Developmental Dynamics最新文献

{"title":"Embryonic cerebrospinal fluid pressure in fetal mice in utero: External factors pressurize the intraventricular space.","authors":"Koichiro Tsujikawa, Reina Muramatsu, Takaki Miyata","doi":"10.1002/dvdy.70047","DOIUrl":"https://doi.org/10.1002/dvdy.70047","url":null,"abstract":"<p><strong>Background: </strong>Previous experiments inducing leakage of embryonic cerebrospinal fluid (CSF) suggest the necessity of intraventricular CSF pressure (P_CSF) for brain morphogenesis. Nevertheless, how embryonic P_CSF occurs is unclear, especially in utero.</p><p><strong>Results: </strong>Using a Landis water manometer, we measured P_CSF in fetal mice isolated from the amniotic cavity (P_CSF-ISO) and found that P_CSF-ISO rose from 20 Pa at embryonic day (E) 10 to 100-110 Pa at E14-16. At E13, intraventricular injections of ≥3 μL of saline elevated P_CSF-ISO by ~30%, whereas those of inhibitors of CSF secretion decreased P_CSF-ISO by ~30%. Shh-mediated cerebral wall expansion did not significantly increase P_CSF-ISO. Removal of the brain-surrounding contractile tissues decreased P_CSF-ISO by 80%-90%. We then found that the intraamniotic pressure measured in utero (P_AF-IU) declined from 2000 Pa at E10 to 500 Pa at E15-18 but was always much greater than P_CSF-ISO. Direct measurement of P_CSF in utero (P_CSF-IU) at E13 and E15 coupled with the measurement of P_CSF-ISO under hydrostatic pressure loading to mimic P_AF-IU at various embryonic ages revealed the following relationship: P_CSF-IU = P_CSF-ISO + P_AF-IU.</p><p><strong>Conclusions: </strong>The P_CSF of mice in utero is influenced by external factors, most strongly by intraamniotic pressure and less strongly by brain-confining tissues.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial highlights","authors":"Paul A. Trainor","doi":"10.1002/dvdy.70049","DOIUrl":"10.1002/dvdy.70049","url":null,"abstract":"&lt;p&gt;Every organism is a model organism for understanding development, evolution, disease, and regeneration, and we have only begun to scratch the surface of the interdisciplinary genetic, molecular, cellular, and developmental mechanisms that regulate these biological processes. These “Highlights” denote exciting advances recently reported in &lt;i&gt;Developmental Dynamics&lt;/i&gt; that illustrate the complex dynamics of developmental biology.&lt;/p&gt;&lt;p&gt;“Elp1 function in placode-derived neurons is critical for proper trigeminal ganglion development” by Margaret and Hines and Lisa Taneyhill, &lt;i&gt;DevDyn&lt;/i&gt; 254.6, pp. 494–512. https://doi.org/10.1002/dvdy.749.&lt;/p&gt;&lt;p&gt;Cranial sensory nerves are part of the peripheral nervous system and are responsible for relaying sensory information to the central nervous system. The trigeminal (V), epibranchial (geniculate (facial VII)), petrosal (glossopharyngeal IX), and nodose (vagal X) ganglia house neuronal cell bodies and supporting glia of the sensory nerves, which innervate the face, tongue, mouth, and digestive tract. The ganglia are derived from two embryonic cell populations, cranial neural crest and neurogenic placodes, however, the molecules and pathways that mediate reciprocal interactions between them during ganglion development remain poorly understood. Recently, the authors identified Elongator acetyltransferase complex subunit 1 (Elp1) as a potential regulator of trigeminal ganglion development, which when perturbed can cause familial dysautonomia, a neurodevelopmental and neurodegenerative disease. Here the authors characterize the spatiotemporal expression of Elp1 in avian embryos as the trigeminal ganglion initially assembles. &lt;i&gt;Elp1&lt;/i&gt; is expressed in migratory cranial neural crest cells and later in undifferentiated neural crest cells and placode-derived neurons that contribute to the trigeminal ganglion. Knockdown of &lt;i&gt;Elp1&lt;/i&gt; in trigeminal placode cells reveal its critical functions in placode-derived neurons during trigeminal ganglion development, providing additional insight into the etiology of trigeminal nerve deficits in familial dysautonomia.&lt;/p&gt;&lt;p&gt;“Spatiotemporal distribution of neural crest cells in the common wall lizard &lt;i&gt;Podarcis muralis&lt;/i&gt;” by Robin Pranter and Nathalie Feiner, &lt;i&gt;DevDyn&lt;/i&gt; 254.6, pp. 551–567. https://doi.org/10.1002/dvdy.758. Neural crest cells are a migratory cell population considered unique to vertebrates and fundamentally important for their evolution and variation. Reptiles which comprise ~12,000 species, are renowned for their numerous morphological adaptions, many of which are neural crest cell derived, which have facilitated their radiation and adaption to nearly every ecological niche on the plant. Hence there is considerable interest in the evolutionary origins of neural crest cells and while studies in squamates have increased our understanding of neural crest cell specification, migration, and differentiation across vertebrates, evolutionary changes in neura","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"254 6","pages":"476-477"},"PeriodicalIF":1.5,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.70049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144214196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA repair during embryonic epidermal stratification.","authors":"Fumiya Meguro, Katsushige Kawasaki, Yoshito Kakihara, Maiko Kawasaki, Makoto Fukushima, Finsa Tisna Sari, Vanessa Utama, Alex Kesuma, Jun Nihara, Takehisa Kudo, Akira Fujita, Kaya Ichikawa, Kazuaki Osawa, Takeyasu Maeda, Koichi Tabeta, Makio Saeki, Atsushi Ohazama","doi":"10.1002/dvdy.70046","DOIUrl":"https://doi.org/10.1002/dvdy.70046","url":null,"abstract":"<p><strong>Background: </strong>Genomes are constantly exposed to a myriad of DNA-damaging agents. Robust DNA repair mechanisms protect DNA by removing or tolerating damage. However, it remains unclear whether these mechanisms are required for organogenesis.</p><p><strong>Results: </strong>Multiple epithelial layers are essential for skin function, including body protection. The epidermis is initiated as a single layer and then stratifies in utero. Stratification did not occur in mice with epithelial conditional deletion of the DNA repair molecule Reptin (Reptin^fl/fl;K14Cre). DNA damage was observed in the mutant epidermis but not in the wild-type epidermis. The mutant epidermis also showed reduced cell proliferation and upregulated p53 expression. Stratification was restored when p53 was deleted in the Reptin mutant mice by generating Reptin and p53 double mutant mice (Reptin^fl/fl;K14Cre;p53^-/-).</p><p><strong>Conclusion: </strong>In the wild-type epidermis, DNA is likely damaged at the initiation of embryonic stratification and promptly repaired by DNA repair mechanisms involving Reptin.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Streamlining asymmetry quantification in fetal mouse imaging: A semi-automated pipeline supported by expert guidance","authors":"S. M. Rolfe,&nbsp;D. Mao,&nbsp;A. M. Maga","doi":"10.1002/dvdy.70028","DOIUrl":"10.1002/dvdy.70028","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Asymmetry is a key feature of numerous developmental disorders and in phenotypic screens is often used as a readout for environmental or genetic perturbations. A better understanding of the genetic basis of asymmetry and its relationship to disease susceptibility will help unravel the complex genetic and environmental factors and their interactions that increase risk in a range of developmental disorders. Large-scale imaging datasets offer opportunities to work with sample sizes necessary to detect and quantify differences in morphology beyond severe deformities but also pose challenges to manual phenotyping protocols.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We introduce a tool for quantifying asymmetry in 3D images and apply it to explore the role of genes contributing to abnormal asymmetry by deep phenotyping 3D fetal microCT images from knockout strains acquired as part of the Knockout Mouse Phenotyping Program. Four knockout strains: <i>Ccdc186</i>, <i>Acvr2a</i>, <i>Nhlh1</i>, and <i>Fam20c</i> were identified with highly significant asymmetry in craniofacial regions, making them good candidates for further analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In this work, we demonstrate an open-source, semi-automated tool to quantify the asymmetry of craniofacial structures that integrates expert anatomical knowledge. This tool can detect abnormally asymmetric phenotypes in fetal mice to explore the relationship between facial asymmetry, perturbed development, and developmental instability.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"254 8","pages":"999-1010"},"PeriodicalIF":1.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences in palatal shelf epithelial stiffness between the lingual/nasal and buccal/oral surfaces during palatal shelf elevation in developing mice.","authors":"Arata Nagasaka, Yasuhiko Bando, Miyuki Toda-Fujii, Go Onozawa, Kaito Suzuki, Takaki Miyata, Osamu Amano","doi":"10.1002/dvdy.70044","DOIUrl":"https://doi.org/10.1002/dvdy.70044","url":null,"abstract":"<p><strong>Background: </strong>During secondary palate formation, bilateral palatal shelves grow vertically to a horizontal position. This morphological change of the palatal shelves, defined as the palatal shelf elevation, occurs from embryonic day (E)-13.5 to E14 in mice. Palatal shelves show regional differences in elevation patterns along the anterior-posterior (AP) axis; however, the underlying mechanisms remain unclear. Material properties of the lingual/nasal and buccal/oral surfaces, especially stiffness, possibly contribute to different elevation patterns.</p><p><strong>Results: </strong>Indentation test using atomic force microscopy was performed to measure the stiffness at the epithelial surface of the palatal shelf. Measurement of palatal shelf stiffness along the AP axis before and after elevation revealed that the lingual/nasal surface was softer than the buccal/oral surface in the posterior region before elevation and that the palatal shelf was stiffer after elevation than before elevation. Moreover, the thickness of epithelial cells on the lingual/nasal side was lower than that on the buccal/oral side before elevation.</p><p><strong>Conclusion: </strong>Overall, our results suggest that epithelial cell thickness affects epithelial surface stiffness, causing regional differences in elevation patterns.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pss knockdown in the midgut causes growth retardation in Drosophila similar to that in human LMHD.","authors":"Kwan-Young Kim, You-Lim Hwang, Sunwoo Yeom, Seung-Hae Kwon, Sang-Hak Jeon","doi":"10.1002/dvdy.70039","DOIUrl":"https://doi.org/10.1002/dvdy.70039","url":null,"abstract":"<p><strong>Background: </strong>Phosphatidylserine synthase (PSS), localized in the mitochondrial membrane, synthesizes phosphatidylserine. In humans, mutations in Pss lead to Lenz-Majewski hyperostotic dwarfism, a disorder affecting growth and development. The effects of Pss mutations on the growth of Drosophila melanogaster are not fully known. Hence, this study was conducted to investigate the effects of Pss knockdown on the growth and development of D. melanogaster.</p><p><strong>Results: </strong>Enterocyte (EC)-specific Pss knockdown resulted in reduced cell size in the gut via reduced Akt signaling. EC-specific Pss knockdown was associated with a decrease in gut size, a change in gut pH, and reduced food intake. These abnormalities affected normal nutrient metabolism in larvae, leading to decreased secretion of Drosophila insulin-like peptides. Consequently, the reduced systemic Akt signaling at the organismal level resulted not only in impaired gut growth but also in abnormal organismal growth and development.</p><p><strong>Conclusion: </strong>These findings highlight the significant role of the Pss gene in the growth and development of D. melanogaster.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein turnover downstream of the Nipbl/CRL4 axis contributes to abnormal development in zebrafish embryos.","authors":"Annie C Sanchez, Niusha Banoukh, Fiona Mensching, Robert V Skibbens, M Kathryn Iovine","doi":"10.1002/dvdy.70037","DOIUrl":"https://doi.org/10.1002/dvdy.70037","url":null,"abstract":"<p><strong>Background: </strong>Mutations in cohesins cause cohesinopathies such as Cornelia de Lange Syndrome (CdLS) and Roberts Syndrome (RBS). Prior findings demonstrate that Esco2 (a cohesin activator) and Smc3 (a core cohesin subunit) regulate the CRL4 E3 ubiquitin ligase. SMC3 mutations, however, account for a small percentage of CdLS. Here, we test whether NIPBL, which when mutated is responsible for 65% of CdLS cases, also regulates CRL4.</p><p><strong>Results: </strong>We report that Nipbl knockdown in zebrafish embryos produces developmental abnormalities and reduces the transcription of ddb1, which encodes a key component of CRL4 E3 ligase. The severity of phenotypes in Nipbl knockdown embryos is partially rescued by exogenous ddb1 mRNA, demonstrating that CRL4 ligase function is downstream of Nipbl. These findings suggest that aberrant accumulation of CRL4 ligase substrates contributes to developmental abnormalities. To test this model, we identified candidate CRL4 substrates in zebrafish embryos by LC-MS. The results reveal that elevated expression of one of these candidates, pparαa, is sufficient to produce developmental defects in zebrafish embryos.</p><p><strong>Conclusions: </strong>Nipbl impacts CRL4 ligase activity via regulation of ddb1 expression. We provide evidence that the aberrant accumulation of substrates is sufficient to produce developmental abnormalities consistent with those observed in RBS and CdLS models.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downstream branches of receptor tyrosine kinase signaling act interdependently to shape the face","authors":"Nicholas Hanne,&nbsp;Diane Hu,&nbsp;Marta Vidal-García,&nbsp;Charlie Allen,&nbsp;M. Bilal Shakir,&nbsp;Wei Liu,&nbsp;Benedikt Hallgrímsson,&nbsp;Ralph Marcucio","doi":"10.1002/dvdy.70041","DOIUrl":"10.1002/dvdy.70041","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Previously we found that increasing fibroblast growth factor (FGF) signaling in the neural crest cells within the frontonasal process (FNP) of the chicken embryo caused dysmorphology that was correlated with reduced proliferation, disrupted cellular orientation, and lower MAPK activation but no change in PLCγ and PI3K activation. This suggests RTK signaling may drive craniofacial morphogenesis through specific downstream effectors that affect cellular activities. In this study we inhibited three downstream branches of RTK signaling to determine their role in regulating cellular activities and how these changes affect morphogenesis of the FNP.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Small molecule inhibitors of MEK1/2, PI3K, and PLCγ were delivered individually and in tandem to the right FNP of chicken embryos. All treatments caused asymmetric proximodistal truncation on the treated side and a mild expansion on the untreated side compared to DMSO control treated FNPs. Inhibiting each pathway caused similar decreased proliferation and disrupted cellular orientation, and only mildly increased apoptosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Since RTK signaling is a ubiquitous and tightly regulated biochemical system, we conclude that the downstream pathways are robust to developmental perturbation through redundant signaling systems.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"254 8","pages":"979-998"},"PeriodicalIF":1.5,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The endocannabinoid system regulates both ependymoglial and neuronal cell responses to a tail amputation in the axolotl.","authors":"Michael Tolentino, Sarah E Walker, Gaynor E Spencer, Robert Carlone","doi":"10.1002/dvdy.70035","DOIUrl":"https://doi.org/10.1002/dvdy.70035","url":null,"abstract":"<p><strong>Background: </strong>The endocannabinoid system is a neuromodulatory system implicated in cellular processes during both development and regeneration. The Mexican axolotl, one of only a few vertebrates capable of central nervous system regeneration, was used to examine the role of the endocannabinoid system in the regeneration of the tail and spinal cord following amputation.</p><p><strong>Results: </strong>The endocannabinoid receptor CB1 was upregulated in the regenerating axolotl spinal cord by 4 hours following tail amputation, and this upregulation persisted for at least 14 days. The endocannabinoid receptor CB2 was upregulated later, between 7 and 14 days after tail amputation. Both CB1 and CB2 were located in ependymoglia and neurons within the regenerating spinal cord. Treatment with inverse agonists to inhibit CB1 (AM251) or CB2 (AM630) inhibited spinal cord and tail regeneration. During the first 7 days after injury, CB1 and CB2 expression was also necessary for the proliferation of ependymoglial cells and the regeneration of axons into the newly regenerated tail tissue. However, only CB1 was necessary for the differentiation of ependymoglia into immature neurons.</p><p><strong>Conclusions: </strong>These studies are the first to examine the role of the endocannabinoid system during spinal cord regeneration in a regeneration-competent vertebrate.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in culturing of the sea star Patiria miniata.","authors":"Vanessa Barone, Luisa Coronado, Deka Ismail, Sareen Fiaz, Deirdre C Lyons","doi":"10.1002/dvdy.70040","DOIUrl":"https://doi.org/10.1002/dvdy.70040","url":null,"abstract":"<p><strong>Background: </strong>The use of the sea star Patiria miniata as a model system has produced groundbreaking advances in a disparate set of biomedical research fields, including embryology, immunology, regeneration, cell biology, and evolution of development. Nonetheless, the life cycle of P. miniata has not yet been closed in the laboratory, precluding the generation of stable transgenic and mutant lines, which would greatly expand the toolset for experimentation with this model system. Rearing P. miniata in the laboratory has been challenging due to limited knowledge about metamorphosis cues, feeding habits of juveniles, and their relatively long generation time.</p><p><strong>Results: </strong>Here we report protocols to rear P. miniata embryos through sexual maturity in a laboratory setting. We provide detailed staging of early embryonic development at different temperatures, and show that larvae can be raised to competence in as little as 15 days. We find that retinoic acid induces metamorphosis effectively and present methods to rear juveniles on commercially available foods. We show that in a flow-through system, juveniles double in size every 2 months and reach sexual maturity in approximately 2 years.</p><p><strong>Conclusions: </strong>We report the first example of P. miniata raised through sexual maturity in a laboratory setting, paving the way for the generation of stable mutant sea star lines.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}