jason W Sinclair, Morgan Kathleen Prochaska, Louis E Dye, Yalan Wu, Liezhen Fu, Yun-Bo Shi, James Iben, Benjamin Feldman, Jeffrey A Farrell","doi":"10.1101/gad.353662.126","DOIUrl":"10.1101/gad.353662.126","url":null,"abstract":"<p><p><i>best4</i> ⁺ cells are a recently described vertebrate intestinal epithelial cell type. <i>best4</i> ^<i>+</i> cells are altered in inflammatory bowel disease and colorectal cancer, suggesting that stimulation of their homeostatic replenishment may have therapeutic potential. However, the development and function of <i>best4</i> ⁺ cells remain unclear. Since mice lack <i>best4</i> ⁺ cells, we established zebrafish as a tractable in vivo model to observe, manipulate, and remove <i>best4</i> ⁺ cells in an organismal context. We dissected <i>best4</i> ⁺ cell developmental regulation in vivo from birth to differentiation and specialization, focusing on factors conserved in <i>best4</i> ⁺ cells across vertebrates. Lineage tracing demonstrated that <i>best4</i> ⁺ cells arise from secretory progenitors, where Notch/Dll4 signaling mediates a decision between <i>best4</i> ⁺ and enterochromaffin cells by triggering <i>meis1b</i> expression. Following specification by <i>meis1b</i>, <i>pbx3a</i> spatially diversifies <i>best4</i> ⁺ cells, which develop regional heterogeneity in gene expression, intracellular pH, and function. In vivo live imaging and removal of <i>best4</i> ⁺ cells showed that <i>best4</i>+ cells sense luminal pH changes and extend dynamic luminal and stromal projections, but are not required to restore global luminal pH after challenge. Altogether, this study experimentally delineates <i>best4</i> ⁺ cell developmental regulation and develops a genetic toolkit to examine their function in vivo, both of which will aid investigating how <i>best4</i> ⁺ cells are altered or can be restored during disease.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1553-1574"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148689120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal expression of bromodomain proteins alters neuronal health and peripheral protein homeostasis to promote longevity.","authors":"Naibedya Dutta, Daniel Hicks, Edgar Esparza, Anna Entin, Priyadharshini Vijayakumar, Caitlin M Lange, Tripti Nair, Elijah A Roditi, Athena Alcala, Maxim Averbukh, Matthew Vega, Rebecca Aviles Barahona, Caitlin McTygue, Veronica Kuo, Juri Kim, Herbert Anson, Aeowynn J Coakley, George Wang, Steven E Pilley, Max A Thorwald, Whitaker Cohn, Sean P Curran, Nicolas Brouilly, Caroline Kumsta, Rachel N Arey, Peter J Mullen, Gilberto Garcia, Ryo Higuchi-Sanabria","doi":"10.1101/gad.353559.125","DOIUrl":"10.1101/gad.353559.125","url":null,"abstract":"<p><p>Longevity and stress resilience require precise coordination of gene expression programs across tissues. Here, we demonstrate that overexpression of the chromatin reader <i>bet-1</i> specifically in neurons of <i>Caenorhabditis elegans</i> promotes organismal longevity and stress resistance via cell-nonautonomous signaling. Neuronal <i>bet-1</i> elicits a neurotransmitter-dependent signal that activates the conserved stress-responsive transcription factor HSF-1 in the intestine, enhancing proteostasis, oxidative stress resistance, metabolic remodeling, and immune defense. Life span extension by neuronal <i>bet-1</i> requires both <i>hsf-1</i> and <i>daf-16</i> in neurons but only requires <i>hsf-1</i> in peripheral tissues. Using bulk RNA sequencing, we reveal distinct prolongevity pathways that include enhanced heat-shock response, proteostasis, increased actin stability, and resistance to pathogens, which likely together coordinate the prolongevity effects of neuronal <i>bet-1</i> Our findings establish BET-1 as a potent nonautonomous regulator of aging and stress response, highlighting chromatin readers as upstream modulators of intertissue signaling and systemic resilience.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1523-1552"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13532663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBM39 modulates UPR signaling through alternative splicing of IRE1α/<i>ERN1</i>.","authors":"Jeongjin J Kim, Amit K Behera, Arun Prasath Damodaran, Shreya Kordale, Thomas Gonatopoulos-Pournatzis","doi":"10.1101/gad.353632.126","DOIUrl":"10.1101/gad.353632.126","url":null,"abstract":"<p><p>The unfolded protein response (UPR) preserves endoplasmic reticulum proteostasis through coordinated signaling pathways, including the IRE1α-XBP1 axis, which promotes adaptive transcriptional programs via noncanonical XBP1 mRNA splicing. However, upstream mechanisms regulating this pathway remain incompletely defined. Here, we apply CRASP-seq, a scalable RNA-coupled CRISPR screening platform, to systematically identify regulators of XBP1 splicing. We uncovered the U2 snRNP auxiliary factor RBM39 as a critical positive regulator of this process. Perturbation of RBM39 or U2 snRNP components induces alternative splicing of <i>ERN1</i>, leading to exon-18 skipping and the production of an unstable transcript subject to nonsense-mediated decay, as well as a truncated IRE1α isoform that acts in a dominant-negative manner to suppress XBP1 splicing. Mechanistically, we show that heat shock reduces RBM39 functional activity and promotes <i>ERN1</i> exon-18 skipping, thereby attenuating IRE1α-XBP1 signaling. Functionally, hyperactivation of this pathway is detrimental under proteotoxic stress, suggesting that exon-18 skipping serves as a stress-adaptive mechanism to limit UPR output. Together, our findings reveal a previously unrecognized regulatory axis linking the canonical splicing machinery to UPR signaling and establish alternative splicing of <i>ERN1</i> as a key modulator of cellular stress responses.</p>","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1448-1465"},"PeriodicalIF":7.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13532665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148689043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}