Developmental Dynamics最新文献

{"title":"A review on recent advances in regenerative medicine for renal diseases: Approaches and challenges.","authors":"Urbi Roy, Ashiq Shibili Pillatt, Mike K S Chan, Mohan Rao Velure RajaRao, Antara Banerjee, Surajit Pathak","doi":"10.1002/dvdy.70193","DOIUrl":"https://doi.org/10.1002/dvdy.70193","url":null,"abstract":"<p><p>Renal diseases such as acute and chronic kidney disease cause loss of nephrons and kidney function, often leading to renal failure. Current treatments like dialysis and transplantation only manage symptoms and extend survival for a few years. Regenerative medicine offers promising approaches for repairing and regenerating renal tissue by targeting underlying disease mechanisms. For this narrative review, relevant original research articles and review articles were retrieved from online databases such as PubMed, Google Scholar, and ScienceDirect by using relevant keywords such as \"renal regeneration,\" \"kidney organoids,\" \"stem cell therapy,\" \"gene therapy,\" \"extracellular vesicles,\" and \"tissue engineering.\" The literature search focused primarily on articles published between 2020 and 2026 to discuss the recent advancements in regenerative approaches for renal disease. Recent advances in regenerative medicine have identified therapies such as stem cells, gene therapy, CRISPR-Cas9, extracellular vesicles, and kidney organoids that promote nephron regeneration, improve vascularization, regulate inflammation, and restore kidney function. This review highlights the cellular and molecular mechanisms underlying renal damage, recent advances in regenerative medicine, and the key challenges and future directions for the safe and effective use of regenerative medicine in treating renal diseases.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180077","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":"Gene expression detection methods in the African turquoise killifish brain","authors":"Emily Whisenant,&nbsp;Arne C Lekven","doi":"10.1002/dvdy.70083","DOIUrl":"10.1002/dvdy.70083","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The short-lived African turquoise killifish (<i>Nothobranchius furzeri</i>) is an important emerging model organism for gene expression studies, with limited tools for transcript and protein detection, especially methods that are both cost-effective and high-resolution. Brain tissue is particularly challenging to analyze due to its opacity and structural complexity, making whole-organ imaging techniques valuable. However, various tissue-clearing protocols adapted for <i>N. furzeri</i> are long and require specialized equipment.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>To address these limitations for gene expression detection techniques, we optimized cryosection-compatible ISH protocols for mRNA detection and adapted the EZ-clear method for whole-brain protein visualization in <i>N. furzeri</i>. Using <i>Gfap</i> and <i>Dat</i> as test markers, we optimized the colorimetric ISH protocol for detecting mRNA in both thick and thin sections, achieved high signal-to-noise ratios, and confirmed expression in expected brain regions. Additionally, we adapted the EZ-clear protocol for brain tissue clearing. We demonstrate the method's compatibility with immunostaining, showing a possible upregulation in Gfap, alongside endogenous fluorescence preservation of transgenic reporter lines.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our protocols add to the existing cost-effective and accessible methods for gene and protein visualization in <i>N. furzeri</i>. The cryosection-amenable ISH and adapted EZ-clear protocols expand the methodological toolkit for studying gene expression in this emerging model system.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 10","pages":"989-998"},"PeriodicalIF":1.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148297","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 Ralph Marcucio, Assistant Editor, University of California San Francisco, United States","authors":"Paul Trevorrow,&nbsp;Ralph Marcucio","doi":"10.1002/dvdy.70163","DOIUrl":"10.1002/dvdy.70163","url":null,"abstract":"&lt;p&gt;&lt;b&gt;Ralph Marcucio&lt;/b&gt; was born in and grew up in Amsterdam, N.Y. Dr. Marcucio began his research career as an intern at The Boyce Thompson Institute while he was an undergraduate at Cornell University in Ithaca, NY. After receiving his bachelor's degree from Cornell University in 1990, Dr. Marcucio was accepted into Cornell University's School of Agriculture PhD program. Ralph Marcucio was born in and grew up in Amsterdam, N.Y. Dr. Marcucio began his research career as an intern at The Boyce Thompson Institute while he was an undergraduate at Cornell University in Ithaca, NY. After receiving his bachelor's degree from Cornell University in 1990, Dr. Marcucio was accepted into Cornell University's School of Agriculture PhD program. He completed his PhD in 1995. For his exemplary performance and dedication as a Graduate Teaching Assistant, Dr. Marcucio was recognized by the Dean of Cornell University's School of Agriculture for his outstanding contribution to undergraduate education. After receiving his PhD, Ralph was awarded a prestigious NIH training grant to study tissue interactions that control development of the musculoskeletal system. Dr. Marcucio spent 5 years in the New York State College of Veterinary Medicine studying the origins of the musculature responsible for moving the head and jaw skeleton. In 2000, Dr. Marcucio joined the Molecular and Cellular Biology Laboratory at the University of California, San Francisco, (UCSF). In this position, he began studying how the skeleton of the face attains its shape and form. In 2003, Dr. Marcucio was appointed to the faculty at UCSF in the Department of Orthopaedic Surgery. His research program focuses on two basic science areas. First, he studies bone fracture healing focusing on the transformation of chondrocytes to osteoblasts and other cell types, as well as the inflammatory process during healing. Second, Dr. Marcucio is examining the role that the brain plays during development of the facial skeleton. Dr. Marcucio is a dedicated and enthusiastic mentor. His students have been invited to participate in university, state, national, and international research competitions.&lt;/p&gt;&lt;p&gt;I originally wanted to be a veterinarian. While I was in high school, I worked for a vet, and in New York State the main pathway into veterinary medicine is through Cornell University, so I went there.&lt;/p&gt;&lt;p&gt;Early on, I was inspired by James Harriet, the well-known English veterinarian who wrote those wonderful books illustrating the life of a countryside vet. Going to Cornell sparked a broader curiosity about science. Over time, I became increasingly interested in research, particularly in the cell cycle and cloning cattle embryos so my PhD focused on that area.&lt;/p&gt;&lt;p&gt;From there, my interests shifted toward developmental biology and embryology, especially more classical, “old-school” embryology. I worked in a lab that used chicken embryos, creating quail–chick chimeras and similar models. Through that experience, ","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 10","pages":"928-930"},"PeriodicalIF":1.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.70163","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224068","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":"Modest alterations in Drosophila denticle morphology reveal genetic interactions between actin disassembly proteins and ck/Myosin VIIA","authors":"Adeline Boettcher,&nbsp;Hannah Jones,&nbsp;Mary Leskovec,&nbsp;Helen Majer,&nbsp;Brooke Allen,&nbsp;Jennifer Sallee","doi":"10.1002/dvdy.70089","DOIUrl":"10.1002/dvdy.70089","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Building and disassembling actin filaments is essential for the remodeling of the actin cytoskeleton. In large structures, like <i>Drosophila</i> bristles, the loss of function of actin disassembly proteins can lead to smaller and misshapen bundled actin. Here we investigate whether mutant alleles of the disassembly genes <i>twinstar</i> (<i>tsr</i>), <i>flare</i> (<i>flr</i>), and <i>twinfilin</i> (<i>twf</i>) show similar phenotypes in smaller embryonic actin-based denticles. We also examined potential genetic interactions between F-actin disassembly proteins and the molecular motor <i>ck</i>/myosin VIIA, a protein necessary for denticle formation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Cuticle preparations of late-stage embryos were examined for denticle hook orientation, height, and width. There were mild morphological phenotypes such as loss of hook polarity across the genes. Single mutants for the disassembly genes showed that loss of <i>tsr</i> caused denticles to be longer, loss of <i>twf</i> resulted in shorter denticles, and mutant <i>flr</i> alleles showed varied effects. Double mutants of <i>tsr</i> and <i>twf</i> showed a genetic interaction in widths of denticles while <i>ck</i> was epistatic to <i>twf</i> and <i>flr</i> for width.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These results demonstrate that actin disassembly proteins and <i>ck</i>/myosin VIIA are involved in denticle formation, and the lack of wild type gene function in <i>tsr</i>, <i>twf</i>, <i>flr</i>, and <i>ck</i> causes measurable defects in denticle morphology.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 10","pages":"977-988"},"PeriodicalIF":1.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145279311","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":"Additive effects on craniofacial development upon conditional ablation of PDGFRα and SHP2 in the mouse neural crest lineage","authors":"Daniel Fuhr,&nbsp;Jessica Johnston,&nbsp;Elliott P. Brooks,&nbsp;Katherine A. Fantauzzo","doi":"10.1002/dvdy.70099","DOIUrl":"10.1002/dvdy.70099","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Activity of the receptor tyrosine kinase PDGFRα and the tyrosine phosphatase SHP2 is critical for vertebrate craniofacial development. SHP2 has been shown to both positively and negatively regulate PDGFR signaling through the recruitment of Grb2 and dephosphorylation of the receptor, respectively. We sought to determine the effect of SHP2 binding to PDGFRα in the facial mesenchyme via phenotypic and biochemical analyses of an allelic series of mouse embryos with combined loss of both proteins in the neural crest lineage.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We demonstrated that SHP2 preferentially binds PDGFRα/α homodimers among the three PDGFR dimers. We showed that double-homozygous mutant embryos exhibit a combination, but not an improvement or worsening, of the phenotypes observed upon conditional ablation of PDGFRα or SHP2 in the neural crest lineage. We further revealed that cell death in the lateral nasal and maxillary processes underlies the upper jaw phenotypes in embryos with loss of SHP2. Finally, we showed that E10.5 <i>Pdgfra</i>^<i>+/fl</i><i>;Shp2</i>^<i>fl/fl</i><i>;Wnt1-Cre</i>^<i>+/Tg</i> embryos have increased phosphorylation of PDGFRα and the downstream effector Erk1/2 compared to control and double-heterozygous embryos.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We propose a putative model in which SHP2 binds and dephosphorylates PDGFRα while simultaneously increasing survival through an Erk1/2-independent mechanism.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 10","pages":"945-960"},"PeriodicalIF":1.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145539417","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 role of Rho GTPases in facial morphogenesis","authors":"Isra Ibrahim,&nbsp;Joy M. Richman","doi":"10.1002/dvdy.70105","DOIUrl":"10.1002/dvdy.70105","url":null,"abstract":"<p>Facial morphogenesis relies on the coordinated regulation of cellular behaviors that sculpt the face from simple facial prominences to the fully confluent lip and nose. Disruptions to migration of cranial neural crest cells and/or the directed growth of the prominences will lead to abnormalities such as orofacial clefts. Here we review what is known about the roles of the actin cytoskeleton and its key regulators, the small RHO GTPases, during neural crest cell migration and facial development. Although small RHO GTPase signaling has been studied in the context of cancer and vascular pathologies, their role in facial development has received limited attention. In this review, we review the experimental data that connects changes in the function of small Rho GTPases to cytoskeletal dynamics and ultimately to facial morphogenesis. We also highlight human craniofacial disorders resulting from germline or somatic variants of small Rho GTPase pathway genes as well as associations between variants in GTPase-activating proteins (GAPs) and guanidine nucleotide exchange factors (GEFs) and the complex trait, non-syndromic cleft lip with or without cleft palate. The review points to a model where the gain or loss of RHO GTPase pathway components could be centrally involved in many craniofacial disorders and that the Rho GTPases are major regulators of homeostasis during normal development.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 10","pages":"931-944"},"PeriodicalIF":1.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.70105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145970730","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":"Editorial highlights","authors":"Paul A. Trainor","doi":"10.1002/dvdy.70196","DOIUrl":"https://doi.org/10.1002/dvdy.70196","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 Ralph Marcucio, Assistant Editor, University of California, San Francisco” by Paul Trevorrow and Ralph Marcucio.&lt;span&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/span&gt; Dr. Marcucio primarily studies the interdependency of brain and facial development and its influence on craniofacial shape and variation, and the implications this has for craniofacial evolution and the etiology and pathogenesis of congenital craniofacial anomalies. Of note, Dr. Marcucio discovered the facial ectoderm zone, a signaling center that controls the growth and shape of the upper face during embryonic development. Dr. Marcucio's lab also investigates the mechanisms underpinning bone fracture healing and repair, and more specifically, how chondrocytes transform into osteoblasts and the role played by inflammation. The prevailing opinion for the past century had been that chondrocytes underwent programmed cell death, with new bone being formed by osteoblasts. However, Dr. Marcucio and colleagues demonstrated that chondrocytes can directly transform into osteoblasts and contribute to the bone lineage themselves. Therefore, a major focus of his ongoing research is defining how that cellular transition occurs.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Craniofacial Morphogenesis&lt;/b&gt; “The role of Rho GTPases in facial morphogenesis” by Isra Ibrahim and Joy Richman.&lt;span&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/span&gt; Facial morphogenesis relies on the coordinated regulation of cellular behaviors, including proliferation, migration, and differentiation. In response to external cues, cells reorganize their subcellular components, changing the polarity of cytoskeletal fibers. Interactions between the cytoskeleton and extracellular matrix facilitate the biophysical forces that drive tissue shape changes, including during craniofacial morphogenesis. In this review article, the authors discuss the roles of the actin cytoskeleton and its key regulators, the small RHO GTPases, during neural crest cell migration and facial development. The authors also highlight human craniofacial disorders known to result from variants in the small Rho GTPase pathway genes, as well as associations between variants in GTPase-activating proteins (GAPs) and guanidine nucleotide exchange factors (GEFs) in the etiology and pathogenesis of non-syndromic cleft lip with or without cleft palate. The authors conclude that gain or loss of RHO GTPase pathway components may be centrally involved in many craniofacial disorders and that the Rho GTPases are major regulators of homeostasis during normal development.&lt;/p&gt;&lt;p&gt;&lt;b&gt;","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 10","pages":"926-927"},"PeriodicalIF":1.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvdy.70196","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149146072","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":"Non-migratory mode of ventral body wall closure: Primary mid-ventral covering is replaced by prospective definitive body wall","authors":"Kengo Buma,&nbsp;Yoshiko Takahashi","doi":"10.1002/dvdy.70106","DOIUrl":"10.1002/dvdy.70106","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>During ventral body wall closure in amniotes, the skeleton and muscles such as sternum, ribs, and pectoral muscles undergo a striking positional change from the dorso-lateral to mid-ventral region. The precise process of ventral body wall closure has poorly been explored. We have presented and examined two opposing models: the invading closure model, in which musculoskeletal components infiltrate into the mid-ventral tissue, and the replacing closure model, in which the original mid-ventral tissue degenerates to be replaced by the dorso-lateral body wall.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We developed a new method that enables direct cell labeling with PKH dyes in late chicken embryos. Our PKH labeling has shown that the original mid-ventral tissue, including both mesodermal and ectodermal cells, is progressively confined to the midline as the closure proceeds, contradicting the invading closure model. Moreover, the dorso-lateral tissue, including not only musculoskeletal but also non-musculoskeletal components, eventually contributes to the mid-ventral region. These results support the replacing closure model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The ventral body wall closure is achieved in a replacing manner. The mid-ventral region of the early body wall is a transient structure to cover the ventral surface, which is eventually eliminated to be replaced by the dorso-lateral region that represents the future definitive body wall.</p>\u0000 </section>\u0000 </div>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":"255 10","pages":"961-976"},"PeriodicalIF":1.5,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809667","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":"Evidence for functional convergence between LZTS2 and DYRK1A during craniofacial development.","authors":"Nicole Cheng, Santiago Lima, Larisa Litovchick, Amanda J G Dickinson","doi":"10.1002/dvdy.70192","DOIUrl":"https://doi.org/10.1002/dvdy.70192","url":null,"abstract":"<p><strong>Background: </strong>Precise control of DYRK1A dosage is essential for embryonic development, including craniofacial morphogenesis. While LZTS2 is among the most consistently identified DYRK1A-interacting proteins, its roles in embryonic development remain incompletely understood, and its potential contribution to craniofacial development has not been examined. Xenopus laevis was used to test the role of LZTS2 in craniofacial development and its functional relationship with DYRK1A.</p><p><strong>Results: </strong>Lzts2 and Dyrk1a showed overlapping expression during craniofacial development, with both proteins present in developing facial tissues. Knockdown of Lzts2 disrupted craniofacial morphogenesis and reduced expression of craniofacial genes. These phenotypes closely resembled those caused by decreasing Dyrk1a function. Sub-phenotypic reductions of Lzts2 and Dyrk1a synergized to produce craniofacial defects, while partial reduction of Lzts2 attenuated aspects of the phenotype caused by Dyrk1a overexpression. Comparative analysis of human phenotypes associated with copy number gains of LZTS2 and DYRK1A revealed striking overlap, consistent with a potential functional interaction between these genes in humans.</p><p><strong>Conclusions: </strong>These findings identify Lzts2 as a previously unrecognized regulator of craniofacial development and support a functional interaction with Dyrk1a during embryogenesis. Modulating LZTS2 or related regulatory partners may provide a strategy to selectively tune DYRK1A-dependent developmental pathways.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135550","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":"Zebrafish hoxba and hoxbb clusters are redundantly required for posterior pharyngeal pouch development.","authors":"Sohju Toyama, Nanami Iwamatsu, Junpei Imagawa, Takumi Sugawara, Renka Fujii, Morimichi Kikuchi, Yuki Kawabe, Yuzuki Tanaka, Akinori Kawamura","doi":"10.1002/dvdy.70195","DOIUrl":"https://doi.org/10.1002/dvdy.70195","url":null,"abstract":"<p><strong>Background: </strong>Pharyngeal pouch formation is fundamental to vertebrate craniofacial development, but molecular mechanisms underlying posterior pouch formation remain incompletely understood. Retinoic acid (RA) signaling is required for posterior pharyngeal development, and Hox genes are established RA targets. However, their genetic requirement in posterior pouch formation has not been established.</p><p><strong>Results: </strong>Zebrafish lacking both hoxba and hoxbb clusters-teleost-specific duplicates of the ancestral HoxB cluster-exhibited severe loss of posterior pharyngeal pouches and associated pharyngeal skeletal elements, accompanied by reduced expression of the pouch marker pax1a. Alcian blue analysis revealed highly similar losses of posterior pharyngeal skeletal elements in hoxba;hoxbb and RA-deficient aldh1a2 mutants. Pharyngeal expression of hoxb1a and hoxb1b was reduced in aldh1a2 mutants. Combined knockdown of hoxb1a and hoxb1b caused variable, incompletely penetrant posterior pouch abnormalities, supporting their contribution to HoxB-cluster function.</p><p><strong>Conclusions: </strong>These results provide genetic evidence that the hoxba and hoxbb clusters are redundantly required for posterior pharyngeal pouch development. The highly similar posterior pharyngeal abnormalities in hoxba;hoxbb and aldh1a2 mutants, together with reduced hoxb1a and hoxb1b expression, support a functional association between RA signaling and HoxB-cluster activity. Together, these findings identify the duplicated HoxB-derived clusters as important genetic components of RA-associated posterior pharyngeal development.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105568","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}