Developmental biology最新文献

{"title":"Redundant and novel functions of scube genes during zebrafish development","authors":"Quoc Duy Tran,&nbsp;Ivana Mirkovic,&nbsp;Lee B. Miles,&nbsp;Joachim Berger,&nbsp;Alasdair J. Wood,&nbsp;Avnika A. Ruparelia,&nbsp;Sara A. Shehni,&nbsp;Peter D. Currie","doi":"10.1016/j.ydbio.2025.09.002","DOIUrl":"10.1016/j.ydbio.2025.09.002","url":null,"abstract":"<div><div>The N-glycoprotein SCUBE family (Scube1, Scube2, and Scube3) plays diverse roles in vertebrate development and disease, yet many specific functions of the three family members remain unclear. These proteins exhibit broad tissue expression patterns, exist as soluble or membrane-tethered forms, and can form homo- or heteromeric complexes with each other, exerting both short- and long-range effects. Individual functional characterisation has proved challenging because of overlapping expression patterns and compensatory mechanisms that likely obscure specific roles. To elucidate Scube function, we generated single, double, and triple mutant combinations of the three <em>scube</em> genes in zebrafish and assessed their roles in Hedgehog signalling. Our findings indicate that all three Scube proteins contribute to muscle development at distinct levels, with triple knockout zebrafish larvae displaying near-complete Hedgehog loss-of-function phenotypes. RNA sequencing analysis revealed potential roles for all three <em>scube</em> genes, and specific functions for Scube1 and Scube3 in apoptosis regulation and macrophage biology were identified. Furthermore, the Scube family contains multiple functional domains, and the role of EGF domains in Hedgehog signalling remains contentious. Comparative rescue analysis revealed that full-length <em>scube2</em> mRNA restored slow muscle fibre numbers more efficiently than EGF domain-truncated constructs in <em>scube2</em> knockout zebrafish, demonstrating the importance of EGF domains in Scube2 function. Our results illustrate both redundant and non-redundant functions among Scube family members and provide new insights into the roles of this enigmatic class of developmental regulators.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 79-90"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005985","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":"Unraveling the developmental heterogeneity of human retinal ganglion cells within the developing retina to study to the continuity of maturation","authors":"Emil Kriukov ,&nbsp;Jonathan R. Soucy ,&nbsp;Everett Labrecque ,&nbsp;Petr Baranov","doi":"10.1016/j.ydbio.2025.08.025","DOIUrl":"10.1016/j.ydbio.2025.08.025","url":null,"abstract":"<div><div>Tissue development is a complex spatiotemporal process with multiple interdependent components. Anatomical, histological, sequencing, and evolutional strategies can be used to profile and explain tissue development from different perspectives. The introduction of single-cell RNA sequencing (scRNAseq) methods and the computational tools allows to deconvolute developmental heterogeneity and draw a decomposed uniform map. In this manuscript, we decomposed the development of a human retina with a focus on the retinal ganglion cells (RGC). To increase the temporal resolution of retinal cell classes maturation state we assumed the working hypothesis that that maturation of retinal ganglion cells is a continuous, non-discrete process. We have assembled the scRNAseq atlas of human fetal retina from fetal week 8 to week 27 and applied the computational methods to unravel maturation heterogeneity into a uniform maturation track. We align RGC transcriptomes in pseudotime to map RGC developmental fate trajectories against the broader timeline of retinal development. Through this analysis, we identified the continuous maturation track of RGC and described the cell-intrinsic (differentially expressed and variable genes, maturation gene profiles, regulons, transcriptional motifs) and -extrinsic profiles (neurotrophic receptors across maturation, cell-cell interactions) of different RGC maturation states. We described the genes involved in the retina and RGC maturation, including de novo RGC maturation drivers. We demonstrate the application of the human fetal retina atlas as a reference tool, allowing automated annotation and universal embedding of scRNAseq data. Altogether, our findings deepen the current knowledge of the retina and RGC maturation by bringing in the maturation dimension for the cell class vs. state analysis. We show how the pseudotime application contributes to developmental-oriented analyses, allowing to order the cells by their maturation state. This approach not only improves the downstream computational analysis but also provides a true maturation track transcriptomics profile.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 91-104"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005990","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":"Reorganization of H3K9me2-modified chromatin regions during mouse embryonic development","authors":"Diana Fulmer ,&nbsp;Emily J. Shields ,&nbsp;Andrey Poleshko ,&nbsp;Jonathan A. Epstein ,&nbsp;Cheryl L. Smith","doi":"10.1016/j.ydbio.2025.09.005","DOIUrl":"10.1016/j.ydbio.2025.09.005","url":null,"abstract":"<div><div>The three-dimensional organization of chromatin in the nucleus is critical in regulating gene expression. There are two classes of large genomic regions demarcated by the repressive chromatin modification histone H3 lysine 9 dimethyl (H3K9me2) and enriched at the nuclear periphery: lamina-associated domains (LADs); and H3K9me2-only domains (KODs) which have minimal lamina contact and are highly enriched for transcriptional enhancers. LADs have been studied in multiple cell types. In contrast, KODs have been characterized only in pluripotent cells and it remains to be determined whether they are fixed or rearrange according to cell type. Analysis of KODs from various embryonic mouse tissues revealed that KODs adopt cell type-specific configurations that correlate with changes in lineage-specific enhancer activity. Within KODs, local cell type-specific depletion of H3K9me2 was enriched for H3K27ac peaks at active lineage-specific enhancers. KODs were also enriched across ultra-long regulatory regions suggesting a role for KODs in long-range gene regulation. These results suggest that KODs are cell-type specific and maintain cell type-specific enhancers in a repressed state to allow for tissue- and stage-specific gene activation.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 188-203"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091276","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":"Scarecrow, a homolog of mammalian Nkx2.1, regulates the temporal progression and glial differentiation of medulla neuroblasts for the optic lobe development in Drosophila melanogaster","authors":"Cheol-Ho Yun ,&nbsp;Kyungjun Seok ,&nbsp;Gyunghee G. Lee ,&nbsp;Jae H. Park ,&nbsp;Siuk Yoo","doi":"10.1016/j.ydbio.2025.09.012","DOIUrl":"10.1016/j.ydbio.2025.09.012","url":null,"abstract":"<div><div>The <em>Drosophila</em> medulla is the largest structure in the adult visual nervous system. It contains a vast population of interneurons comprising over 80 different cell types generated by medulla neuroblasts (NBs). Aging NBs express a series of temporal transcription factors (tTFs) that contribute to neuronal diversity. Recent studies have shown that an NK-2 homeobox gene <em>scarecrow</em> (<em>scro</em>) works as a tTF covering from middle to late temporal windows; however, how its expression is established over multiple windows and what roles it plays in individual windows remain largely elusive. We found the lack of <em>scro</em> expression in the middle of the Dichaete (D) domain, implying its expression is not in a continuum as previously eluded. Overexpression and knockdown assays of <em>scro</em> or other tTFs using various <em>tTF-Gal4</em> drivers further revealed distinctive roles played by Scro at each window, including the last one. The oldest NBs positive for Tll and Scro found at the most proximal region of the developing medulla field attained expression of Gcm (the master factor of glial differentiation) and Nerfin-1 (a suppressor of dedifferentiation via Notch suppression), which in turn led to NB-to-glia differentiation. Downregulation of either <em>gcm</em> or <em>nerfin-1</em> resulted in the formation of ectopic NBs at the expense of glial cells. Moreover, <em>scro-</em>knockdown led to a loss of Gcm, Nerfin-1, and Prospero expression, misregulation of Notch expression, formation of ectopic NBs, and a substantial reduction in glial cell population, suggesting that Scro acts upstream of Gcm and Nerfin-1. The chromatin-immunoprecipitation (ChIP) assays support that Scro regulates the expression of <em>gcm</em>, <em>nerfin-1</em>, and <em>pros</em>, as well as several tTFs, the expression of which overlaps with Scro. In summary, this study not only verified previously suggested roles of Scro but also uncovered novel features of this gene in various temporal windows, including the promotion of NB-to-glial transition and discontinuous expression within the D domain.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 277-294"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085417","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":"Injury-induced Neuregulin-EGFR signaling from muscle mobilizes stem cells for whole-body regeneration in acoels","authors":"Brian Stevens ,&nbsp;Riley Popp ,&nbsp;Heather Valera ,&nbsp;Kyle Krueger ,&nbsp;Christian P. Petersen","doi":"10.1016/j.ydbio.2025.08.024","DOIUrl":"10.1016/j.ydbio.2025.08.024","url":null,"abstract":"<div><div>The activation of progenitor cells near wound sites is a common feature of regeneration across species, but the conserved signaling mechanisms responsible for this step in whole-body regeneration are still incompletely understood. The acoel <em>Hofstenia miamia</em> undergoes whole-body regeneration using Piwi + pluripotent adult stem cells (neoblasts) that accumulate at amputation sites early in regeneration. The EGFR signaling pathway has broad roles in controlling proliferation, migration, differentiation, and cell survival across metazoans. Using candidate RNAi screening, we identify the <em>Hofstenia</em> EGFR <em>egfr-1</em> and Neuregulin <em>nrg-1</em> genes as essential for blastema formation. Structure prediction of NRG-1 and EGFR-1 proteins suggests these factors interact directly. After amputation injuries, <em>nrg-1</em> expression is induced in body-wall muscle cells at the wound site by 6 h and localizes to the tip of the outgrowing blastema by 24 h and sustains for several days, while <em>egfr-1</em> is broadly expressed, including in muscle and neoblasts. The early phase of <em>nrg-1</em> expression occurs at incision sites that repair through wound healing while the late phase is specific to blastema formation. Under <em>nrg-1(RNAi)</em> and <em>egfr-1(RNAi)</em> conditions that impair blastema formation, animals still undergo the earliest responses to injury to activate expression of the Early Growth Response transcription factor <em>egr</em>. In addition, RNAi of <em>nrg-1</em> only after amputation results in regeneration failure, indicating regeneration requires new <em>nrg-1</em> expression. <em>nrg-1(RNAi)</em> and <em>egfr-1(RNAi)</em> animals possess Piwi+ and H3P + mitotic neoblasts which hyperproliferate normally after amputation, but these cells fail to accumulate at the wound site. Therefore, muscle provides a source for Neuregulin-EGFR signaling after injury and is necessary for the mobilization of proliferative progenitors to enable blastema outgrowth for whole-body regeneration in <em>Hofstenia</em>. These results indicate a shared functional requirement for muscle signaling to enable regeneration between planarians and acoels across 550 million years of evolution.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 105-116"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022973","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":"Nuclear hormone receptor regulation of PAL-1/Caudal mediates ventral nerve cord assembly in C. elegans","authors":"Nathaniel Noblett ,&nbsp;Tony Roenspies ,&nbsp;Stephane Flibotte ,&nbsp;Antonio Colavita","doi":"10.1016/j.ydbio.2025.08.023","DOIUrl":"10.1016/j.ydbio.2025.08.023","url":null,"abstract":"<div><div>The regulatory network governed by CDX/<em>Caudal</em> family transcription factors plays critical roles in shaping embryonic neural development. In <em>C. elegans</em>, we found that proper expression of <em>pal-1</em>, the <em>C. elegans Caudal</em> homologue, is required for correct positioning of motor neuron cell bodies in the first larval stage ventral nerve cord (VNC). We identified an upstream regulatory region within the <em>pal-1</em> promoter that drives <em>pal-1</em> expression in a subset of DD and DA neuronal progenitors. We also show that SEX-1, a nuclear hormone receptor, is required for motor neuron positioning in the VNC. Loss of <em>sex-1</em> results in neuronal positioning defects similar to those observed in <em>pal-1</em> mutants. This is in part due to a requirement for SEX-1 in promoting <em>pal-1</em> expression in DD and DA neuronal progenitors during VNC assembly. Double mutant analysis further suggests that <em>sex-1</em> also has <em>pal-1</em>-independent functions. Together, these findings define a transcriptional hierarchy in which the SEX-1 nuclear hormone receptor regulates the tissue-specific activity of PAL-1 to promote proper motor neuron positioning in the VNC and highlight a conserved role for NHR and CDX/Caudal family proteins in central nerve cord formation.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 13-26"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144989802","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":"Intraocular vasculature formation precedes extraocular vasculature penetration of mouse eyes","authors":"Satoshi Imanishi ,&nbsp;Yohei Tomita ,&nbsp;Kazuno Negishi ,&nbsp;Kazuo Tsubota ,&nbsp;Toshihide Kurihara","doi":"10.1016/j.ydbio.2025.09.010","DOIUrl":"10.1016/j.ydbio.2025.09.010","url":null,"abstract":"<div><div>The posterior ocular circulatory system comprises choroidal vasculature and central retinal and posterior ciliary arteries (PCAs) that are fundamental for ocular tissue maintenance. Much is known about the development of the retinal vascular system, but that of the posterior ocular circulation system remain obscure. Therefore, we aimed to clarify the development of the intraocular vasculature involved in the posterior ocular circulation system. Choriocapillaris and hyaloid capillaries are formed <em>in situ</em> and <em>de novo</em> through the endothelial differentiation of hemangioblasts. The intraocular segments of the hyaloid artery penetrate the retina before extraocular segments appear. The intraocular segments of PCAs arise from the hyaloid artery before the extraocular segments reach the eye. The posterior ocular circulation system apparently synchronizes with events throughout the entire process of ocular development. The intraocular vasculature notably formed before the extraocular segments reached the eyes. Our findings provide a novel perspective on ocular development and might facilitate understanding of eye diseases in humans.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 152-162"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085397","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":"Overexpression of potassium channel Kcna5 alters skeletal patterning in the zebrafish regenerating fin","authors":"Alexander W. Seaver,&nbsp;Xinxhao Li,&nbsp;M. Kathryn Iovine","doi":"10.1016/j.ydbio.2025.09.001","DOIUrl":"10.1016/j.ydbio.2025.09.001","url":null,"abstract":"<div><div>Skeletal patterning relies on a complex network of molecular and genetic regulators. However, our understanding of pathways governing joint placement and morphogenesis remains incomplete. Prior studies have demonstrated that medially located Cx43 mediated gap junctional intercellular communication (GJIC) inhibits joint formation by the adjacent lateral skeletal precursor cells, and thereby determines skeletal patterning in the teleost regenerating fin. Here, we test the model that Cx43-GJIC regulates joint formation by propagating changes in membrane potential (ΔV_m). To provide evidence that ΔV_m is sufficient to influence joint formation, we generated a transgenic line that expresses the <em>X. laevis voltage-gated channel, shaker-related subfamily, member 5</em> (<em>kcna5</em>) behind the temperature-inducible <em>heat shock protein 70</em> (<em>hsp70</em>) promoter. Using this line, we demonstrate that <em>Xl</em>-<em>kcna5</em> overexpression delays <em>evx1</em> expression and causes longer segments. Moreover, the increased segment length in response to Xl-Kcna5 overexpression requires Cx43. These findings support a model whereby potassium channels act together with gap junction channels to influence joint formation, and therefore skeletal patterning, in the zebrafish regenerating fin.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 57-65"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145005933","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":"Mouse variants in Taf1c result in reduced survival to birth","authors":"Jennifer L. Watts ,&nbsp;Logan Willeke ,&nbsp;Rolf W. Stottmann","doi":"10.1016/j.ydbio.2025.09.011","DOIUrl":"10.1016/j.ydbio.2025.09.011","url":null,"abstract":"<div><div>Ribosome biogenesis is a key cellular function and disruptions in this process can lead to congenital anomalies or “ribosomopathies” with varying phenotypes including craniofacial malformations and neurodevelopment symptoms. Classically, the mouse is a robust model to understand the molecular mechanisms underlying ribosomopathies to further elucidate human pathogenesis. We identified novel compound heterozygous missense variants in the <em>TATA-box binding protein associated factor, RNA polymerase I subunit C</em> (<em>TAF1C</em>) locus in a patient with some phenotypes consistent with ribosomopathies. <em>TAF1C</em> encodes a subunit of the SL1 complex which is critical for the RNA <em>Pol</em>I complex to initiate ribosomal RNA transcription. We hypothesized that functional <em>TAF1C</em> is required at developmental stages critical for craniofacial and neurodevelopment. To test this hypothesis, we created mouse <em>Taf1c</em> variants orthologous to the human variants using CRISPR-CAS9 technology (<em>Taf1c</em>^{<em>R202Q</em>} and <em>Taf1c</em>^{<em>S428A</em>}). We also created an 11bp deletion to complement the missense variants (<em>Taf1c</em>^{<em>11bpdel</em>}). We created multiple allelic combinations to determine the roles for <em>Taf1c</em> in survival and craniofacial development. Homozygous mice for any of these novel variants were underrepresented at organogenesis stages. We did not observe craniofacial anomalies in any surviving mice. Our results suggest that these specific <em>TAF1C</em> variants are not the cause of any human phenotype present in the patient motivating the study. However, we showed that <em>Taf1c</em> is required for embryonic survival and our studies contribute to knowledge about the role of ribosome biogenesis machinery throughout organogenesis.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 143-151"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069002","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":"VEGF and its receptors expression in relation to reduced vasculature phenotype in heme oxygenase 1 knockout mouse embryos","authors":"Meenakshi Rana ,&nbsp;Gouri Nandi ,&nbsp;Sidhant Jain ,&nbsp;Divya Bajaj","doi":"10.1016/j.ydbio.2025.09.018","DOIUrl":"10.1016/j.ydbio.2025.09.018","url":null,"abstract":"<div><div>Vascular development is a pivotal aspect of embryogenesis, and its disruption can lead to developmental abnormalities or lethality. Although numerous studies have demonstrated a significant association between heme oxygenase 1 (Hmox1) and vascular biology, this link has not been reported so far during mouse embryonic development. Hmox1 is the rate-limiting enzyme that catalyzes the breakdown of heme to equimolar amounts of biliverdin, carbon monoxide, and ferrous iron. Here, we report that embryos lacking Hmox1 exhibit significant reductions in superficial blood vessel formation during mid-gestation, accompanied by organ-specific disruptions in vascular patterning. A comparative analysis of VEGF, VEGFR2, and CD31 revealed tissue-specific disruptions in angiogenic signaling and endothelial integrity in the brain, heart, and lungs of Hmox1-deficient embryos. The localization and abundance of these molecules were altered in affected organs, with isoform- and receptor subtype–specific expression changes raising the possibility of an impact on the structural integrity of developing vascular networks. These findings suggest that the absence of Hmox1 disrupts essential regulatory mechanisms required for angiogenesis, potentially contributing to the partial prenatal lethality observed in knockout embryos. Our results point to a previously unrecognized role for Hmox1 in regulating organ-specific vascular development during late gestation, with its deficiency leading to tissue-specific disruptions in angiogenesis and impaired blood vessel formation.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 264-276"},"PeriodicalIF":2.1,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181844","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}