Journal of Developmental Biology最新文献

{"title":"Vestigial-like 4 Regulates Neurogenesis and Neural Crest Formation During <i>Xenopus</i> Development.","authors":"Pierre Thiébaud, Emilie Simon, François Moisan, Sandrine Fedou, Hamid-Reza Rezvani, Nadine Thézé","doi":"10.3390/jdb14010008","DOIUrl":"10.3390/jdb14010008","url":null,"abstract":"<p><p>VESTIGIAL-LIKE proteins constitute a family of evolutionarily conserved proteins that act as cofactors in regulating gene expression through their binding to TEAD transcription factors. Among the four members of this family in vertebrates, VESTIGIAL-LIKE 4 has emerged as a tumor suppressor that competes with YAP in binding TEADs, thus inhibiting the HIPPO pathway downstream of YAP. Nevertheless, very few studies have addressed its function during early vertebrate development. Here, we used gain- and loss-of-function strategies to investigate the role of vestigial-like 4 during <i>Xenopus laevis</i> development. Our data show that vestigial-like 4 is a key regulator of neurogenesis and neural crest formation. In embryos depleted of vestigial-like 4, neurogenesis is severely impaired, and neither neurog1 nor neurod1 is able to stimulate neurogenesis. Vestigial-like 4 is also required for neural crest formation through <i>pax3</i> and sox9 regulation, and this property does not necessarily require its interaction with tead. Collectively, our findings demonstrate that vestigial-like 4 is an important regulator of neurogenesis and neural crest formation. Although vestigial-like 4 can bind to tead proteins in the embryo, its function does not depend solely on this interaction, suggesting a complex level of regulation with which vestigial-like 4 regulates early steps in development and differentiation.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12922143/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional State of Lampbrush Chromosomes in Early Vitellogenic Oocytes of Hibernating Frogs <i>Rana temporaria</i>.","authors":"Nadya V Ilicheva, Olga I Podgornaya","doi":"10.3390/jdb14010007","DOIUrl":"10.3390/jdb14010007","url":null,"abstract":"<p><p>Lampbrush chromosomes (LBCs) are a feature of amphibian oocytes and are typically associated with high levels of transcription during active oocyte growth. However, their state during winter hibernation has not been studied. Here, we investigated LBCs in early vitellogenic oocytes (early stage 4) of the grass frog <i>Rana temporaria</i> during winter hibernation. We found that the chromosomes retained their lampbrush morphology, and the phosphorylated form of RNA polymerase II resided on the lateral loops. Transcription on the lateral loops was reduced but detectable at cold conditions and significantly increased when the oocytes were transferred at room temperature. Satellite S1a transcripts were detected at the lateral loops of the chromosomes by RNA FISH. The possible significance of maintaining chromosomes in the lampbrush form during hibernation is discussed.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12921996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Female Aging Affects Coilin Pattern in Mouse Cumulus Cells.","authors":"Alexey S Anisimov, Dmitry S Bogolyubov, Irina O Bogolyubova","doi":"10.3390/jdb14010006","DOIUrl":"10.3390/jdb14010006","url":null,"abstract":"<p><p>Cumulus cells (CCs) are a distinct population of granulosa cells (GCs) that surround the developing and ovulated mammalian oocyte. The features of their structural organization and the expression pattern of key genes significantly affect oocyte viability. Changes in the functional activity of the nucleus are often expressed in changes in the structure of nuclear bodies (NBs), including Cajal bodies (CBs). The diagnostic protein of CBs is coilin, which maintains their structural integrity. Using fluorescent and electron microscopy, we examined maternal aging-associated changes in coilin pattern in mouse CCs. We found that older mice had a decrease in the number of coilin-positive bodies, while external transcriptome data analysis revealed no significant changes in <i>Coil</i> and <i>Smn1</i> gene expression. We hypothesized that the age-related dynamics of coilin-containing bodies are determined not by changes in the expression level of key components of these bodies, but by age-related changes in CC metabolism. Considering that CCs are a by-product of IVF protocols, making them available for analysis in sufficient quantities, age-related changes in the number and size of coilin-positive NBs in CCs may serve as a promising biomarker for assessing ovarian functional aging.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of Obstructive Uropathy on Cyst Formation and Nephrogenesis: Insights from a Fetal Lamb Model.","authors":"Kohei Kawaguchi, Takuya Kawaguchi, Juma Obayashi, Yasuji Seki, Kunihide Tanaka, Kei Ohyama, Junki Koike, Shigeyuki Furuta, Kevin C Pringle, Hiroaki Kitagawa","doi":"10.3390/jdb14010005","DOIUrl":"10.3390/jdb14010005","url":null,"abstract":"<p><p>Obstructive uropathy (OU) during fetal development induces a fetal cystic dysplastic kidney. The mechanisms of cyst formation and the onset of renal dysfunction remain unclear. Determining whether nephrogenic potential persists during fetal life may suggest whether early intervention could preserve renal development. We aimed to evaluate residual nephrogenic activity in fetal cystic dysplastic kidneys using β-catenin and CD10 immunostaining, and to assess whether the site of obstruction influences cystogenesis. After appropriate approval, 20 timed-gestation fetal lambs had OU created at 60 days. Males underwent urethral and urachal ligation (<i>n</i> = 8, 3 lost), and females underwent unilateral ureteric ligation (<i>n</i> = 8, 1 lost). Fetuses were sacrificed at 80 days (<i>n</i> = 6) and 140 days (term, <i>n</i> = 10), comparing kidneys with normal controls of the same gestational age using immunohistochemical staining for β-catenin and CD10. Developing fetal cystic dysplastic kidneys were identified at 80 days. β-catenin staining showed the absence of granular cytoplasmic expression in cystic regions, indicating arrested nephrogenesis. In male models, cysts originated exclusively from proximal tubules. Female models exhibited mixed proximal and distal tubular involvement. CD10 staining confirmed the loss of proximal tubular markers. Renal development remained arrested at term. Cyst formation disrupts renal development early in gestation, which persists until term. Differences in cystogenesis between the models suggest that the site of obstruction influences pathogenic mechanisms.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Discovery of New Markers for Haemogenic Endothelium and Haematopoietic Progenitors in the Mouse Yolk Sac.","authors":"Guillermo Diez-Pinel, Alessandro Muratore, Christiana Ruhrberg, Giovanni Canu","doi":"10.3390/jdb14010004","DOIUrl":"10.3390/jdb14010004","url":null,"abstract":"<p><p>Erythro-myeloid progenitors (EMPs) originate from the haemogenic endothelium in the yolk sac via an endothelial-to-haematopoietic transition (EHT) to generate blood and immune cells that support embryo development. Yet, the transitory nature of EHT and the limited availability of molecular markers have constrained our understanding of the origin, identity, and differentiation dynamics of EMPs. Here, we have refined the annotation of yolk sac haemato-vascular populations in publicly available single-cell RNA sequencing (scRNAseq) datasets from mouse embryos to identify novel molecular markers of haemogenic endothelium and EMPs. By sub-clustering key cell populations followed by pseudotime analysis, we refined cluster annotations and then reconstructed differentiation trajectories. Subsequent differential gene expression analysis between clusters identified novel cell surface markers for haemogenic endothelial cells (<i>Fxyd5</i> and <i>Scarf1</i>) and EMPs (<i>Fcer1g</i>, <i>Tyrobp,</i> and <i>Mctp1</i>). Further, we have identified candidate signalling and metabolic pathways that may regulate yolk sac haematopoietic emergence and differentiation. The specificity of FXYD5, SCARF1, and FCER1G for haemogenic endothelium and EMPs was validated by immunostaining of the mouse yolk sac. These insights into the transcriptional dynamics in the yolk sac should support future investigation of EHT and haematopoietic differentiation during early mammalian development.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Interplay of One-Carbon Metabolism, Mitochondrial Function, and Developmental Programming in Ruminant Livestock.","authors":"Kazi Sarjana Safain, Kendall C Swanson, Joel S Caton","doi":"10.3390/jdb14010003","DOIUrl":"10.3390/jdb14010003","url":null,"abstract":"<p><p>Maternal nutrition during gestation profoundly influences fetal growth, organogenesis, and long-term offspring performance through developmental programming. Among the molecular mechanisms responsive to maternal nutrient availability, one-carbon metabolism plays a central role by integrating folate, methionine, choline, and vitamin B₁₂ pathways that regulate methylation, nucleotide synthesis, and antioxidant defense. These processes link maternal nutritional status to epigenetic remodeling, cellular proliferation, and redox balance during fetal development. Mitochondria act as nutrient sensors that translate maternal metabolic cues into bioenergetic and oxidative signals, shaping tissue differentiation and metabolic flexibility. Variations in maternal diet have been associated with shifts in fetal amino acid, lipid, and energy metabolism, suggesting adaptive responses to constrained intrauterine environments. This review focuses on the molecular interplay between one-carbon metabolism, mitochondrial function, and metabolomic adaptation in developmental programming of ruminant livestock. Understanding these mechanisms offers opportunities to design precision nutritional strategies that enhance fetal growth, offspring productivity, and long-term resilience in livestock production systems.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Zebrafish Seizure Model of cblX Syndrome Reveals a Dose-Dependent Response to mTor Inhibition.","authors":"Claudia B Gil, David Paz, Briana E Pinales, Victoria L Castro, Claire E Perucho, Annalise Gonzales, Giulio Francia, Sepiso K Masenga, Antentor Hinton, Anita M Quintana","doi":"10.3390/jdb14010002","DOIUrl":"10.3390/jdb14010002","url":null,"abstract":"<p><p>Mutations in the transcriptional co-factor HCFC1 cause methylmalonic aciduria and homocystinemia, cblX type (<i>cblX</i>) (MIM#309541), non-syndromic X-linked intellectual disability (XLID), and focal epilepsy. Zebrafish studies have revealed increased activation of the Akt/mTor signaling pathway after mutation of <i>hcfc1a</i>, one ortholog of <i>HCFC1</i>. mTOR hyperactivation is linked to seizures, and its inhibition alleviates epilepsy in other preclinical models. We hypothesized that mTor overactivity in <i>hcfc1a</i> mutant zebrafish increases seizure susceptibility and/or severity. We employed a two-concentration model of the seizure-inducing agent, pentylenetetrazol (PTZ), with or without pretreatment of the mTor inhibitor, torin1. Mutation of <i>hcfc1a</i> did not alter the response to PTZ at sub-optimal concentrations, and the pharmaceutical inhibition of mTor using the compound Torin1 reduced response to 1 µM PTZ, but only in a dose-dependent manner. Higher doses of mTor inhibition did not reduce the seizure response in mutant larvae but were effective in wildtype siblings. These data suggest that inhibition of mTor in an <i>hcfc1a</i>-deficient background leads to a reaction that differs from the traditional response observed in wildtype siblings. Collectively, we present a model that can be used to test dose-response and the development of combinatorial treatment approaches in a high-throughput manner.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Epithelial Egg Tooth of the Chicken Shares Protein Markers with the Embryonic Subperiderm and Feathers.","authors":"Attila Placido Sachslehner, Julia Steinbinder, Claudia Hess, Veronika Mlitz, Leopold Eckhart","doi":"10.3390/jdb14010001","DOIUrl":"10.3390/jdb14010001","url":null,"abstract":"<p><p>The epithelial egg tooth is used by birds to open the eggshell for hatching. This ectodermal structure consists of a multilayered periderm and a hard cornified portion, the caruncle or actual egg tooth. Here, we determined the protein composition of the egg tooth of the chicken and compared the proteins to markers of other epithelia identified in previous studies. The egg tooth and the upper beak of chicken embryos of Hamburger and Hamilton (HH) stage 44 were subjected to mass spectrometry-based proteomics. We found that scaffoldin, a marker of the embryonic periderm and the feather sheath, was enriched in the egg tooth relative to the beak. Likewise, Epidermal Differentiation protein containing DPCC Motifs (EDDM) and Epidermal Differentiation protein starting with a MTF motif and rich in Histidine (EDMTFH), which had previously been characterized as markers of the subperiderm on embryonic scutate scales and the barbs of feathers, were also enriched in the egg tooth. The expression of EDDM and EDMTFH was confirmed RT-PCR analysis. Our data suggest that the epithelial egg tooth is related to the subperiderm and feathers, a hypothesis with potentially important implications for the evolution of the avian integument.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"14 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146010685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiology and Management of Placenta Accreta Spectrum.","authors":"Lana Shteynman, Genevieve Monanian, Gilberto Torres, Giancarlo Sabetta, Deborah M Li, Zhaosheng Jin, Tiffany Angelo, Bahaa E Daoud, Morgane Factor","doi":"10.3390/jdb13040045","DOIUrl":"10.3390/jdb13040045","url":null,"abstract":"<p><p>Placenta Accreta Spectrum (PAS) disorders, including placenta accreta, increta, and percreta, are serious obstetric conditions characterized by abnormal placental adherence to the uterine wall. With increasing incidence, PAS poses significant risks, primarily through massive hemorrhage during or after delivery, often necessitating hysterectomy. Key risk factors include prior cesarean sections, uterine surgery, and placenta previa diagnosis. In this review, we will examine the pathophysiology of PAS, with a focus on the mechanisms underlying abnormal trophoblast invasion and defective decidualization. We will highlight the role of uterine scarring, extracellular matrix remodeling, dysregulated signaling pathways, and immune and vascular alterations in disrupting the maternal-fetal interface, ultimately predisposing to morbid placentation and delivery complications. We will also discuss the life-threatening complications of PAS, such as shock and multi-organ failure, which require urgent multidisciplinary intensive care, as well as the optimization of management through preoperative planning and intraoperative blood loss control to reduce maternal morbidity and mortality.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"13 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12733690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145819517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac Aftermath of Gestational Diabetes-From Intrauterine Impact to Lifelong Complications: A Systematic Review.","authors":"Sophia Tsokkou, Ioannis Konstantinidis, Antonios Keramas, Vasileios Anastasiou, Alkis Matsas, Maria Florou, Alexandra Arvanitaki, Emmanouela Peteinidou, Theodoros Karamitsos, George Giannakoulas, Themistoklis Dagklis, Theodora Papamitsou, Antonios Ziakas, Vasileios Kamperidis","doi":"10.3390/jdb13040044","DOIUrl":"10.3390/jdb13040044","url":null,"abstract":"<p><p><b>Background</b>. Gestational diabetes mellitus (GDM) induces maternal hyperglycemia, which may alter fetal cardiac structure and function, increasing short- and long-term cardiovascular risks. <b>Purpose</b>. To systematically review the evidence on the fetal cardiac structural and functional effects of GDM, to explore the diagnostic role of novel imaging and biochemical biomarkers, and to summarize the long-term cardiovascular complications associated with GDM. <b>Materials and Methods</b>. A systematic search of PubMed, Scopus, and Cochrane Library was conducted according to the PRISMA guidelines. All studies comparing cardiac outcomes in GDM and non-GDM pregnancies were included. Data on myocardial hypertrophy, diastolic and systolic function, imaging modalities, and biomarkers were extracted and qualitatively synthesized. <b>Results</b>. A total of twelve eligible studies were identified. Fetal cardiac hypertrophy and diastolic and early systolic dysfunction are common among GDM pregnancies and can be detected by dual-gate Doppler and speckle-tracking echocardiography. Abnormalities are observed in indices such as the myocardial performance index, E/A, E/e' ratios, and global longitudinal and circumferential strain in fetuses and may persist in the neonatal period. Alterations may be more pronounced for the right ventricle compared to the left. Septal hypertrophy is associated with elevated umbilical cord pro-brain natriuretic peptide. The risk of early-onset cardiovascular disease in the progeny of diabetic mothers is 29% higher, as evidenced by population-based cohort data. <b>Conclusions</b>. GDM is linked to fetal cardiac remodeling and an increased long-term cardiovascular risk. Early detection and customized interventions to reduce adverse outcomes may be achieved by integrating advanced echocardiographic techniques and biomarkers into prenatal surveillance.</p>","PeriodicalId":15563,"journal":{"name":"Journal of Developmental Biology","volume":"13 4","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12733427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145819533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}