Tianqi Xu, Dan Fang, Fulei Li, Zhiqiang Wang, Yuan Liu
{"title":"Vitamin B6 resensitizes mcr-carrying Gram-negative bacteria to colistin.","authors":"Tianqi Xu, Dan Fang, Fulei Li, Zhiqiang Wang, Yuan Liu","doi":"10.1038/s42003-025-07911-5","DOIUrl":"10.1038/s42003-025-07911-5","url":null,"abstract":"<p><p>Antimicrobial resistance poses a severe threat to human health, with colistin serving as a critical medication in clinical trials against multidrug-resistant Gram-negative bacteria. However, the efficacy of colistin is increasingly compromised due to the rise of MCR-positive bacteria worldwide. Here, we reveal a notable metabolic disparity between mcr-positive and -negative bacteria through transcriptome and metabolomics analysis. Specifically, pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, was significantly diminished in mcr-positive bacteria. Conversely, supplementing with PLP could reverse the metabolic profile of drug-resistant bacteria and effectively restore colistin's bactericidal properties. Mechanistically, PLP was found to augment bacterial proton motive force by inhibiting the Kdp transport system, a bacterial K<sup>+</sup> transport ATPase, thereby facilitating the binding of the positively charged colistin to the negatively charged bacterial membrane components. Furthermore, PLP supplementation triggers ferroptosis-like death by accumulating ferrous ions and inducing lipid peroxidation. These two modes of action collectively resensitize mcr-harboring Gram-negative bacteria to colistin therapy. Altogether, our study provides a novel metabolic-driven antibiotic sensitization strategy to tackle antibiotic resistance and identifies a potentially safe antibiotic synergist.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"459"},"PeriodicalIF":5.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143662873","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}
Qiang Liu, Lu Yan, Tao Wu, Qinghua Wu, Ben Ke, Wen Shen
{"title":"Peli1, regulated by m<sup>6</sup>A modification, suppresses NLRP3 inflammasome activation in atherosclerosis by inhibiting YB-1.","authors":"Qiang Liu, Lu Yan, Tao Wu, Qinghua Wu, Ben Ke, Wen Shen","doi":"10.1038/s42003-025-07839-w","DOIUrl":"10.1038/s42003-025-07839-w","url":null,"abstract":"<p><p>The activation of pyrin domain-containing-3 (NLRP3) inflammasome in macrophages is a risk factor accelerating the progression of atherosclerosis (AS). Here, the function of pellino 1 (Peli1) in regulating the activation of NLRP3 inflammasome during the development of AS was investigated. Our results showed that Y-box binding protein 1 (YB-1) knockdown could inhibit the progression of AS in vivo, and YB-1 silencing repressed oxidized low-density lipoprotein (ox-LDL)-mediated lipid accumulation and inflammation in macrophages by inactivating NLRP3 inflammasome. E3 ubiquitination ligase Peli1 mediated ubiquitination-dependent degradation of YB-1 during AS progression. Moreover, it was found that YTH domain-containing 2 (YTHDC2) recognized methyltransferase-like 3 (METTL3)-mediated Peli1 N6-methyladenosine (m<sup>6</sup>A) modification and mediated Peli1 mRNA degradation. Rescue studies revealed that YB-1 upregulation abrogated the repressive effect of Peli1 upregulation on AS progression both in vitro and in vivo. Taken together, Peli1, regulated by m<sup>6</sup>A modification, inhibited YB-1-mediated activation of NLRP3 inflammasome in macrophages by promoting YB-1 ubiquitination to suppress the progression of AS.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"457"},"PeriodicalIF":5.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656237","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}
Caitlin D Palmer, Yara Ghnamah, Nurit Livnat-Levanon, Oded Lewinson, Amy C Rosenzweig
{"title":"The Escherichia coli AZY operon links copper uptake to antibiotic resistance.","authors":"Caitlin D Palmer, Yara Ghnamah, Nurit Livnat-Levanon, Oded Lewinson, Amy C Rosenzweig","doi":"10.1038/s42003-025-07884-5","DOIUrl":"10.1038/s42003-025-07884-5","url":null,"abstract":"<p><p>Copper import to the bacterial cytoplasm has been underinvestigated as bacterial cuproenzymes are extracytoplasmic. However, copper must access the cytoplasm to interact with metal-dependent transcription factors. In particular, the multiple drug antibiotic resistance (mar) operon is induced by a copper signal, the source of which has not been established. Here we show that the Escherichia coli AZY operon, which encodes the copper-binding periplasmic proteins YobA and YebY and the putative copper importer YebZ, mediates copper uptake. Copper uptake by YebZ depends on two conserved histidine residues and is modulated by YobA and YebY. Moreover, the AZY proteins are necessary for activation of the mar operon and mediate resistance to multiple antibiotics in a copper-dependent fashion. AZY-like operons are widespread in gram-negative bacteria, suggesting that this previously unknown link between copper and antibiotic resistance is a general mechanism that may offer an alternative therapeutic target for multidrug resistance.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"458"},"PeriodicalIF":5.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923076/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143662844","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":"IL-27 alleviates high-fat diet-induced obesity and metabolic disorders by inhibiting adipogenesis via activating HDAC6.","authors":"Yinsheng Zhong, Shujun Yang, Shuangmei Li, Sijun Yuan, Xuxiang Chen, Huibao Long, Haidong Wu, Yajie Guo, Tong Wang","doi":"10.1038/s42003-025-07918-y","DOIUrl":"10.1038/s42003-025-07918-y","url":null,"abstract":"<p><p>Obesity arises from an imbalance between adipogenesis and adipocyte thermogenesis. Interleukin-27 (IL-27), a heterodimer cytokine, is known to promote thermogenesis in brown adipose tissue. However, its role in adipogenesis remains unclear. This study aims to investigate the effects of IL-27 on adipogenesis both in vitro and in vivo, and to elucidate the underlying mechanisms. In vitro, an adipogenic differentiation model of adipose-derived mesenchymal stem cells (ADSCs) demonstrate that IL-27 is non-cytotoxic to ADSCs and inhibits ADSCs adipogenic differentiation. In vivo, using a high-fat diet (HFD)-induced obese mouse model and a targeted adipose tissue-specific IL-27 overexpression adeno-associated viral (AAV) vector, we confirm that IL-27 suppresses adipogenesis, prevents weight gain, and improves glucose and lipid metabolic homeostasis in obese mice. Additionally, the inhibition of adipogenesis by IL-27 is mediated through HDAC6 activation of the TGFβ/Smad3 signaling pathway. Our study suggests that IL-27 is a potential therapeutic target for obesity and metabolic disorders.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"460"},"PeriodicalIF":5.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143662839","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}
Yunyue Chen, Siyifei Wang, Luhao Zhang, Dandan Peng, Ke Huang, Baohua Ji, Junfen Fu, Yingke Xu
{"title":"POT, an optogenetics-based endogenous protein degradation system.","authors":"Yunyue Chen, Siyifei Wang, Luhao Zhang, Dandan Peng, Ke Huang, Baohua Ji, Junfen Fu, Yingke Xu","doi":"10.1038/s42003-025-07919-x","DOIUrl":"10.1038/s42003-025-07919-x","url":null,"abstract":"<p><p>Precise regulation of protein abundance is critical for cellular homeostasis, whose dysfunction may directly lead to human diseases. Optogenetics allows rapid and reversible control of precisely defined cellular processes, which has the potential to be utilized for regulation of protein dynamics at various scales. Here, we developed a novel optogenetics-based protein degradation system, namely Peptide-mediated OptoTrim-Away (POT) which employs expressed small peptides to effectively target endogenous and unmodified proteins. By engineering the light-induced oligomerization of the E3 ligase TRIM21, POT can rapidly trigger protein degradation via the proteasomal pathway. Our results showed that the developed POT-PI3K and POT-GPX4 modules, which used the iSH2 and FUNDC1 domains to specifically target phosphoinositide 3-kinase (PI3K) and glutathione peroxidase 4 (GPX4) respectively, were able to potently induce the degradation of these endogenous proteins by light. Both live-cell imaging and biochemical experiments validated the potency of these tools in downregulating cancer cell migration, proliferation, and even promotion of cell apoptosis. Therefore, we believe the POT offers an alternative and practical solution for rapid manipulation of endogenous protein levels, and it could potentially be employed to dissect complex signaling pathways in cell and for targeted cellular therapies.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"455"},"PeriodicalIF":5.2,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920400/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656239","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}
Lisa Weixler, Roko Žaja, Nonso J Ikenga, Jonas Siefert, Ganga Mohan, Gülcan Aydin, Sven Wijngaarden, Dmitri V Filippov, Bernhard Lüscher, Karla L H Feijs-Žaja
{"title":"Family-wide analysis of human macrodomains reveals novel activities and identifies PARG as most efficient ADPr-RNA hydrolase.","authors":"Lisa Weixler, Roko Žaja, Nonso J Ikenga, Jonas Siefert, Ganga Mohan, Gülcan Aydin, Sven Wijngaarden, Dmitri V Filippov, Bernhard Lüscher, Karla L H Feijs-Žaja","doi":"10.1038/s42003-025-07901-7","DOIUrl":"10.1038/s42003-025-07901-7","url":null,"abstract":"<p><p>ADP-ribosylation is well-known as protein posttranslational modification and was recently also identified as RNA posttranscriptional modification. When macrodomain proteins were identified as protein ADP-ribosylhydrolases, several ADP-ribosylation substrates were not yet identified. Therefore, the majority of macrodomain-containing proteins have not been tested towards these additional substrates and were considered to be inactive. Here, we compare in vitro activities of the human macrodomains on a range of ADP-ribosylated substrates. We confirm recent findings that PARP9macro1 and PARP14macro1 can remove ADP-ribose from acidic residues and provide evidence that also PARP14macro2 and PARP15macro2 can function as ADP-ribosylhydrolases. In addition, we find that both PARP9macro1 and PARP14macro1 are active as ADPr-RNA decapping protein domains. Notwithstanding these in vitro activities, our data furthermore indicate that in HEK293 cells, PARG is the major ADPr-RNA decapping enzyme. Our findings thus expand the spectrum of known catalytic activities of human macrodomains and demonstrate their different efficiencies towards nucleic acid substrates.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"453"},"PeriodicalIF":5.2,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656277","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}
Gülben Gürhan, Kenan Sevinç, Can Aztekin, Mert Gayretli, Alperen Yılmaz, Abdullah Burak Yıldız, Elif Naz Ervatan, Tunç Morova, Elif Datlı, Oliver D Coleman, Akane Kawamura, Nathan A Lack, Hamzah Syed, Tamer Önder
{"title":"A chromatin-focused CRISPR screen identifies USP22 as a barrier to somatic cell reprogramming.","authors":"Gülben Gürhan, Kenan Sevinç, Can Aztekin, Mert Gayretli, Alperen Yılmaz, Abdullah Burak Yıldız, Elif Naz Ervatan, Tunç Morova, Elif Datlı, Oliver D Coleman, Akane Kawamura, Nathan A Lack, Hamzah Syed, Tamer Önder","doi":"10.1038/s42003-025-07899-y","DOIUrl":"10.1038/s42003-025-07899-y","url":null,"abstract":"<p><p>Cell-autonomous barriers to reprogramming somatic cells into induced pluripotent stem cells (iPSCs) remain poorly understood. Using a focused CRISPR-Cas9 screen, we identified Ubiquitin-specific peptidase 22 (USP22) as a key chromatin-based barrier to human iPSC derivation. Suppression of USP22 significantly enhances reprogramming efficiency. Surprisingly, this effect is likely to be independent of USP22's deubiquitinase activity or its association with the SAGA complex, as shown through module-specific knockouts, and genetic rescue experiments. USP22 is not required for iPSC derivation or maintenance. Mechanistically, USP22 loss during reprogramming downregulates fibroblast-specific genes while activating pluripotency-associated genes, including DNMT3L, LIN28A, SOX2, and GDF3. Additionally, USP22 loss enhances reprogramming efficiency under naïve stem cell conditions. These findings reveal an unrecognized role for USP22 in maintaining somatic cell identity and repressing pluripotency genes, highlighting its potential as a target to improve reprogramming efficiency.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"454"},"PeriodicalIF":5.2,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656273","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}
Jiashuo Liu, Jingjing Zhang, Tingting Zhao, Mengya Zhao, Min Su, Ye Chen, Zheying Huang, Yuyan Wang, Chaoyue Zhong, Zheng Hu, Ping Zhou, Rui Tian, Dan He
{"title":"SunTag-PE: a modular prime editing system enables versatile and efficient genome editing.","authors":"Jiashuo Liu, Jingjing Zhang, Tingting Zhao, Mengya Zhao, Min Su, Ye Chen, Zheying Huang, Yuyan Wang, Chaoyue Zhong, Zheng Hu, Ping Zhou, Rui Tian, Dan He","doi":"10.1038/s42003-025-07893-4","DOIUrl":"10.1038/s42003-025-07893-4","url":null,"abstract":"<p><p>Prime editing (PE) holds tremendous potential in the treatment of genetic diseases because it can install any desired base substitution or local insertion/deletion. However, the full-length PE effector size (6.3-kb) is beyond the packaging capacity of adeno-associated virus (AAV), hindering its clinical translation. Various splitting strategies have been used to improve its delivery, but always accompanied by compromised PE efficiency. Here, we developed a modular and efficient SunTag-PE system that splits PE effectors into GCN4-nCas9 and single-chain variable fragment (scFv) tethered reverse transcriptase (RT). We observed that SunTag-PEs with 1×GCN4 in the N terminus of nCas9 was the most efficient configuration rather than multiple copies of GCN4. This SunTag-PE strategy achieved editing levels comparable to canonical fused-PE (nCas9 and RT are linked together) and higher than other split-PE strategies (including sPE and MS2-PE) in both PE2 and PE3 forms with no increase in insertion and deletion (indel) byproducts. Moreover, we successfully validated the modularity of SunTag-PE system in the Cas9 orthologs of SauCas9 and FrCas9. Finally, we employed dual AAVs to deliver SunTag-ePE3 and efficiently corrected the pathogenic mutation in HBB mutant cell line. Collectively, our SunTag-PE system provides an efficient modular splitting strategy for prime editing and further facilitate its transformation in clinics.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"452"},"PeriodicalIF":5.2,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647595","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":"The differentiated impacts and constraints of allometry, phylogeny, and environment on the ruminants' ankle bone.","authors":"Orgebin Pierre, Dziomber Laura, Aiglstorfer Manuela, Mennecart Bastien","doi":"10.1038/s42003-025-07898-z","DOIUrl":"10.1038/s42003-025-07898-z","url":null,"abstract":"<p><p>The astragalus is a hinged bony organ common to many tetrapods. Several factors, including allometry, phylogeny, and environment, constrain its morphology. Due to the underlying risk of these factors being confounding, previous works have frequently highlighted the difficulty in discerning the specific influence of each factor. Here, we conducted allometric and size-adjusted clade and ecomorphological analyses to assess the contribution of each of these three parameters to the morphological variation of the astragalus in ruminant artiodactyls. 3D geometric morphometric analyses confirm the astragalus' highly integrated structure and multifactorial morphological responses. Sturdier astragali are correlated with heavier bodies. Bovids tend to display larger proximal trochlear ridges, and moschids show a prominent posterior process. The degree of development of areas where joints and ligaments intersect reflects the degree of freedom of the ankle and the locomotion type. This study provides new perspectives on the evolution of ruminants and their interactions with their environment.</p>","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"456"},"PeriodicalIF":5.2,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656244","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}
Alejandro Martínez, Stefano Bonaglia, Maikon Di Domenico, Gustavo Fonseca, Jeroen Ingels, Katharina M Jörger, Christopher Laumer, Francesca Leasi, Daniela Zeppilli, Elisa Baldrighi, Holly Bik, Diego Cepeda, Marco Curini-Galletti, Asher D Cutter, Giovanni Dos Santos, Simone Fattorini, Dagmar Frisch, Sabine Gollner, Ulf Jondelius, Alexandra Kerbl, Kevin M Kocot, Nabil Majdi, Stefano Mammola, José M Martín-Durán, André Menegotto, Paul A Montagna, Francisco J A Nascimento, Nicolas Puillandre, Anne Rognant, Nuria Sánchez, Isaac R Santos, Andreas Schmidt-Rhaesa, Michaela Schratzberger, Federica Semprucci, Mauricio Shimabukuro, Paul J Sommerfield, Torsten H Struck, Martin V Sørensen, Andreas Wallberg, Katrine Worsaae, Hiroshi Yamasaki, Diego Fontaneto
{"title":"Fundamental questions in meiofauna research highlight how small but ubiquitous animals can improve our understanding of Nature.","authors":"Alejandro Martínez, Stefano Bonaglia, Maikon Di Domenico, Gustavo Fonseca, Jeroen Ingels, Katharina M Jörger, Christopher Laumer, Francesca Leasi, Daniela Zeppilli, Elisa Baldrighi, Holly Bik, Diego Cepeda, Marco Curini-Galletti, Asher D Cutter, Giovanni Dos Santos, Simone Fattorini, Dagmar Frisch, Sabine Gollner, Ulf Jondelius, Alexandra Kerbl, Kevin M Kocot, Nabil Majdi, Stefano Mammola, José M Martín-Durán, André Menegotto, Paul A Montagna, Francisco J A Nascimento, Nicolas Puillandre, Anne Rognant, Nuria Sánchez, Isaac R Santos, Andreas Schmidt-Rhaesa, Michaela Schratzberger, Federica Semprucci, Mauricio Shimabukuro, Paul J Sommerfield, Torsten H Struck, Martin V Sørensen, Andreas Wallberg, Katrine Worsaae, Hiroshi Yamasaki, Diego Fontaneto","doi":"10.1038/s42003-025-07888-1","DOIUrl":"10.1038/s42003-025-07888-1","url":null,"abstract":"","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"449"},"PeriodicalIF":5.2,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914145/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647589","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}
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
