Biology of Reproduction最新文献

{"title":"Equine endometrial organoids preserve tissue structure and cycle-stage transcriptional identity†.","authors":"Margo Helene Verstraete, Fianne Kuijpers, William Holl, Jamie Norris, Machteld van Heule, Soledad Martin-Pelaez, Christina Heard, José Uribe-Salazar, Anibal Armien, Alan Conley, Ward De Spiegelaere, Mariano Carossino, Peter Daels, Pouya Dini","doi":"10.1093/biolre/ioaf232","DOIUrl":"10.1093/biolre/ioaf232","url":null,"abstract":"<p><p>The endometrium is a hormonally responsive tissue that undergoes cyclic remodeling. Although endometrial organoids have been established in several species, detailed characterization remains limited. Here, we assessed the structural and molecular fidelity of equine endometrial organoids across reproductive cycle stages and during extended culture. Organoids were generated from biopsies collected during estrus and diestrus and analyzed using histology, immunohistochemistry, electron microscopy, and bulk- and single-cell RNA sequencing. Organoids formed polarized cystic structures composed of columnar cells with microvilli, tight junctions, and secretory vesicles. Compared to native tissue, organoids showed higher expression of genes involved in proliferation and metabolism, and lower expression of genes related to differentiation, angiogenesis, and immune responses. Single-cell analysis identified diverse epithelial and stromal populations in both tissue and organoids. While most cell types were preserved, organoids were enriched in progenitor-like cells but underrepresented in ciliated, proliferative glandular, endothelial, smooth muscle, and antigen-presenting cells. Cycle-specific differences were observed in morphology, hormone receptor expression, and gene expression profiles. Estrus-derived organoids showed increased proliferation and metabolic activity. Although organoids retained transcriptional signatures reflective of the hormonal cycle stage of the source tissue, these signatures faded with prolonged culture, despite overall transcriptomic stability. In summary, equine endometrial organoids replicate key features of the native tissue, retain reproductive cycle characteristics, and maintain transcriptomic stability over time. Endometrial organoids provide a robust platform to study the equine endometrium, though native tissue differences should be considered in the experimental design and data interpretation.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":"835-854"},"PeriodicalIF":3.0,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13017593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGF-β3 promotes trophoblast development in sheep embryos via ACSS2-dependent permissive lipid metabolism†.","authors":"Francesca Boffa, Marika Domenicone, Margherita Moncada, Martina Lo Sterzo, Luca Palazzese, Aurora Scudieri, Emanuele Capra, Barbari Lazzari, Luca Valbonetti, Luisa Gioia, Ramiro Alberio, Domenico Iuso, Pasqualino Loi, Marta Czernik","doi":"10.1093/biolre/ioaf220","DOIUrl":"10.1093/biolre/ioaf220","url":null,"abstract":"<p><p>Transforming growth factor-beta (TGF-β) supports the in vitro maintenance of embryonic and trophoblast stem cells. Here, we demonstrated that, in a sheep embryo model, the transition from morula to blastocyst is positively regulated by TGF-β3, primarily through its promotion of trophoblast development. Our results indicate that morulae treated with TGF-β3 develop at a higher rate into blastocysts, characterized by an expanded trophoblast layer marked by CDX-2 expression. In blastocysts, TGF-β3 mediates transcriptional activation of genes involved in cell adhesion and lipid metabolism pathways, leading to remarkable in vitro outgrowth expansion and a substantial increase in trophoblast lipid droplet content. Functional analysis reveals that the positive effects of TGF-β3 are mitigated by inhibition of Acetyl-CoA Synthetase Short-Chain Family Member 2 (ACSS2), a key enzyme upregulated by TGF-β3 and a promoter of de novo lipogenesis. These findings suggest that TGF-β3 modulates lipid metabolism during blastocyst formation and may play a potential role in regulating implantation and placental development.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":"773-783"},"PeriodicalIF":3.0,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13017937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The EDIcebreaker: a new educational inclusive tool.","authors":"Nour Abou Nader, Adélaïde Allais, Maryse Michèle Um, Hugh Clarke, Géraldine Delbès, Gustavo Zamberlam","doi":"10.1093/biolre/ioag057","DOIUrl":"https://doi.org/10.1093/biolre/ioag057","url":null,"abstract":"","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reciprocal embryo transfer and newborns cross-fostering between mouse lines selected for high or low swim stress-induced analgesia.","authors":"Łukasz Jankowski, Agata Nawrocka, Piotr Poznański, Jacek Z Kubiak, Jacek A Modliński, Anna Piliszek, Mariusz Sacharczuk","doi":"10.1093/biolre/ioag062","DOIUrl":"https://doi.org/10.1093/biolre/ioag062","url":null,"abstract":"<p><p>Pain tolerance varies significantly among humans, with disparities attributable to genetic factors and environmental influences. The developmental origins of health and disease approach postulate that pre- and early postnatal maternal environment affects individuals' health and well-being. In the present study, we aimed to determine the influence of prenatal and early postnatal maternal environment and care on the offspring's physiology and pain response. To this end, we analysed the influence of bidirectional embryo transfer (ET) and cross-fostering (CF) between two mouse lines divergently selected for high (HA) and low (LA) swim stress-induced analgesia (SSIA) on offspring phenotype, SSIA-related traits and opioid component of SSIA. Our findings reveal that both the fetal development and early maternal care significantly influence the level of SSIA in mice. HA mice born after ET to LA surrogate mothers showed reduced SSIA levels alongside a diminished effect of the opioid antagonist naloxone, suggesting a decreased opioid component in SSIA regulation. This effect was preserved in the F2 generation of individuals originating from ET, but not CF. Additionally, both ET and CF resulted in changes in body weight and body temperature towards an average value of the surrogate or foster maternal line; however, these changes were not preserved in the F2 generation. Together, our findings indicate that maternal influence during fetal development and the early postnatal period may influence physiological parameters, as well as traits associated with stress response. Maternal influence is more pronounced in progeny subject to ET, indicating a stronger influence of the prenatal period.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of KIT signaling in ovarian development and function: Insights from multisystem biology.","authors":"Wonmi So, Ashley E Pak, Amirhossein Abazarikia, Anat Chemerinski, Nataki Douglas, So-Youn Kim","doi":"10.1093/biolre/ioag061","DOIUrl":"10.1093/biolre/ioag061","url":null,"abstract":"<p><p>KIT signaling is a fundamental regulatory pathway that preserves cellular homeostasis and controls cell development and fate across a wide range of organs and cell types. Consistent with this pleiotropic role, mutations in c-KIT/Kit have been associated with a wide range of phenotypes, including sterility, piebaldism, nevus formation, mastocytosis, and multiple malignancies. The contribution of c-KIT/Kit to reproductive function has attracted sustained attention for several decades, underscoring its essential role in fertility and gonadal biology. KIT expression is observed in oocytes - localized to the oocyte membrane and the cytoplasm - as well as in theca cells and interstitial cells, suggesting a multifaceted role in follicular development. Notably, all Kit mutant models develop primary ovarian insufficiency (POI) with variable onset, characterized by endocrine dysfunction, impaired folliculogenesis, and eventual female infertility. These findings collectively establish KIT signaling as a critical regulator of ovarian integrity, as both gain- or loss-of-function mutations in Kit consistently recapitulate POI-associated phenotypes. However, despite substantial progress, the precise molecular mechanisms by which KIT signaling integrates these pathways to preserve primordial follicle survival and prevent POI remain incompletely understood. Here, we summarize current knowledge of KIT expression and the functional consequences of Kit mutations, with particular emphasis on oocytes across ovarian cell populations and in comparison to other organ systems in humans and mice. We further evaluate the physiological and pathological significance of ovarian KIT signaling in female fertility and highlight crucial knowledge gaps that must be addressed to fully elucidate its role in maintaining ovarian function.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteomic profiling reveals potential mechanisms regulating acquisition of luteolytic capacity in the bovine corpus luteum†.","authors":"Jillian M Hughes-Brown, Elizabeth H Medich, Joy L Pate, Camilla H K Hughes","doi":"10.1093/biolre/ioag059","DOIUrl":"https://doi.org/10.1093/biolre/ioag059","url":null,"abstract":"<p><p>The corpus luteum (CL) produces progesterone to support pregnancy but undergoes luteolysis in response to prostaglandin F2A (PGF2A) when pregnancy is absent. Developing CL resist PGF2A-induced regression. This acquisition of luteolytic capacity (ALC) occurs around day 5 of the estrous cycle in cattle. To understand the mechanisms underlying ALC, we evaluated transcriptomic and proteomic changes in the CL on days 4 and 6 of the estrous cycle. 1190 transcripts were greater on day 4 and 119 were greater on day 6 (Padj <0.05, log2FC > |1|). In the proteomics dataset, 2 proteins were greater on day 4, with 12 greater on day 6 (Padj <0.05, log2FC > |1|). Data were integrated with datasets of luteal changes during luteolysis and during early pregnancy, and gene ontology analysis was used to identify candidate pathways regulating luteal PGF2A responsiveness, including apoptosis, cellular stress response, and cytokine signaling. Apoptosis regulators increased on day 6 and increased in response to PGF2A in vivo, indicating a likely role in luteolytic cell death. Changes to regulators of antigen presentation and T cell programming suggested increased T cell activation on day 6. A luteal cell culture experiment revealed that apoptosis pathways were regulated by interferon gamma and immune pathways were regulated by luteinizing hormone in vitro. In summary, integration across datasets from multiple luteal states allowed identification of proposed mediators governing luteal survival and PGF2A response. Apoptosis and immune-related pathways, changes indicating increased activated T cells, may poise the CL to regress in response to PGF2A.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Secretogranin II-Derived Peptide Secretoneurin Differentially Stimulates Luteinizing Hormone Secretion by Age and Sex in Ex Vivo Murine Pituitaries†.","authors":"Ashley K Herdman, Alex Lagasse, Cole R Bolen, Milla M Reddick, Anessa Haney, Victoria G Ortega, Ulrich Boehm, Angus M MacNicol, Melanie C MacNicol, Tiffany K Miles, Gwen V Childs, Angela K Odle","doi":"10.1093/biolre/ioag058","DOIUrl":"https://doi.org/10.1093/biolre/ioag058","url":null,"abstract":"<p><p>Secretoneurin (SN) is a small, bioactive proteolytic product of secretogranin II (SCG2), a chromogranin protein involved in secretory vesicle packaging. SCG2 co-aggregates with luteinizing hormone (LH) in pituitary gonadotrope secretory granules and thus has long been associated with GnRH-regulated LH secretion. Previously, the SCG2-derived peptide SN has been identified as a regulator of LH production and secretion in fish and a murine gonadotrope-like cell line (LβT2). Though high levels of SCG2/SN are present in the mammalian pituitary, the role of pituitary SN has not been identified in mammals. It is further unknown if pituitary SN function varies with age and sex. Here, we identify a decrease in levels of precursor SCG2, and a trend towards increased levels of SN throughout postnatal developmental, particularly in females, following the onset of puberty. Additionally, proteomic and bioinformatic analyses of adult male and female pituitaries revealed protein-protein interactions between SCG2 and various peptides, many associated with prohormone processing and regulated secretion. Furthermore, we demonstrate for the first time that SN is capable of stimulating LH secretion from ex vivo mouse pituitaries, an effect previously documented only in non-mammalian vertebrate species and LβT2 cells. Exogenous SN stimulation significantly increased LH release from adult male (1.4x; p<0.01) and proestrous female (2.4x; p<0.0001) murine pituitaries. Notably, we found that SN treatment had no observed effect on LH secretion in prepubertal (PND14) male and female pituitaries, indicating that SN may function primarily in mature gonadotropes to promote fertility and estrous cycle progression.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147376101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fetal Hypothyroidism Induces Sex-Specific Epigenetic and Transcriptomic Alterations in the Porcine Placenta.","authors":"Sarah M Innis, J Alex Pasternak, Ryan Cabot","doi":"10.1093/biolre/ioag050","DOIUrl":"https://doi.org/10.1093/biolre/ioag050","url":null,"abstract":"<p><p>The placenta is critical for fetal development, supporting nutrient transport, while also isolating the developing conceptus from adverse maternal signals. The porcine placenta creates an enzymatic barrier for thyroid hormones following activation of the fetal endocrine system in early gestation. Perturbation of the fetal thyroid system can have significant developmental consequences. However, research examining the relationship between fetal thyroid hormone availability, the placental epigenome, and global effects on placental gene expression is limited, particularly in swine. Existing work on select placental genes suggests a potential compensatory response to fetal endocrine disruption during late gestation. We hypothesize that global placental epigenetic and transcriptomic changes may arise in response to induced fetal hypothyroidism. To address this hypothesis, we analyzed placental tissues from gestation day 86 fetuses exposed to 21-day maternal methimazole (MMI) treatment and matched controls. CUT&RUN profiling revealed differential histone mark enrichment, with enrichment of both marks predominantly gained in MMI samples. The placental histone mark status from female fetuses was more substantially altered in response to maternal MMI treatment than placental tissue from male fetuses. In contrast, while differential gene expression was apparent between control and MMI conditions, transcriptional changes were more pronounced in placental tissue from male fetuses. Integration of these datasets revealed treatment- and sex-dependent epigenetic and transcriptional variation. This work expands our understanding of the intricate interplay between fetal thyroid hormone levels and placental gene expression regulation and provides novel insights into the existence of sex-specific differences in placental epigenetic and transcriptomic responses to fetal endocrine disruption.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147376024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-carnitine ameliorates fibrosis and reproductive dysfunction in intrauterine adhesion via restoration of mitochondrial fatty acid oxidation.","authors":"Ke Peng, Congquan Wu, QiaoWen Lu, Yudong Wang, Mingqing Li, Qiliang Cai, Shujun Gao","doi":"10.1093/biolre/ioag054","DOIUrl":"https://doi.org/10.1093/biolre/ioag054","url":null,"abstract":"<p><strong>Introduction: </strong>Intrauterine adhesion (IUA) is a leading cause of secondary infertility, characterized by fibrosis and impaired endometrial regeneration. Although inflammation and fibrotic pathways have been studied, the metabolic mechanisms remain unclear. This study aimed to identify metabolic alterations in intrauterine adhesion and to evaluate whether L-carnitine (LCA) supplementation could restore mitochondrial function and alleviate fibrosis.</p><p><strong>Material and methods: </strong>Untargeted metabolomic profiling was performed on endometrial tissues from patients with IUA and controls using liquid chromatography-tandem mass spectrometry. An ethanol-induced mouse model of IUA was established and treated with LCA by intraperitoneal injection. Histological, immunohistochemical, and ultrastructural analyses assessed fibrosis, inflammation, and mitochondrial integrity. In vitro, lipopolysaccharide-stimulated endometrial epithelial cells were used to evaluate fatty acid oxidation (FAO), lipid droplet accumulation, mitochondrial function, reactive oxygen species (ROS) production, lipid peroxidation, and transforming growth factor beta secretion after L-carnitine treatment.</p><p><strong>Result: </strong>Metabolomics revealed profound depletion of carnitine and derivatives in IUA, accompanied by enrichment of pro-inflammatory prostaglandins and fibrosis-associated metabolites. LCA treatment in mice restored uterine morphology, reduced apoptosis, fibrosis, and inflammation, and improved pregnancy outcomes. In vitro, LCA restored FAO activity, reduced lipid droplet accumulation, preserved mitochondrial membrane potential, suppressed ROS and lipid peroxidation, and decreased TGF-β secretion in LPS-stimulated cells.</p><p><strong>Conclusion: </strong>This study establishes carnitine deficiency as a key driver of IUA, demonstrating that it disrupts mitochondrial FAO, promotes oxidative stress, and culminates in fibrosis. LCA supplementation not only restores metabolic homeostasis and reduces fibrotic progression but also improves reproductive outcomes, positioning it as a mechanistically grounded therapy for IUA.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147376070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RAB3B regulates vesicle uptake and tight junction integrity in amniotic epithelial cells and is downregulated in premature rupture of membranes.","authors":"Shuguang Su, Qiantao Ye, Feilong Chen, Qin Tian, Caixia Gan, Yanqiu Li","doi":"10.1093/biolre/ioag048","DOIUrl":"https://doi.org/10.1093/biolre/ioag048","url":null,"abstract":"<p><strong>Background: </strong>Premature rupture of membranes (PROM) is a major cause of preterm birth and neonatal mortality. Tight junctions are critical for maintaining fetal membrane barrier integrity. Ras-related protein Rab-3B (RAB3B), a key regulator of vesicle trafficking, may influence barrier homeostasis; however, its role in PROM remains unclear.</p><p><strong>Methods: </strong>Whole-transcriptome RNA sequencing was performed on fetal membrane tissues from 31 PROM patients and 10 full-term controls to identify differentially expressed genes. A PROM mouse model was established to access RAB3B expression and related pathological changes. In vitro, RAB3B was overexpressed or slienced in human amniotic epithelial cells (hAECs) to evaluate its effect on cell migration, epithelial-mesenchymal transition (EMT), epithelial permeability, and tight junction integrity. Extracellular vesicles (EVs) were isolated to explore the role of RAB3B in EV internalization and EV-mediated regulation of tight junctions.</p><p><strong>Results: </strong>RAB3B expression was significantly downregulated in fetal membranes from PROM patients and PROM mice. PROM mice exhibited increased membrane permeability, enhanced apoptosis, elevated pro-inflammatory cytokine levels, and reduced expression of tight junction proteins. In hAECs, RAB3B overexpression promoted cell migration, suppressed EMT, reduced epithelial permeability, and upregulated tight junction proteins, whereas RAB3B knockdown produced opposite effects. Furthermore, RAB3B enhanced EV internalization and potentiated the beneficial effects EVs on tight junction integrity.</p><p><strong>Conclusion: </strong>RAB3B is markedly downregulated in PROM and plays a critical role in maintaining fetal membrane barrier integrity. By enhancing tight junctions and promoting EV-mediated material transport, RAB3B contributes to fetal membrane repair, highlighting its potential as a therapeutic target for PROM prevention and treatment.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147368903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}