The International journal of developmental biology最新文献

{"title":"Promoter strength delimits enhancer threshold in the early Drosophila embryo.","authors":"Miroo Hong, Joung-Woo Hong","doi":"10.1387/ijdb.240230jh","DOIUrl":"10.1387/ijdb.240230jh","url":null,"abstract":"<p><p>The enhancer threshold is defined as the minimum concentration of transcription factors (TFs) required to elicit an enhancer response in a given time and space. Here, evidence is presented that the enhancer threshold is relative to promoter strength in the early <i>Drosophila</i> embryo. The apparently inactive <i>even-skipped</i> (<i>eve</i>) minimal stripe element (MSE), in which a single Hunchback (Hb)-binding site is deleted, is functionally complemented by the <i>hsp70</i> promoter in transgenic embryos. Forced pause release of RNA polymerase II (Pol II) and transcription bubble assays show that both <i>eve</i> and <i>heat shock protein 70</i> (<i>hsp70</i>) promoters exhibit paused Pol II. However, bioinformatics analyses and transient transfection assays indicate that the strength of the <i>hsp70</i> promoter is much stronger than that of the <i>eve</i> promoter. Consistently, inactive MSE function is also restored by promoters stronger than the <i>eve</i> promoter. It is conceivable that the functional complementarity between enhancer and promoter strengths defines the enhancer threshold, thus determining whether a genomic locus acts as an enhancer for a particular promoter.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":"69 2","pages":"81-90"},"PeriodicalIF":1.3,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144304205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal dynamics of lineage-specific epithelial maturation in the developing mouse stomach.","authors":"Masashi Nishide, Yuki Taira, Akira Kurisaki, Hitomi Takada","doi":"10.1387/ijdb.250171ht","DOIUrl":"https://doi.org/10.1387/ijdb.250171ht","url":null,"abstract":"<p><p>At birth, the gastric epithelium is immature and progressively matures during postnatal development to establish adult tissue architecture and function. Although this process has been investigated at functional, proteomic and transcriptomic levels, the precise temporal and spatial dynamics by which individual epithelial lineages initiate differentiation, exit proliferative states and establish adult homeostasis remain incompletely understood. Here, we performed a comprehensive immunofluorescence analysis of the mouse stomach from mid-gestation through adulthood, examining fetal markers, lineage-specific functional epithelial markers, and the proliferation marker KI67. By integrating functional epithelial marker expression with proliferative status, we delineated distinct maturation trajectories for pit, parietal, and chief cell lineages. Notably, parietal and chief cells exhibited a robust proliferative phase from late gestation to early postnatal stages, followed by a marked decline in proliferative activity, whereas pit cells showed the emergence of proliferative progenitors primarily during later postnatal stages. Moreover, we identified region-specific differences in the timing of maturation between the corpus and the antrum. Together, our study establishes a spatiotemporal <i>in situ</i> atlas of gastric epithelial maturation and provides a framework for understanding lineage- and region- specific mechanisms governing postnatal gastric development.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":"69 4","pages":"203-215"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The <i>Hydra</i> FGF family - dispersed across the genome and expressed locally.","authors":"Kerstin Ohler, Lisa Reichart, Lars Kneifert, Susanne Önel, Monika Hassel","doi":"10.1387/ijdb.250118mh","DOIUrl":"10.1387/ijdb.250118mh","url":null,"abstract":"<p><p>Although the nonbilaterian <i>Hydra</i> has a simple body architecture, its signaling systems are as complex as those of Bilateria. We here add data to the fibroblast growth factor signaling system which has previously been identified in <i>Hydra</i> as essential for bud detachment. The localized expression patterns of its, now fifteen, FGFs indicate additional, yet unidentified, functions in sometimes very small subsets of cells at the body termini and/or during budding or in testes. Presence of a typical signal sequence (prediction >93%) in only 30% of the <i>Hydra</i> FGFs suggests mechanisms of action (and/or secretion) other than the canonical ones. A knockdown approach using siRNA revealed a potential role for Hv-FGF-c in tentacle morphogenesis. Our results document a high complexity of FGF signaling sites in <i>Hydra</i> and open the field for a detailed analysis of their functions.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":" ","pages":"173-185"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145936767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melastatin family Transient Receptor Potential channels support spermatogenesis in planarian flatworms.","authors":"Haley Nicole Curry, Roger Huynh, Labib Rouhana","doi":"10.1387/ijdb.240180lr","DOIUrl":"10.1387/ijdb.240180lr","url":null,"abstract":"<p><p>The Transient Receptor Potential superfamily of proteins (TRPs) form cation channels that are abundant in animal sensory systems. Amongst TRPs, the Melastatin-related family (TRPMs) is composed of members that respond to temperature, pH, sex hormones, and various other stimuli. Some TRPMs exhibit enriched expression in the gonads of vertebrate and invertebrate species, but their contributions to germline development remain to be determined. We identified twenty-one potential TRPMs in the planarian flatworm <i>Schmidtea mediterranea</i> and analyzed their anatomical distribution of expression by whole-mount <i>in situ</i> hybridization. Enriched expression of two TRPMs (<i>Smed-TRPM-c</i> and <i>Smed-TRPM-l</i>) was detected in testis, whereas eight TRPM genes had detectable expression in patterns representative of neuronal and/or sensory cell types. Functional analysis of TRPM homologs by RNA-interference (RNAi) revealed that disruption of normal levels of <i>Smed-TRPM-c</i> expression impaired sperm development, indicating a role for this receptor in supporting spermatogenesis. <i>Smed-TRPM-l</i> RNAi alone did not result in a detectable phenotype, but it did increase sperm development deficiencies when combined with <i>Smed-TRPM-c</i> RNAi. Fluorescence <i>in situ</i> hybridization revealed expression of <i>Smed-TRPM-c</i> in early spermatogenic cells within testes, suggesting cell-autonomous regulatory functions in germ cells for this gene. In addition, <i>Smed-TRPM-c</i> RNAi resulted in reduced numbers of presumptive germline stem cell clusters in asexual planarians, suggesting that <i>Smed-TRPM-c</i> supports the establishment, maintenance, and/or expansion of spermatogonial germline stem cells. While further research is needed to identify the factors that trigger Smed-TRPM-c activity, these findings reveal one of the few known examples for TRPM function in the direct regulation of sperm development.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":"69 1","pages":"21-34"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12421698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039564","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":"Three Decades of the Spanish Society for Developmental Biology (SEBD): Insights and Emerging Perspectives from the 18th Spanish Society for Developmental Biology Meeting (SEBD 2024).","authors":"Eloisa Herrera, Sandra Acosta, María Almuedo, Victor Borrell, Cristian Cañestro, Sergio Casas-Tintó, Luis M Escudero, Nicole Gorfinkiel, Esteban Hoijman, José Carlos Pastor-Pareja, Barbara Pernaute, Teresa Rayón, Murielle Saade, Jordi Solana, Vikas Trivedi, Elisa Martí, Cristina Pujades, Sofia J Araújo","doi":"10.1387/ijdb.250034sa","DOIUrl":"10.1387/ijdb.250034sa","url":null,"abstract":"<p><p>The Spanish Society for Developmental Biology (SEBD) organized its 18^th meeting in October 2024 (hereafter SEBD2024), coinciding with the society's 30^th anniversary and serving as the stage for its celebrations. This article provides an overview of the event, including the speakers, scientific sessions and the different activities related to the anniversary.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":"69 1","pages":"1-9"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of COX2 impairs angiogenesis and causes vascular defects in developing zebrafish embryos.","authors":"Lakshmi Pillai, Vishakha Nesari, Dhanush Danes, Suresh Balakrishnan","doi":"10.1387/ijdb.240222sb","DOIUrl":"10.1387/ijdb.240222sb","url":null,"abstract":"<p><p>This study investigated the role of cyclooxygenase-2 (COX2) in angiogenesis during zebrafish embryogenesis by inhibiting COX2 activity with etoricoxib. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis confirmed the successful penetration of etoricoxib into zebrafish embryos, leading to selective inhibition of COX2 without affecting COX1 activity. COX2 inhibition caused a significant reduction in prostaglandin E₂ levels throughout development. Phenotypically, treated embryos exhibited pericardial edema, bradycardia, and defective vascular development, including delays in intersegmental vessel (ISV) sprouting, incomplete dorsal longitudinal anastomotic vessel (DLAV) formation by 48 hpf, and impaired vascular networks by 72 hpf. Confocal imaging and AngioTool analysis revealed reduced vessel length, area and increased lacunarity. Molecular analysis showed significant downregulation of <i>vascular endothelial growth factor A (vegfa), kdr</i>, <i>pi3k</i> and <i>akt</i> transcripts, as well as reduced VEGFA, EP4 and Akt protein levels, disrupting VEGFA-PI3K-Akt signaling. Additionally, reduced expression of <i>ephrinb</i> and <i>prox1</i> affected arterial and venous identity formation. These results demonstrate that COX2 is essential for proper angiogenesis during zebrafish development, and its inhibition leads to significant vascular defects, underscoring COX2's crucial role in regulating VEGFA-mediated angiogenesis.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":" ","pages":"11-20"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling hepatic consequences of intrauterine growth restriction and catch-up growth: insights from histological, biochemical and metabolomic analysis in rats.","authors":"Mukaddes Esrefoğlu, Sahabettin Selek, Fatmanur Koktasoglu, Nihan Bayindir, Emine-Rumeysa Hekimoglu, Seda Kirmizikan, Fatma-Bedia Karakaya-Cimen, Halime Dulun-Agac, Mehtap Alim, Birsen Elibol, Ozge Pasin, Somer Bekiroglu","doi":"10.1387/ijdb.240147me","DOIUrl":"10.1387/ijdb.240147me","url":null,"abstract":"<p><p>Intrauterine growth restriction (IUGR) is increasingly recognized as a significant risk factor for metabolic disorders in adulthood. Employing a multi-faceted approach encompassing histopathological, immunohistochemical, biochemical, Western-blotting, and metabolomics analyses, this study aimed to elucidate potential metabolite markers of IUGR, and catch-up growth-related metabolic disturbances and the underlying metabolic pathways implicated in IUGR pathogenesis. This study cohort comprised 54 male siblings from 20 Sprague-Dawley female young rats. On the 19th day of gestation, half of the pregnant rats underwent bilateral uterine artery ligation, while the remaining half underwent a simulated surgical intervention involving solely peritoneal incisions. Blood and liver samples were collected from the pups after attaining catch-up growth at the postnatal weeks 2, 4, and 8. IUGR rats exhibited a spectrum of changes including histological abnormalities, altered apoptosis rates, oxidative stress markers, and mitochondrial energy metabolism. Metabolomic analysis revealed dysregulation in multiple metabolic pathways encompassing galactose, propanoate, glycerolipid, cysteine, methionine, and tyrosine metabolism, among others. Notably, disturbances were observed in butanoate, glutathione metabolism, valine, leucine, and isoleucine biosynthesis and degradation, citrate cycle, aminoacyl-tRNA biosynthesis, as well as glycolysis/gluconeogenesis. Our metabolomics analysis provides insights into the potential disease susceptibility of individuals born with IUGR, including obesity, diabetes, heart failure, cancer, mental retardation, kidney and liver diseases, and cataracts. These findings underscore the intricate interplay between intrauterine conditions and long-term metabolic health outcomes, highlighting the need for further investigation into preventive and therapeutic strategies aimed at mitigating the risk of metabolic diseases in individuals with a history of IUGR.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":" ","pages":"35-50"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Placental transcriptome reveals the placental brain axis genes and pathways of gestational diabetes mellitus (GDM) affecting offspring neurodevelopment.","authors":"Jianhua Li, Qian Liu, Xuhui Liu, Yunyun Wang, Yuxia Jin, Weikai Wang, Bin Yi, Yanxia Wang","doi":"10.1387/ijdb.240170jl","DOIUrl":"10.1387/ijdb.240170jl","url":null,"abstract":"<p><p>This study aims to analyze the pathways and the placental brain axis genes of gestational <i>diabetes mellitus</i> (GDM) affecting offspring neurodevelopment. Differentially expressed genes (DEGs) were identified through transcriptome sequencing of placental tissues. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed on DEGs. A protein-protein interaction (PPI) network was constructed and annotated using the STRING online software. The expression of neurodevelopment-related genes was analyzed by qPCR. Hubgenes were analyzed using Cytoscape 3.7.1 software. The correlation between Hubgenes and placental brain axis genes was analyzed through literatures alignment. The pathways of GDM affecting offspring neural development were predicted using the KEGG database. The placental transcriptome revealed that there were 404 DEGs between GDM and Normal groups. Among these DEGs, 125 were upregulated and 279 were downregulated. GO analysis indicated that DEGs were mainly involved in intracellular calcium activated chloride channel activity, anion channel activity, G protein-coupled peptide receptors, etc. Additionally, KEGG analysis revealed that DEGs were predominantly involved in neuroactive ligand receptor interaction pathways. STRING online software analysis revealed that the DLGAP1, NXNL2, SCG2, SLC18A2, LYNX1, GRM1, DLGAP1, BIRC7 genes were associated with neurodevelopment. PCR validation of these 8 genes was consistent with transcriptome results (<i>P</i><0.05). Literatures alignment showed that DLGAP1, GRM1 and SLC18A2 are placental brain axis genes that influence offspring neurodevelopment. The placental brain axis genes DLGAP1, GRM1, SLC18A2 have been found to influence GDM offspring neurodevelopment through the regulation of the Gq/PLC/PKC pathway.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":"69 1","pages":"51-59"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144048930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sialylated glycoproteins and sialyltransferases involved in mesoderm-derived organ formation during embryogenesis.","authors":"Ingrid Fliniaux, Pélagie Douchez, Yoshiko Takeda-Uchimura, Marin Matthieu, Alain Martoriati, Nao Yamakawa, Caroline Molinaro, Jean François Bodart, Anne Harduin-Lepers, Katia Cailliau","doi":"10.1387/ijdb.250129km","DOIUrl":"https://doi.org/10.1387/ijdb.250129km","url":null,"abstract":"<p><p>Most major organs, like muscles, bones, vessels and kidneys, develop from the mesoderm, one of three germ cell layers in triploblastic organisms. Sialic acids significantly affect embryonic development by regulating cell division, migration and death through signaling pathways and cell adhesion, which support morphogenesis. Loss of early biosynthetic enzymes reduces embryonic viability and leads to complex phenotypes, while the loss of terminal enzymes primarily results in tissue-specific defects in mesoderm-derived organs. Key sialylated glycoproteins involved in the developmental processes of mesoderm and mesoderm-derived organs have been identified across various species as major effectors. These enzymes and glycoproteins are of significant interest and are discussed in the present review.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":"69 4","pages":"161-172"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynein axonemal assembly factors (<i>dnaaf</i>) 5 and 9 are expressed in ciliated organs of zebrafish embryos.","authors":"Usharani Nayak, Kalyani Sahoo, Rajeeb K Swain","doi":"10.1387/ijdb.250162rs","DOIUrl":"https://doi.org/10.1387/ijdb.250162rs","url":null,"abstract":"<p><p>Dynein axonemal assembly factors (DNAAFs) play crucial roles in the formation and function of motile cilia, and their dysfunction often results in primary ciliary dyskinesia (PCD). We report the spatio-temporal expression patterns of <i>dnaaf5</i> and <i>dnaaf9</i> mRNA in zebrafish embryos, providing insight into their possible functions during development. We show that <i>dnaaf5</i> and <i>dnaaf9</i> mRNAs are expressed in motile ciliated tissues, such as the Kupffer's vesicle, pronephros, floor plate, brain and olfactory placode. The <i>dnaaf5</i> and <i>dnaaf9</i> crispants develop ciliopathic defects during zebrafish development. These data suggest that <i>dnaaf5</i> and <i>dnaaf9</i> may regulate motile cilia biogenesis and function in zebrafish. Our findings suggest functional redundancy and divergence among dynein arm assembly factors in vertebrates.</p>","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":"69 4","pages":"195-202"},"PeriodicalIF":1.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}