Genes & development最新文献_第7页

Mechanisms coordinating exit from the stem cell state in mammals. 哺乳动物干细胞状态的协调退出机制。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353584.125

Emily J Park, Florencia Levin-Ferreyra, Bruno Di Stefano

{"title":"Mechanisms coordinating exit from the stem cell state in mammals.","authors":"Emily J Park, Florencia Levin-Ferreyra, Bruno Di Stefano","doi":"10.1101/gad.353584.125","DOIUrl":"10.1101/gad.353584.125","url":null,"abstract":"Differentiation requires coordinated exit from the stem cell state, during which gene regulatory networks sustaining self-renewal are dismantled, while lineage-specific programs are activated. This transition is governed by chromatin modifications, transcriptional networks, RNA processing, translational control, and metabolic rewiring that must operate with temporal precision. Despite significant progress in identifying individual regulatory components, understanding how these layers integrate to orchestrate irreversible cell fate commitment remains a fundamental challenge. This review examines common and unique regulatory principles governing stem cell exit, from totipotency during early embryogenesis to tissue-specific stem cell differentiation in adults. We synthesize recent findings on regulatory mechanisms across mammalian species, highlight species-specific adaptations, and explore the concept of reversibility in differentiation. Elucidating these principles has broad implications for regenerative medicine, cellular reprogramming, and diseases in which differentiation programs are corrupted.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"982-1011"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13267984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971763","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}

引用次数: 0

Evolutionarily conserved spliceosome-exosome pathway in nuclear mRNA surveillance. 核mRNA监测中的进化保守剪接体-外泌体途径。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353594.125

Daniel K Abbas, Fabien Bonneau, Max E Wilkinson, Steffen Schüssler, Jérôme Basquin, Elena Conti

{"title":"Evolutionarily conserved spliceosome-exosome pathway in nuclear mRNA surveillance.","authors":"Daniel K Abbas, Fabien Bonneau, Max E Wilkinson, Steffen Schüssler, Jérôme Basquin, Elena Conti","doi":"10.1101/gad.353594.125","DOIUrl":"10.1101/gad.353594.125","url":null,"abstract":"Intron-containing mRNAs are cotranscriptionally spliced and assembled into messenger ribonucleoprotein (mRNP) particles, a process monitored by surveillance pathways. Here, we combined biochemical and structural approaches to elucidate the mechanisms by which mRNPs are sorted between two opposing fates: nuclear degradation and cytoplasmic export. While the human GANP-PCID2 complex is known to connect mRNPs to nuclear export, our data indicate that the LENG8-PCID2 complex operates as an mRNP decay connector, coupling nuclear mRNPs to the RNA-degrading exosome via the PAXT adaptor complex. Both recognize the mRNP component UAP56, but LENG8-PCID2 uniquely associates with early splicing factors through a direct interaction with U1A and RRP1B. Similarly, the Thp3-Csn12 ortholog in budding yeast couples the early splicing factors Mud2-Bbp with the nuclear exosome. The spliceosome-exosome mRNP decay pathway we uncovered reveals molecular principles that remain strikingly conserved across evolution, despite the fundamental differences in splicing and decay between humans and budding yeast.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1119-1132"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948273","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}

引用次数: 0

MYC serine 62 phosphorylation promotes its association with DNA double-strand breaks to facilitate repair and cell survival under genotoxic stress. MYC丝氨酸62磷酸化促进其与DNA双链断裂的关联，以促进基因毒性应激下的修复和细胞存活。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.352832.125

Gabriel M Cohn, Colin J Daniel, Jennifer R Eng, Alannah S MacDonald, Jonathan St-Germain, Nadja M Pieper, Toshita Kannan, Xiao-Xin Sun, Carl Pelz, Ariffin Ali, Koei Chin, Alexander Smith, Charles D Lopez, Jonathan R Brody, Brian Raught, Linda Z Penn, Martin Eilers, Mu-Shui Dai, Rosalie C Sears

{"title":"MYC serine 62 phosphorylation promotes its association with DNA double-strand breaks to facilitate repair and cell survival under genotoxic stress.","authors":"Gabriel M Cohn, Colin J Daniel, Jennifer R Eng, Alannah S MacDonald, Jonathan St-Germain, Nadja M Pieper, Toshita Kannan, Xiao-Xin Sun, Carl Pelz, Ariffin Ali, Koei Chin, Alexander Smith, Charles D Lopez, Jonathan R Brody, Brian Raught, Linda Z Penn, Martin Eilers, Mu-Shui Dai, Rosalie C Sears","doi":"10.1101/gad.352832.125","DOIUrl":"10.1101/gad.352832.125","url":null,"abstract":"Genomic instability is a hallmark of cancer, driving oncogenic mutations that enhance tumor aggressiveness and drug resistance. MYC, a master transcription factor that is deregulated in nearly all human tumors, paradoxically induces replication stress and associated DNA damage while also increasing expression of DNA repair factors and mediating resistance to DNA-damaging therapies. Emerging evidence supports a nontranscriptional role for MYC in preserving genomic integrity at sites of active transcription and protecting stalled replication forks under stress. Understanding how MYC's genotoxic and genoprotective functions diverge may reveal new therapeutic strategies for MYC-driven cancers. Here, we identify a noncanonical role of MYC in DNA damage response (DDR) through its association with DNA breaks. We show that phosphorylation at serine 62 (pS62-MYC) is crucial for the efficient recruitment of MYC to damage sites, its interaction with repair factors BRCA1 and RAD51, and effective DNA repair to support cell survival under stress. Proteomic profiling of the MYC interactome confirms a conserved interaction with components of the DDR pathway. These findings establish pS62-MYC as a key regulator of genomic stability and a potential therapeutic target in cancers.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1152-1172"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948232","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}

引用次数: 0

MLL4/KMT2D histone methyltransferase and JUNB cooperate in a feed-forward loop to support AP-1-dependent TGF-β signaling. MLL4/KMT2D组蛋白甲基转移酶和JUNB在前馈环路中合作，支持ap -1依赖性TGF-β信号传导。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353313.125

Timothy En Haw Chan, Md Saiful Islam, Omid Fotouhi, Mert Bozkurt, Sheikh Nizamuddin, Katrin M Schüle, Sebastian J Arnold, H T Marc Timmers

{"title":"MLL4/KMT2D histone methyltransferase and JUNB cooperate in a feed-forward loop to support AP-1-dependent TGF-β signaling.","authors":"Timothy En Haw Chan, Md Saiful Islam, Omid Fotouhi, Mert Bozkurt, Sheikh Nizamuddin, Katrin M Schüle, Sebastian J Arnold, H T Marc Timmers","doi":"10.1101/gad.353313.125","DOIUrl":"10.1101/gad.353313.125","url":null,"abstract":"Transforming growth factor β (TGF-β) signaling is a highly pleiotropic pathway with an important role in development, homeostasis, and cancer. Chromatin regulators contribute to the regulation of TGF-β-responsive transcription. The requirement of subunits of the MLL3/MLL4 histone methyltransferase complexes for TGF-β responses has been reported. However, their exact roles are not fully understood. To investigate the functions of these complexes, we employed CRISPR/Cas9 genome editing to inactivate the KMT2C/MLL3 or KMT2D/MLL4 genes in human diploid epithelial cells. Time-course RNA-seq experiments revealed the requirement of MLL4 but not of MLL3 for TGF-β transcriptional responses. CUT&RUN experiments showed that MLL4 binding increases after TGF-β treatment and is especially enriched at AP-1 transcription factor binding sites. Interestingly, TGF-β-induced chromatin binding of MLL4 correlates with increases in H3K27ac but not in H3K4me1 modifications. Furthermore, TGF-β treatment sets off SMAD2-induced JUNB expression, which forms a feed-forward loop with MLL4. By inhibiting the activities of AP-1, the BAF chromatin remodeler, or the CBP/p300 histone acetyltransferase, we found that AP-1 binding and these chromatin regulators are all necessary for TGF-β induction of MLL4 binding and transcriptional activation of its genomic targets. Taken together, our study reveals distinctive roles for the MLL3 and MLL4 paralogs in the transcriptional response to TGF-β. In contrast to MLL3, MLL4 forms a feed-forward loop of JUNB, the BAF complex, and CBP/p300 to sustain transcription activation by TGF-β.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1012-1028"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147768989","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}

引用次数: 0

Coupling of translesion synthesis with the replisome stabilized at stalled replication forks by ATR. ATR在停滞复制叉上稳定的复制体与翻译合成的耦合。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353474.125

Jung-Hoon Yoon, Karthi Sellamuthu, Robert E Johnson, Louise Prakash, Satya Prakash

{"title":"Coupling of translesion synthesis with the replisome stabilized at stalled replication forks by ATR.","authors":"Jung-Hoon Yoon, Karthi Sellamuthu, Robert E Johnson, Louise Prakash, Satya Prakash","doi":"10.1101/gad.353474.125","DOIUrl":"10.1101/gad.353474.125","url":null,"abstract":"By promoting replication through DNA lesions, translesion synthesis (TLS) DNA polymerases protect against chromosomal instability and tumorigenesis. However, it is not known whether TLS in mammalian cells operates in conjunction with the replisome or in postreplicational gaps and how that impacts genomic stability. Here we show that TLS in human cells operates in close coordination with the replisome and that ATR stabilizes the replisome at the stalled replication fork (RF). In ATR-inhibited cells, the CMG helicase and DNA synthesis components of the replisome disassemble from RFs stalled at DNA lesions, and the composition of TLS and DNA synthesis components and the ensuing TLS and replication mechanisms at the stalled RFs are altered drastically from those in ATR-proficient cells. These alterations include the lack of requirement for Rad18-dependent PCNA ubiquitination for TLS by Polη and primer synthesis by the newly identified PrimPol--PolA1/PolA2 Polα complex. These results reveal the coupling of TLS to DNA replication, thus providing a means for protection against chromosome instability.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1059-1079"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948180","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}

引用次数: 0

CDK1 and CEP97 cooperatively control centriole length to orchestrate ciliogenesis and developmental patterning. CDK1和CEP97共同控制中心粒长度，协调纤毛发生和发育模式。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353426.125

Yue Liu, Zhengmao Wang, Tanvi Sinha, Kathy H Li, Robert J Chalkley, Vicente Herranz-Pérez, Chang Xie, Bradley K Yoder, Alma L Burlingame, Brian L Black, Jeremy F Reiter

{"title":"CDK1 and CEP97 cooperatively control centriole length to orchestrate ciliogenesis and developmental patterning.","authors":"Yue Liu, Zhengmao Wang, Tanvi Sinha, Kathy H Li, Robert J Chalkley, Vicente Herranz-Pérez, Chang Xie, Bradley K Yoder, Alma L Burlingame, Brian L Black, Jeremy F Reiter","doi":"10.1101/gad.353426.125","DOIUrl":"10.1101/gad.353426.125","url":null,"abstract":"Architecture is critical for organelle function. The lengths of centrioles, key components of centrosomes, are tightly regulated. We adapted centrosome purification approaches to measure centrosomal protein phosphorylation. Centrosome-specific phosphoproteomics with and without cyclin-dependent kinase 1 (CDK1) activity revealed that CDK1 phosphorylates many centriolar proteins involved in centriole length control, including Centrobin. CDK1 regulated centriole length synergistically with CEP97-CCP110, a local centriolar complex. CEP97 restricted Centrobin localization to centrioles, whereas CDK1-dependent phosphorylation suppressed Centrobin's ability to promote centriole elongation. Thus, CDK1 and CEP97-CCP110 both restrict centriole elongation by inhibiting the function of Centrobin, a centriole elongation factor, but via different mechanisms. Overelongated centrioles failed to support ciliogenesis in human cells and in mouse embryos. Removing CEP97 during mouse development caused centriole overelongation, impaired ciliogenesis and attenuated Hedgehog (HH) signaling, disrupting mouse heart development. We conclude that CEP97-CCP110 and CDK1 cooperatively restrict Centrobin function to control centriole length, critical for mammalian development.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1133-1151"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948191","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}

引用次数: 0

Corrigendum: Inhibition of Myc family proteins eradicates KRas-driven lung cancer in mice. 更正：抑制Myc家族蛋白可根除kras驱动的小鼠肺癌。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353956.126

Laura Soucek, Jonathan R Whitfield, Nicole M Sodir, Daniel Massó-Vallés, Erika Serrano, Anthony N Karnezis, Lamorna Brown Swigart, Gerard I Evan

引用次数: 0

DDX3X-mediated translation of structured cardiac mRNAs is essential for female heart development. ddx3x介导的结构化心脏mrna翻译对女性心脏发育至关重要。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353320.125

Kayla K Mason, Seohyun K Park, James I Emerson, Yao Wei Lu, Da-Zhi Wang, William F Marzluff, Frank L Conlon

{"title":"DDX3X-mediated translation of structured cardiac mRNAs is essential for female heart development.","authors":"Kayla K Mason, Seohyun K Park, James I Emerson, Yao Wei Lu, Da-Zhi Wang, William F Marzluff, Frank L Conlon","doi":"10.1101/gad.353320.125","DOIUrl":"10.1101/gad.353320.125","url":null,"abstract":"Sex differences influence congenital heart disease (CHD) development, yet underlying molecular mechanisms remain largely unclear. We demonstrate that the X-linked RNA helicase DDX3X associates in the heart with ribosomal subunit proteins, and eCLIP mapping reveals its preferential binding to cardiac mRNAs with long, structured 5' untranslated regions (UTRs) that can hinder translation. Using a cardiomyocyte-specific mouse Ddx3x knockout model, we show that female embryos lacking Ddx3x die at midgestation from heart failure due to impaired translation of key cardiac regulators, whereas male littermates survive. Ribosome profiling and proteomics demonstrate that DDX3X is required for efficient translation of female differential cardiac mRNAs. Reporter assays confirm that translation of essential cardiac genes such as Srf and Rcor2 depends on their 5' UTRs and requires DDX3X. These findings uncover a sex-specific posttranscriptional mechanism by which DDX3X safeguards female heart development through selective mRNA translation, providing insight into how X-linked dosage-sensitive regulators contribute to CHD.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1029-1044"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147768938","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}

引用次数: 0

The competition between splicing and 3' processing shapes the human transcriptome. 剪接和3'加工之间的竞争塑造了人类转录组。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353718.126

Lindsey V Soles, Shuangyu Li, Liang Liu, Kristianna S K Sarkan, Erik G Alvstad, Lusong Tian, Yoseop Yoon, Marielle Valdez, Ivan Marazzi, Yongsheng Shi

{"title":"The competition between splicing and 3' processing shapes the human transcriptome.","authors":"Lindsey V Soles, Shuangyu Li, Liang Liu, Kristianna S K Sarkan, Erik G Alvstad, Lusong Tian, Yoseop Yoon, Marielle Valdez, Ivan Marazzi, Yongsheng Shi","doi":"10.1101/gad.353718.126","DOIUrl":"10.1101/gad.353718.126","url":null,"abstract":"Eukaryotic pre-mRNA processing steps, including splicing and 3' processing, are tightly coordinated, yet the underlying mechanisms remain incompletely understood. U1 snRNP has been proposed to inhibit 3' processing at intronic polyadenylation (IPA) sites through a splicing-independent mechanism termed telescripting. In contrast, we discovered that disrupting splicing by using six different methods-targeting various key components such as U1 snRNP, U2 snRNP, U2AF, and SF3b-activates 3' processing at thousands of IPA sites. Notably, splicing inhibition, especially of U1 snRNP, induced widespread premature transcription termination within gene bodies through both IPA-coupled and IPA-independent mechanisms. Inhibition of different splicing factors activated overlapping and distinct sets of IPA sites, reflecting their specific contributions to transcription and spliceosome function. Conversely, inhibition of 3' processing enhanced splicing globally. These findings support a model in which splicing and 3' processing are competing processes that intersect with transcription to shape the transcriptome landscape.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1099-1118"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948239","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}

引用次数: 0

Cleavage of the RNA polymerase II general transcription factor TFIIB tunes transcription during stress. RNA聚合酶II一般转录因子TFIIB的断裂调节应激期间的转录。

IF 7.4 1区生物学

Genes & development Pub Date : 2026-07-01 DOI: 10.1101/gad.353187.125

Leah Gulyas, Azra Lari, Sahil B Shah, Britt A Glaunsinger

{"title":"Cleavage of the RNA polymerase II general transcription factor TFIIB tunes transcription during stress.","authors":"Leah Gulyas, Azra Lari, Sahil B Shah, Britt A Glaunsinger","doi":"10.1101/gad.353187.125","DOIUrl":"10.1101/gad.353187.125","url":null,"abstract":"Cellular stressors often cause widespread repression of RNA polymerase II (RNAP II) activity, which is thought to facilitate a focused transcriptional output toward stress resolution. In many cases, however, the underlying regulatory mechanisms remain unknown. Here, we demonstrate that stress-induced downregulation of the general transcription factor TFIIB tempers expression of specific stimulus response genes. Following a variety of stressors, TFIIB is proteolytically cleaved between its cyclin folds at conserved aspartic acid residue D207 by caspase-3 and caspase-7. Cleavage in this portion of the protein significantly reduces the ability of TFIIB to form a TBP-TFIIB-DNA promoter complex in vitro. Using both overexpression and endogenous base editing, we found that B and T cells that are unable to cleave TFIIB upregulate expression of a select gene set during apoptosis. These TFIIB-sensitive genes are primarily short, stimulus-responsive, and proto-oncogenic loci, and cleavage of TFIIB temporally restricts their expression. Failure to cleave TFIIB during stress leads to aberrant lymphocyte proliferation during chemical perturbation. Hence, caspase targeting of TFIIB destabilizes transcription to tune gene expression, allowing for proper stress resolution.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":" ","pages":"1045-1058"},"PeriodicalIF":7.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13263058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147928489","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}

引用次数: 0