Developmental Dynamics最新文献

{"title":"foxe1 mutant zebrafish show indications of a hypothyroid phenotype and increased sensitivity to ethanol for craniofacial malformations","authors":"Sophie T. Raterman,&nbsp;Frank A. D. T. G. Wagener,&nbsp;Jan Zethof,&nbsp;Vincent Cuijpers,&nbsp;Peter H. M. Klaren,&nbsp;Juriaan R. Metz,&nbsp;Johannes W. Von den Hoff","doi":"10.1002/dvdy.745","DOIUrl":"10.1002/dvdy.745","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>FOXE1 mutations in humans are associated with cleft palate and hypothyroidism. We previously developed a <i>foxe1</i> mutant zebrafish demonstrating mineralization defects in larvae. In the present study, we investigate the thyroid status and skeletal phenotype of adult <i>foxe1</i> mutants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Mutant fish have increased expression of <i>tshβ</i> in the pituitary, and of hepatic <i>dio1</i> and <i>dio2</i>. In plasma, we found higher Mg levels. Together these findings are indicative of hypothyroidism. We further observed mineralization defects in scales due to enhanced osteoclast activity as measured by increased expression levels of <i>tracp</i>, <i>ctsk</i>, and <i>rankl</i>. Gene–environment interactions in the etiology of FOXE1-related craniofacial abnormalities remain elusive, which prompts the need for models to investigate genotype–phenotype associations. We here investigated whether ethanol exposure increases the risk of developing craniofacial malformations in <i>foxe1</i> mutant larvae that we compared to wild types. We found in ethanol-exposed mutants an increased incidence of developmental malformations and marked changes in gene expression patterns of cartilage markers (<i>sox9a</i>), apoptotic markers (<i>casp3b</i>), retinoic acid metabolism (<i>cyp26c1</i>), and tissue hypoxia markers (<i>hifaa, hifab</i>).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Taken together, this study shows that the <i>foxe1</i> mutant zebrafish recapitulates phenotypes associated with FOXE1 mutations in human patients and a clear <i>foxe1</i>-ethanol interaction.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"254 3","pages":"240-256"},"PeriodicalIF":2.0,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.745","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364776","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":"Hypoxia regulate developmental coronary angiogenesis potentially through VEGF-R2- and SOX17-mediated signaling","authors":"Halie E. Vitali,&nbsp;Bryce Kuschel,&nbsp;Chhiring Sherpa,&nbsp;Brendan W. Jones,&nbsp;Nisha Jacob,&nbsp;Syeda A. Madiha,&nbsp;Sam Elliott,&nbsp;Eddie Dziennik,&nbsp;Lily Kreun,&nbsp;Cora Conatser,&nbsp;Bhupal P. Bhetwal,&nbsp;Bikram Sharma","doi":"10.1002/dvdy.750","DOIUrl":"10.1002/dvdy.750","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The development of coronary vessels in embryonic mouse heart involves various progenitor populations, including sinus venosus (SV), endocardium, and proepicardium. ELA/APJ signaling is known to regulate coronary growth from the SV, whereas VEGF-A/VEGF-R2 signaling controls growth from the endocardium. Previous studies suggest hypoxia might regulate coronary growth, but its specific downstream pathways are unclear. In this study, we further investigated the role of hypoxia and have identified SOX17- and VEGF-R2-mediated signaling as the potential downstream pathways in its regulation of developmental coronary angiogenesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>HIF-1α stabilization by knocking out von Hippel Lindau (VHL) protein in the myocardium (cKO) disrupted normal coronary angiogenesis in embryonic mouse hearts, resembling patterns of accelerated coronary growth. VEGF-R2 expression was increased in coronary endothelial cells under hypoxia in vitro and in VHL cKO hearts in vivo. Similarly, SOX17 expression was increased in the VHL cKO hearts, while its knockout in the endocardium disrupted normal coronary growth.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings provide further evidence that hypoxia regulates developmental coronary growth potentially through VEGF-R2 and SOX17 pathways, shedding light on mechanisms of coronary vessel development.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"254 2","pages":"174-188"},"PeriodicalIF":2.0,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364777","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":"Analysis of Meis2 knockout mice reveals Sonic hedgehog-mediated patterning of the cochlear duct.","authors":"Hei Yeun Koo, Jae Hwan Oh, María Beatriz Durán Alonso, Iris López Hernández, Margarita González-Vallinas, María Teresa Alonso, Juan J Tena, Alejandro Gil-Gálvez, Fernando Giraldez, Jinwoong Bok, Thomas Schimmang","doi":"10.1002/dvdy.747","DOIUrl":"https://doi.org/10.1002/dvdy.747","url":null,"abstract":"<p><strong>Background: </strong>The mechanisms underlying the formation of complex structures such as during the outgrowth of the cochlear duct are still poorly understood.</p><p><strong>Results: </strong>We have analyzed the morphological and molecular changes associated with cochlear development in mouse mutants for the transcription factor Meis2, which show defective coiling of the cochlea. These morphological abnormalities were accompanied by the formation of ectopic and extra rows of sensory hair cells. Gene profiling of otic vesicles from Meis2 mutants revealed a dysregulation of genes that are potentially involved in Sonic hedgehog (Shh)-mediated patterning of the cochlear duct. Like in Shh mutants, Meis2 defective mice showed a loss of genes that are expressed in the apical part of the cochlear duct.</p><p><strong>Conclusions: </strong>Taken together, these data reveal that the loss of Meis2 leads to a phenotype that resembles Shh mutants, suggesting that Meis2 is instrumental for cochlear Shh signaling. The modulation of the same subset of genes provides an interesting insight into which Shh responsive genes are essential for outgrowth and patterning of the cochlear duct.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343560","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.748","DOIUrl":"10.1002/dvdy.748","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;Blood Development&lt;/b&gt; “Establishment of a Diamond-Blackfan anemia like (DBAL) model in zebrafish”, by Yiming Ling, Jiaye Wu, Yushi Liu, Panpan Meng, Ying Sun, Dejian Zhao, and Qing Lin; &lt;i&gt;Dev Dyn&lt;/i&gt; 253:10, pp. 906–921. https://doi.org/10.1002/dvdy.703. Red blood cells (erythrocytes), which have a typical lifespan of 90–120 days, are essential for oxygen delivery throughout the body. Deficiencies in erythrocyte number or morphology, or hemoglobin levels can result in anemia. Zebrafish, which have transparent embryos, are a powerful model for studying human hematological disorders. In this study, the authors generated &lt;i&gt;epoa&lt;/i&gt;-deficient zebrafish as a model of Diamond–Blackfan anemia like (DBAL), which occurs in humans in association with recessive loss-of-function mutations in EPO. EPO is crucial for erythrocyte development and oxygen transport and &lt;i&gt;epoa&lt;/i&gt;&lt;sup&gt;&lt;i&gt;szy8/zy8&lt;/i&gt;&lt;/sup&gt; mutants carrying the human EPO mutation c.530G&gt;A, developed DBAL due to reduced &lt;i&gt;EPO&lt;/i&gt; expression. The severe anemia observed in &lt;i&gt;epoa&lt;/i&gt;&lt;sup&gt;&lt;i&gt;szy8/zy8&lt;/i&gt;&lt;/sup&gt; mutant zebrafish can be used to screen drugs for treating epoa-deficiency anemia, and recombinant human EPO significantly improved erythrocyte numbers. Zebrafish &lt;i&gt;epoa&lt;/i&gt; models of DBAL are therefore beneficial for in vivo assessments of patient-derived &lt;i&gt;EPO&lt;/i&gt; variants, and for developing potential therapeutic approaches for treating DBAL.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Craniofacial and Hair Development&lt;/b&gt; “Lineage-specific requirements of Alx4 function in craniofacial and hair development” by Yu Lan, Zhaoming Wu, Han Liu, and Rulang Jiang; &lt;i&gt;Dev Dyn&lt;/i&gt; 253:10, pp. 940–948. https://doi.org/10.1002/dvdy.705. The ALX family of transcription factors are key regulators of craniofacial development. Variants in &lt;i&gt;ALX4&lt;/i&gt; have been associated with autosomal dominant parietal foramina and autosomal recessive frontonasal dysplasia with alopecia in humans, but the mechanisms connecting their etiology and pathogenesis remain poorly understood. &lt;i&gt;Alx4&lt;/i&gt; is broadly expressed throughout development, making it difficult to determine its cell-autonomous and non-cell autonomous functions. Here the authors report the generation and characterization of &lt;i&gt;Alx4&lt;/i&gt;&lt;sup&gt;&lt;i&gt;fx/fx&lt;/i&gt;&lt;/sup&gt; conditional mice as a valuable new resource for investigating the pathogenic mechanisms underlying ALX4-related developmental disorders and alopecia. &lt;i&gt;Alx4&lt;/i&gt; tissue-specific loss-of-function in neural crest cells and limb bud mesenchyme, results in craniofacial and limb bud developmental def","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"253 10","pages":"880-881"},"PeriodicalIF":2.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.748","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343565","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":"Patterns of early embryogenesis and growth in the olfactory system of chick (Gallus gallus domesticus) based on iodine-enhanced micro-computed tomography.","authors":"Aneila V C Hogan, Donald G Cerio, Gabriel S Bever","doi":"10.1002/dvdy.746","DOIUrl":"https://doi.org/10.1002/dvdy.746","url":null,"abstract":"<p><strong>Background: </strong>The vertebrate olfactory system entails a complex set of neural/support structures that bridge morphogenetic regions. The developmental mechanisms coordinating this bridge remain unclear, even for model organisms such as chick, Gallus gallus. Here, we combine previous growth data on the chick olfactory apparatus with new samples targeting its early embryogenesis. The purpose is to illuminate how early developmental dynamics integrate with scaling relationships to produce adult form and, potentially, evolutionary patterns. Olfactory structures, including epithelium, turbinate, nerve, and olfactory bulb, are considered in the context of neighboring nasal and brain structures.</p><p><strong>Results: </strong>Axonal outgrowth from the olfactory epithelium, which eventually connects receptor neurons with the brain, begins earlier than previously established. This dynamic marks the beginning of a complex pattern of early differential growth wherein the olfactory bulbs scale with positive allometry relative to both brain volume and turbinate area, which in turn scale isometrically with one another.</p><p><strong>Conclusions: </strong>The mechanisms driving observed patterns of organogenesis and growth remain unclear awaiting experimental evidence. We discuss competing hypotheses, including the possibility that broad-based isometry of olfactory components reflects constraints imposed by high levels of functional/structural integration. Such integration would include the frontonasal prominence having a strong influence on telencephalic patterning.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343563","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":"Knockout of rbm24a and rbm24b genes in zebrafish impairs skeletal and cardiac muscle integrity and function during development.","authors":"Audrey Saquet, Ziwei Ying, De-Li Shi, Raphaëlle Grifone","doi":"10.1002/dvdy.743","DOIUrl":"https://doi.org/10.1002/dvdy.743","url":null,"abstract":"<p><strong>Backgound: </strong>Skeletal and cardiac muscles are contractile tissues whose development and function are dependent on genetic programs that must be precisely orchestrated in time and space. In addition to transcription factors, RNA-binding proteins tightly regulate gene expression by controlling the fate of RNA transcripts, thus specific proteins levels within the cell. Rbm24 has been identified as a key player of myogenesis and cardiomyogenesis in several vertebrates, by controlling various aspects of post-transcriptional regulation, including pre-mRNA alternative splicing and mRNA stabilization. In zebrafish, knockdown of rbm24a or rbm24b also causes skeletal and cardiac muscle phenotypes, but how their combined loss affects muscle integrity and function remains elusive.</p><p><strong>Results: </strong>By genome editing, we have generated rbm24a and rbm24b single mutants as well as double mutants. Structural analyses indicate that homozygous rbm24a and rbm24b double mutants exhibit severe somitic muscle and cardiac phenotypes, although rbm24b single mutants are obviously normal. We further show that the loss of rbm24a and rbm24b disrupts sarcomere organization, impairing functional contractility and motility of skeletal and cardiac muscles.</p><p><strong>Conclusion: </strong>The rbm24 mutant zebrafish represents a new genetic tool for in-depth studies of Rbm24-mediated post-transcriptional regulation of skeletal and cardiac muscle development, disease and regeneration.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343562","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":"Ventral body wall closure: Mechanistic insights from mouse models and translation to human pathology","authors":"Caroline Formstone,&nbsp;Bashar Aldeiri,&nbsp;Mark Davenport,&nbsp;Philippa Francis-West","doi":"10.1002/dvdy.735","DOIUrl":"10.1002/dvdy.735","url":null,"abstract":"<p>The ventral body wall (VBW) that encloses the thoracic and abdominal cavities arises by extensive cell movements and morphogenetic changes during embryonic development. These morphogenetic processes include embryonic folding generating the primary body wall; the initial ventral cover of the embryo, followed by directed mesodermal cell migrations, contributing to the secondary body wall. Clinical anomalies in VBW development affect approximately 1 in 3000 live births. However, the cell interactions and critical cellular behaviors that control VBW development remain little understood. Here, we describe the embryonic origins of the VBW, the cellular and morphogenetic processes, and key genes, that are essential for VBW development. We also provide a clinical overview of VBW anomalies, together with environmental and genetic influences, and discuss the insight gained from over 70 mouse models that exhibit VBW defects, and their relevance, with respect to human pathology. In doing so we propose a phenotypic framework for researchers in the field which takes into account the clinical picture. We also highlight cases where there is a current paucity of mouse models for particular clinical defects and key gaps in knowledge about embryonic VBW development that need to be addressed to further understand mechanisms of human VBW pathologies.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"254 2","pages":"102-141"},"PeriodicalIF":2.0,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.735","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343564","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":"Expression analysis of genes including Zfhx4 in mice and zebrafish reveals a temporospatial conserved molecular basis underlying craniofacial development","authors":"Shujie Liu,&nbsp;Lin Xu,&nbsp;Makoto Kashima,&nbsp;Rika Narumi,&nbsp;Yoshifumi Takahata,&nbsp;Eriko Nakamura,&nbsp;Hirotoshi Shibuya,&nbsp;Masaru Tamura,&nbsp;Yuki Shida,&nbsp;Toshihiro Inubushi,&nbsp;Yuko Nukada,&nbsp;Masaaki Miyazawa,&nbsp;Kenji Hata,&nbsp;Riko Nishimura,&nbsp;Takashi Yamashiro,&nbsp;Junichi Tasaki,&nbsp;Hiroshi Kurosaka","doi":"10.1002/dvdy.740","DOIUrl":"10.1002/dvdy.740","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Embryonic craniofacial development involves several cellular and molecular events that are evolutionarily conserved among vertebrates. Vertebrate models such as mice and zebrafish have been used to investigate the molecular and cellular etiologies underlying human craniofacial disorders, including orofacial clefts. However, the molecular mechanisms underlying embryonic development in these two species are unknown. Therefore, elucidating the shared mechanisms of craniofacial development between disease models is crucial to understanding the underlying mechanisms of phenotypes in individual species.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We selected mice and zebrafish as model organisms to compare various events during embryonic craniofacial development. We identified genes (<i>Sox9</i>, <i>Zfhx3</i> and <i>4</i>, <i>Cjun</i>, and <i>Six1</i>) exhibiting similar temporal expression patterns between these species through comprehensive and stage-matched gene expression analyses. Expression analysis revealed similar gene expression in hypothetically corresponding tissues, such as the mice palate and zebrafish ethmoid plate. Furthermore, loss-of-function analysis of <i>Zfhx4/zfhx4</i>, a causative gene of human craniofacial anomalies including orofacial cleft, in both species resulted in deformed skeletal elements such as the palatine and ethmoid plate in mice and zebrafish, respectively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These results demonstrate that these disease models share common molecular mechanisms, highlighting their usefulness in modeling craniofacial defects in humans.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"254 3","pages":"257-271"},"PeriodicalIF":2.0,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.740","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142343561","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":"Effects of life history strategies and habitats on limb regeneration in plethodontid salamanders.","authors":"Vivien Bothe, Hendrik Müller, Neil Shubin, Nadia Fröbisch","doi":"10.1002/dvdy.742","DOIUrl":"https://doi.org/10.1002/dvdy.742","url":null,"abstract":"<p><strong>Background: </strong>Salamanders are the only tetrapods that exhibit the ability to fully regenerate limbs. The axolotl, a neotenic salamander, has become the model organism for regeneration research. Great advances have been made providing a detailed understanding of the morphological and molecular processes involved in limb regeneration. However, it remains largely unknown how limb regeneration varies across salamanders and how factors like variable life histories, ecologies, and limb functions have influenced and shaped regenerative capacities throughout evolution.</p><p><strong>Results: </strong>This study focuses on six species of plethodontid salamanders representing distinct life histories and habitats. Specimens were examined for regeneration ability after bite injuries as well as after controlled amputations. Morphological investigations revealed great regenerative abilities in all investigated species and frequent anatomical limb anomalies. Correlations were observed with respect to speed of regeneration and habitat.</p><p><strong>Conclusions: </strong>Investigating regeneration in non-model salamander taxa is essential for disentangling shared features of the regeneration process versus those that may be more taxon-specific. Gaining insights into variable aspects of regeneration under natural conditions and after conspecific biting rather than controlled amputations adds important new datapoints for understanding the evolutionary framework of regeneration and provides a broader context for interpreting findings made in the model organism axolotl.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281898","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":"Stage-by-stage exploration of normal embryonic development in the Arabian killifish, Aphanius dispar.","authors":"Amena Alsakran, Rashid Minhas, Atyaf S Hamied, Rod W Wilson, Mark Ramsdale, Tetsuhiro Kudoh","doi":"10.1002/dvdy.738","DOIUrl":"https://doi.org/10.1002/dvdy.738","url":null,"abstract":"<p><strong>Background: </strong>Arabian killifish, Aphanius dispar, lives in marine coastal areas of the Middle East, as well as in streams that experience a wide range of salinities and temperatures. It has been used as a mosquito control agent and for studying the toxicities of environmental pollutants. A. dispar's eggshell (chorion) and embryos are highly transparent and are suitable for high resolution microscopic observations, offering excellent visibility of live tissues.</p><p><strong>Results: </strong>In this study, the staging of normal embryonic development of A. dispar was described and investigated at different temperatures. Embryonic development was then examined under different thermal environments from 26 to 34°C. Our data suggest that temperature has a significant effect on embryonic development, with accelerated development at higher temperatures.</p><p><strong>Conclusion: </strong>A. dispar exhibits broad thermal tolerance and extended independent feeding capabilities, making it a promising model organism for toxicology and pathogenesis studies conducted over an extended period of time (12 days post-fertilization).</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281899","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}