Developmental Dynamics最新文献

{"title":"Mycn regulates vascular development through PI3K signaling pathway in zebrafish","authors":"Guo-Qin Zhao,&nbsp;Tao Cheng,&nbsp;Peng-Yun Wang,&nbsp;Jing Mo,&nbsp;Feng Yu,&nbsp;Yang Dong,&nbsp;Yun-Fei Li,&nbsp;Yu Feng,&nbsp;Peng-Fei Xu,&nbsp;Li-Ping Shu","doi":"10.1002/dvdy.70104","DOIUrl":"10.1002/dvdy.70104","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Mycn, a MYC gene family member, is implicated in both carcinogenesis through amplification and Feingold syndrome through its deficiency. Previous studies have indicated that increased Mycn expression enhances vascularization in human neuroblastomas, yet its precise role in vascular development remains elusive.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In this study, we utilized single-cell RNA-seq and live imaging analyses to confirm that <i>mycn</i> is expressed during zebrafish vasculogenesis. We investigated vascular development in zebrafish using a genetically engineered <i>mycn</i> mutation. Our findings reveal that <i>mycn</i>-deficient zebrafish exhibit reduced intersegmental vessels and malformed subintestinal vessels, primarily due to decreased cell proliferation in vascular endothelial cells. Importantly, we discovered that activation of PI3K signaling significantly ameliorates these vascular abnormalities.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our study establishes Mycn as a key regulator of vascular development in zebrafish, acting through the PI3K signaling pathway.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 9","pages":"881-895"},"PeriodicalIF":1.5,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145818031","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":"Membrane lipid metabolism as a regulatory frontier in neural crest biology: Roles for sphingolipids, cholesterol, and lipid rafts.","authors":"Allison E Mancini, Mallorie P Jenne, Michael L Piacentino","doi":"10.1002/dvdy.70182","DOIUrl":"https://doi.org/10.1002/dvdy.70182","url":null,"abstract":"<p><p>Neural crest cells are multipotent, migratory stem-like cells essential for vertebrate development that contribute broadly to many tissues including the craniofacial skeleton, peripheral nervous system, and pigment-producing cells. Their development progresses through phases of induction, specification, delamination, migration, and differentiation. Importantly, advancement through these phases requires detecting and responding to extracellular cues through the plasma membrane. While the gene regulatory networks and the signals that govern neural crest development are well characterized, plasma membrane lipid composition as a regulatory layer controlling these transitions remains underexplored. Despite technical limitations in quantitative lipid measurements from vertebrate embryos, genetic and molecular studies have inferred roles of key lipid metabolites. Here we review how membrane lipid metabolism and composition regulate neural crest behavior, focusing primarily on sphingolipids, cholesterol, and lipid raft domains. We examine how morphogen signaling is modified and organized by lipids, how modulating lipid content alters the biophysical state of the neural crest plasma membrane, and the deleterious effects of dysregulated lipid metabolism in neurocristopathies. Drawing parallels to other developmental and disease contexts, we highlight membrane lipid metabolism as a critical frontier in neural crest biology with broad implications for understanding developmental mechanisms and congenital disorders.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148864000","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":"MIT/TFE family transcription factors, Mitf and Tfec, redundantly promote pigment cell differentiation and retinal epithelium pigmentation in teleosts.","authors":"James Lister, Keisuke Sugiwaka, Tetsuaki Kimura, Rieko Tanaka, Makoto Goda, Hikaru Kobayashi, Chikako Inoue, Kawilarang W A Masengi, Kazunori Yamahira, Kiyoshi Naruse, Satoshi Ansai, Robert N Kelsh, Masahiko Hibi, Hisashi Hashimoto","doi":"10.1002/dvdy.70183","DOIUrl":"https://doi.org/10.1002/dvdy.70183","url":null,"abstract":"<p><strong>Background: </strong>Transcription factors of the MIT/TFE family-mitfa, mitfb, and tfec-play essential roles in specifying pigment cells derived from neural crest cells in vertebrates. In teleosts, which possess multiple pigment cell types, these factors exhibit partially redundant but largely distinct functions across different pigment lineages. We previously reported that the combined loss of mitfa and mitfb leads to a complete absence of melanophores, xanthophores, and leucophores in medaka.</p><p><strong>Results: </strong>Here, we describe newly generated hypomorphic alleles of mitfa and mitfb, which result in delayed melanophore development. Using these hypomorphic mutants in combination with a newly generated null allele of tfec, we show that Tfec can partially compensate for the loss of Mitfa and Mitfb in melanophore, xanthophore, and leucophore differentiation. Consistent with previous findings in zebrafish, loss of tfec alone results in the complete absence of iridophores. Importantly, simultaneous null mutations in all three genes cause a complete loss of all four chromatophore types and lead to defective pigmentation of the retinal pigmented epithelium (RPE), which is not derived from the neural crest in both Oryzias species and in zebrafish. Using an RPE-specific marker, we further show that the RPE is specified and structurally intact but fails to melanize.</p><p><strong>Conclusions: </strong>These findings indicate that the redundant functions of Mitfa, Mitfb, and Tfec are not only essential for the specification of diverse pigment cell types but also critical for RPE pigmentation.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839583","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":"A proteomic investigation of forebrain regeneration in the leopard gecko (Eublepharis macularius).","authors":"Alexandra I Noble, Samantha L Payne, Matthew K Vickaryous","doi":"10.1002/dvdy.70181","DOIUrl":"https://doi.org/10.1002/dvdy.70181","url":null,"abstract":"<p><strong>Background: </strong>The ability to replace lost or damaged neurons following an injury is termed reactive neurogenesis. Although reactive neurogenesis has been reported in several lizard species, the molecular mechanisms underlying this response remain largely unknown. Here, we investigate ontogenetic, injury-, and regeneration-associated proteomic changes to the forebrain of subadult leopard geckos (Eublepharis macularius), focusing on an area of the cerebral hemispheres that includes the medial and dorsomedial cortices, septum, and neighboring tissues.</p><p><strong>Results: </strong>Among control (untreated) geckos, the proteome of the forebrain changes during a one-month period, providing evidence of an ontogenetically driven proteomic shift. To initiate reactive neurogenesis, we administered the neurotoxin 3-acetylpyridine (3-AP). Using liquid chromatography-tandem mass spectrometry, we found that 3-AP induces differential expression of proteins associated with cell death, immune activation, and neurogenesis. However, by 30 days post-injury, the proteomic profile of the forebrain was returning toward that of age-matched controls.</p><p><strong>Conclusions: </strong>Our findings demonstrate that structural regeneration of the gecko forebrain is associated with the differential expression of proteins involved in brain development and repair in mammals and provides a resource for future evolutionary studies of neurogenesis.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789502","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.70178","DOIUrl":"10.1002/dvdy.70178","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;&lt;b&gt;Meet the editorial team&lt;/b&gt; “An interview with Lisa A. Taneyhill, assistant editor, University of Maryland” by Paul Trevorrow and Lisa Taneyhill.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; Dr. Taneyhill studies how two critical embryonic cell populations, neural crest cells and placode cells, form and later interact to generate new anatomical structures. Neural crest cells undergo via an epithelial to mesenchymal transition to acquire migratory capacity and Dr. Taneyhill's lab is investigating the function of proteases that cleave proteins without which cells can't move. Neural crest cells join together with placodes to form the neurons and glia of the cranial ganglia, and although much is known about how motor neurons reach their targets, the sensory nerves have received far less attention. Dr. Taneyhill is therefore interested in how the sensory nerves of the trigeminal ganglion target tissues like the eye or jaw, and how the nerves transmit signals back that help shape those tissues. This fundamental developmental biology research has translational impact in the form of a better understanding of neurodevelopmental disorders such as Familial Dysautonomia and their potential treatment.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Diabetes and pancreas regeneration&lt;/b&gt; “Pancreatic injury induces β-cell regeneration in axolotl” by Connor Powell, Hani Singer, Ashley Juarez, Ryan Kim, Elane Kim, Duygu Payzin-Dogru, Aaron Savage, Noah Lopez, Kara Thornton, Steven Blair, Adnan Abouelela, Anita Dittrich, Stuart Akeson2, Miten Jain2, and Jessica L. Whited.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; Diabetes is a condition in which insulin homeostasis is compromised. This can lead to complications including heart failure, kidney disease, and tissue necrosis requiring amputation. Diabetes is caused by a loss of pancreatic β-cell function, and this study investigated the capacity for pancreas regeneration in axolotl. The authors initially characterized pancreatic islets in the axolotl and observed that axolotl pancreatic islets closely resemble those in mice and humans, as demonstrated by the conservation of several key pancreatic gene markers. The authors then used partial pancreatectomy to study the pancreatic response to injury. Following pancreatic resection, whole-organ β-cell proliferation occurred without the formation of a blastemal structure, which is analogous to other models of compensatory congestion in axolotl. Lineage tracing will still be needed in the future to ascertain whether new β-cells originate from existing β-cells or from pancreatic stem cells.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Limb develop","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 8","pages":"742-743"},"PeriodicalIF":1.5,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.70178","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683770","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":"Easily adaptable Fiji macro for mean linear intercept measurement of peripheral respiratory airspace","authors":"Brielle Patlin,&nbsp;Yongjun Yin,&nbsp;Ling Li,&nbsp;David M. Ornitz","doi":"10.1002/dvdy.70078","DOIUrl":"10.1002/dvdy.70078","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Mean linear intercept (MLI) is a method of evaluating lung structure and pathology that is widely used in clinical and research settings. Unfortunately, no widely available software for automation of this process is available, and many clinicians and scientists still perform these measurements manually.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>To increase the speed and accuracy of obtaining MLI measurements, we have developed a macro for Fiji is just ImageJ (Fiji) to semi-automate the acquisition of these measurements. Twenty to 25 images from each of 43 mouse lungs, a total of 1042 images, were analyzed manually and by macro (automated) to validate the accuracy of the MLI macro. No significant difference was recorded between the manual and automated methods in mouse lung tissue of either different age (P14, P21, 8 weeks) or different condition (healthy vs. emphysema). Optimization of MLI macro parameters showed that additional measurements beyond three lines per image did not further improve accuracy. We also provide an Excel macro that summarizes the airspace data for each image and averages all the image data in a given batch of images.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This Fiji macro can be used to automate MLI measurement in histological sections of lung tissue faster and with lower variance.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 8","pages":"824-833"},"PeriodicalIF":1.5,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039419","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":"Multiple gene knockouts in newts reveal novel functions of 5′ Hox genes in limb development along the anterior–posterior and proximal–distal axes","authors":"Kohei Urakawa,&nbsp;Yu Ito,&nbsp;Haruka Matsubara,&nbsp;Ken-ichi T. Suzuki,&nbsp;Masatoshi Matsunami,&nbsp;Shuji Shigenobu,&nbsp;Toshinori Hayashi,&nbsp;Gembu Abe,&nbsp;Takashi Takeuchi","doi":"10.1002/dvdy.70080","DOIUrl":"10.1002/dvdy.70080","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>5' Hox</i> genes play crucial roles in limb patterning along the proximal–distal and anterior–posterior axes in mice. However, their functional conservation across tetrapods remains unclear. We previously found that newt <i>Hox13</i> is essential for digit formation during both development and regeneration. In contrast, the functions of other <i>5' Hox</i> genes (Hox9–Hox12) in newts remain u[WLYJ-108]nknown. Therefore, we generated <i>5' Hox</i> knockout newts (<i>Pleurodeles waltl</i>) using CRISPR–Cas9.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Individual knockouts of <i>Hox9</i>, <i>Hox10</i>, and <i>Hox12</i> disrupted all respective paralogs; however, these newts displayed no apparent abnormalities in limb skeletons. In contrast, <i>Hox11</i> knockout newts exhibited skeletal defects in the posterior zeugopod and autopod of both the forelimbs and hindlimbs. Moreover, compound knockouts of <i>Hox9</i> and <i>Hox10</i> caused substantial loss of stylopod and anterior zeugopod/autopod elements specifically in the hindlimbs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings indicate that <i>Hox9</i> and <i>Hox10</i> redundantly regulate stylopod formation in the hindlimbs. Furthermore, <i>Hox9/Hox10</i> and <i>Hox11</i> contribute to the development of the anterior and posterior regions of the zeugopod/autopod in the hindlimbs, respectively. These novel roles of <i>5' Hox</i> genes identified in newts suggest the functional diversification of <i>5' Hox</i> genes in tetrapod limb development.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 8","pages":"761-781"},"PeriodicalIF":1.5,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184990","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":"Identification of novel genes regulating the development of the palate","authors":"Ashwin Bhaskar,&nbsp;Sophie Astrof","doi":"10.1002/dvdy.70066","DOIUrl":"10.1002/dvdy.70066","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The International Mouse Phenotyping Consortium (IMPC) has generated thousands of knockout mouse lines, many of which exhibit embryonic or perinatal lethality. Using micro-computed tomography (micro-CT), the IMPC has created and publicly released three-dimensional image data sets of embryos from these lethal and subviable lines. In this study, we leveraged this data set to screen homozygous null mutants for anomalies in secondary palate development. We analyzed optical sections from 2987 embryos at embryonic days E15.5 and E18.5, representing 484 homozygous mutant lines.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results and Conclusions</h3>\u0000 \u0000 <p>Our analysis identified 44 novel genes implicated in palatogenesis. Gene set enrichment analysis highlighted biological processes and pathways relevant to palate development and uncovered 18 genes jointly regulating the development of the eye and the palate. These findings present a valuable resource for further research, offer novel insights into the molecular mechanisms underlying palatogenesis, and provide important context for understanding the etiology of rare human congenital disorders involving malformations of the palate and other organs.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 8","pages":"808-823"},"PeriodicalIF":1.5,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768473","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":"Commensal skin bacteria interact with the innate immune system to promote tail regeneration in Xenopus laevis tadpoles","authors":"Phoebe A. Chapman,&nbsp;Robert C. Day,&nbsp;Daniel T. Hudson,&nbsp;Joanna M. Ward,&nbsp;Xochitl C. Morgan,&nbsp;Caroline W. Beck","doi":"10.1002/dvdy.70088","DOIUrl":"10.1002/dvdy.70088","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Tadpoles of the clawed frog <i>Xenopus laevis</i> can regenerate their tails following partial amputation, replacing the missing spinal cord, muscles, and fin. However, for a brief period of development this response becomes unstable, leading to a proportion of tadpoles that undergo wound healing rather than regenerative programme. Inspired by a growing number of links between the microbiome and human inflammatory disease, we asked how the tadpole skin microbiome and innate immunity influence the regeneration of a complex appendage. We previously showed that tadpoles raised in antibiotics such as gentamicin or penicillin/streptomycin or with reduced Toll-like receptor 4 signaling regenerated tails poorly, while adding exogenous lipopolysaccharide promoted or rescued tail regeneration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Here, we show that CRISPR/Cas9 knockdown of Toll-like receptor 2 also reduces tadpole tail regeneration. Conversely, addition of the pathogen-associated molecular pattern peptidoglycan to the medium at the time of amputation increases the likelihood of regeneration. While we have previously shown that tadpoles acquire most of their early skin microbiome from their mothers, analysis of mitochondrial haplotypes did not support a genetic maternal explanation of regenerative bias. Levels of endogenous lipopolysaccharides on tail tips were also not predictive of regenerative success, and shotgun sequencing indicated that there was no difference in bacterial loads. To see if the composition of native microbiome was associated with regenerative success, we sequenced the 16S rRNA genes of 503 tadpole tail tips from 12 sibships and mapped these to the regenerative outcome of each tadpole. While no one taxon was found to be associated with regenerative success, higher proportions of Gram-positive genera overall correlated with improved regeneration outcomes. Supporting this finding, when tadpoles were raised with the antibiotic vancomycin, to select against Gram-positive bacteria, the number of individuals undergoing tail regeneration was significantly decreased.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Taken together, our results suggest a previously undocumented role for Tlr2, possibly activated by peptidoglycan from Gram-positive commensal skin bacteria, in tipping the balance from wound repair to regenerative programmes in <i>Xenopus laevis</i> refractory stage tadpoles.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 8","pages":"782-807"},"PeriodicalIF":1.5,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145307100","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":"Meet the editorial team. An interview with Lisa A. Taneyhill, assistant editor, University of Maryland","authors":"Lisa A. Taneyhill,&nbsp;Paul Trevorrow","doi":"10.1002/dvdy.70129","DOIUrl":"10.1002/dvdy.70129","url":null,"abstract":"","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 8","pages":"744-747"},"PeriodicalIF":1.5,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147490741","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}