DEVELOPMENTAL BIOLOGY发育生物学
DEVELOPMENTAL BIOLOGY(英文缩写 DEV BIOL),ISSN 0012-1606,eISSN 1095-564X,中文译名:发育生物学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.148 | Q2 |
| 2022 | 2.700 | Q2 |
| 2023 | 2.500 | Q2 |
| 2024 | 2.100 | Q3 |
| 2025 | 2.100 | Q3 |
DEVELOPMENTAL BIOLOGY 最新收录文献
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1. Botulinum toxin dysregulates calcium activity and prevents Dpp/BMP secretion from epithelial cells in the developing fly wing.
PMID:日期:2026-11-01It has long been thought that neurons are the only cells to utilize ion flux to temporally regulate secretion for cell-to-cell signaling, but we discovered that ectoderm and mesenchymal cells are excitable, undergo voltage-dependent calcium waves, and harness calcium influx to control secretion of essential morphogens, bone morphogenetic proteins (BMPs). Furthermore, altering ion flux during morphogenesis results in craniofacial and limb abnormalities in organisms as diverse as insects and mammals, suggesting that the role for electrical signaling is conserved. In neurons, calcium activates the SNARE complex to drive fusion of secretory vesicles to temporally regulate secretion. Our discoveries inspired the hypothesis that calcium induces the SNARE complex to control BMP secretion. Here, we use pharmacological inhibition of the SNARE complex (Botulinum toxin, BoNT-C) and genetic tools in Drosophila to test this hypothesis in the wing primordia (wing disc). To test whether the SNARE complex is important in epithelial cells for BMP secretion, we apply BoNT-C to the wing disc and measure BMP secretion and calcium activity. We found that BoNT-C inhibits BMP secretion and increases endogenous calcium activity in the epithelial cells of the wing disc, as it does in neurons. Furthermore, expression of BoNT-C in the BMP-producing cells significantly reduces measures of downstream signaling. These data open the possibility that the SNARE complex may control the secretion of other developmental morphogens. Furthermore, our data suggest that pharmacological inhibition of the SNARE complex may not be specific to neuronal targets.
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2. Shedding light on the proteolytically released ectodomains of membrane-bound Semaphorins.
PMID:日期:2026-11-01Semaphorins (Semas) are secreted and membrane-bound molecules classically characterized as axonal guidance cues in nervous system development. However, it is now widely appreciated that Semas have essential functions in the development of many systems including the cardiovascular, endothelial, and immune systems. Secreted Semas enable functionality distant from the site of release, while membrane-bound Semas mediate localized contact-dependent signaling. Interestingly, functional soluble ectodomains have been discovered in each of the four vertebrate membrane-bound classes which can drive change in the nature and reach of Sema signaling. This review highlights the discovery of these soluble Sema ectodomains, the mechanisms of their release, and their known roles in development and pathological states.
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3. Notch-regulated hematopoiesis in Drosophila: Parallels and contrasts with vertebrate blood development.
PMID:日期:2026-11-01Drosophila melanogaster offers a genetically tractable model for dissecting the molecular logic of blood cell development. With a simple repertoire of blood cell types, Drosophila hematopoiesis relies on a conserved set of developmental pathways, among which Notch signaling emerges as a central regulator. In this review, we examine how Notch governs successive steps of blood cell development, including the initial specification of hematopoietic progenitors from the cardiogenic mesoderm, niche-dependent progenitor maintenance in the larval lymph gland, and fate decisions that include crystal cell specification, maturation, and transdifferentiation from plasmatocytes. We further address how Notch output is shaped by intracellular trafficking through the endolysosomal pathway, and how metabolic and environmental inputs are integrated to fine-tune lineage specification. Finally, we discuss how attenuation of Notch signaling in progenitors is required to permit lamellocyte differentiation in response to immune challenge. Throughout, we draw comparisons with vertebrate hematopoiesis, identifying conserved regulatory logic in progenitor emergence, niche-mediated stem cell maintenance, and binary fate decisions, while noting species-specific differences that reflect the distinct complexity of each system. Together, these analyses position Notch as a multifunctional developmental regulator whose activity underlies both homeostatic and adaptive blood cell production, and whose dysregulation is linked to hematological malignancies in humans.
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4. Limitations of serial cloning in mammals: unresolved donor-cell genomic integrity challenges broad claims of cloning limits.
PMID:日期:2026-11-01Wakayama et al. describe an extraordinary 20-year serial cloning study in mice, concluding that serial cloning in mammals is ultimately limited by the accumulation of genetic anomalies. However, their whole-genome sequencing (WGS) analysis characterized selected cloned animals but did not include matched genomic profiling of the corresponding cumulus cell (CC)-donor mice, the source CC populations, or developmental stages. Because each reconstructed embryo originated from a single CC nucleus and re-cloned animals were used to advance the lineage, pre-existing somatic variation could have entered the lineage and subsequently been propagated. Consequently, variants detected in later generations cannot be assigned definitively to pre-existing donor-cell mosaicism, donor-cell handling, somatic cell nuclear transfer manipulation, or early embryogenesis. Thus, the observed decline cannot be attributed exclusively to genetic lesions arising during repeated cloning, but the unresolved genomic status of the lineage-founding donor cells remains a plausible but unproven contributor. The study therefore demonstrates the transmission and propagation of genetic lesions through serial cloning more directly than it establishes that all initiating lesions arose because of repeated cloning. Paired genomic profiling of donor-cell populations, embryos, and offspring would help resolve the origins of accumulated genetic lesions and determine whether donor-cell screening could extend serial cloning.
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7. The first 25 years of the NICHD structural birth defects initiative.
PMID:日期:2026-11-01Initiated by NICHD and crafted with clinicians and laboratory scientists, the Structural Birth Defects (SBD) Initiative has supported research into the clinical, genetic, biochemical, mechanistic, developmental, and environmental basis of human disorders with structural anomalies for 25 years. The SBD Initiative has supported and continues to fund research teams studying a broad spectrum of single gene (Mendelian) disorders along with defining loci and susceptibility genes in oligogenic phenotypes, including genetic and environmental risk modifiers. The Initiative required and currently convenes biennial meetings of SBD investigators to share data, exchange ideas and initiate collaborations. In alternate years, online trainee symposia provide a platform for medical fellows, postdoctoral fellows and graduate students to present their data, with the goal of attracting and retaining this future generation of investigators in SBD research. In addition to determining their etiology, the SBD Initiative has supported remarkable progress in developing a fundamental mechanistic understanding of this diverse group of phenotypes. Together, scientific progress has led to translational benefits that include 1) widespread diagnostic testing for families with these disorders, both within the United States and across the world, and 2) pharmacological treatments for affected individuals. This progress has fulfilled the promise of the vision of the architects of the program, which is reviewed in this article, and continues to drive the field forward.
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8. Phase separation and condensates in craniofacial development.
PMID:日期:2026-11-01Biomolecular condensates formed by liquid-liquid phase separation (LLPS) have emerged as a major mode of intracellular organization, and their roles in craniofacial development are only beginning to be defined. In this review, we synthesize evidence that phase separation and condensate biology influences craniofacial morphogenesis at multiple levels, from transcriptional control in neural crest-derived lineages to signaling integration, mechanosensing, and the formation of mineralized tissues. Nuclear condensates formed by transcription factors and chromatin regulators are implicated in clefting and craniofacial syndromes are highlighted as modulators of local gene expression programs and cell fate decisions. Condensate-mediated regulation of mechanosensitive pathways and nucleolar function in osteogenic and chondrogenic cells is discussed in relation to craniofacial bone, cartilage, and sutural growth. In parallel, we examine extracellular phase-separation-like and LLPS-adjacent phenomena in enamel and dentin biomineralization, including self-assembly of enamel matrix proteins and polymer-induced liquid precursors that concentrate ions and guide apatite organization. Shared principles, conceptual distinctions, and outstanding questions are outlined, with emphasis on experimental strategies that link condensate or phase-behavior properties to craniofacial development, malformation and tissue repair.
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9. Amiodarone-mediated thyroid hormone disruption induces mitochondrial apoptosis and G1 arrest during chick embryogenesis.
PMID:日期:2026-11-01Thyroid hormones (THs) coordinate proliferation, apoptosis, and tissue remodeling during vertebrate development, yet how TH signaling constrains embryonic cell death in avian embryos remains unclear. Here, we used amiodarone, a pharmacological disruptor of TH signaling with reported effects on TH receptors and deiodinase-mediated hormone metabolism, to perturb TH signaling at the onset of incubation in chick embryos and integrate systems-level and functional readouts. In silico docking predicted favorable binding of amiodarone to all three deiodinase isoforms (DIO1-3), while whole-embryo assays showed a progressive reduction in total embryonic deiodinase capacity from day 2 to day 4. Treated embryos developed lateral plate mesoderm-associated craniofacial, limb, and ventral body-wall defects and exhibited widespread apoptosis, as evidenced by Nile blue sulfate staining, DNA laddering, TUNEL, Annexin V/propidium iodide flow cytometry, and cleaved CASPASE-3 immunolocalization. qRT-PCR and immunoblotting demonstrated downregulation of BCL2 and PCNA with upregulation of BAX, P53, BAD, caspases, and cleaved CASPASE-3, indicating activation of mitochondrial apoptotic signaling accompanied by increased P53 expression. High-resolution proteomics further supported induction of apoptotic and mitochondrial stress-associated pathways alongside suppression of vesicle trafficking and mitochondrial translation proteins. Cell-cycle profiling showed accumulation of cells in sub-G0/G1 and G0/G1 phases, indicating G1 checkpoint arrest and reduced proliferative capacity. Promoter analysis predicted putative thyroid hormone response elements in selected apoptotic regulators, suggesting potential TH-responsive regulatory sites requiring functional validation. Together, these data support an important role for early TH signaling in maintaining the proliferation-apoptosis balance during chick embryonic morphogenesis.
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10. Notch receptors involved in the choice between intestinal secretory and enterocytes and differentiation of Bestrophin4 cells.
PMID:日期:2026-11-01During the first half of embryogenesis, the intestinal epithelium is a simple layer of cuboidal cells surrounded by lateral plate splanchnic mesoderm. As embryogenesis proceeds, the epithelium differentiates to include a variety of enterocytes and secretory cells. During the period of epithelial cell differentiation a number of signaling pathways are used to generate the full complement of cell types. Notch signaling is important for the choice between enterocytes and secretory cells. Following the initial choice, both enterocytes and secretory cells continue differentiating into a number of different subtypes of each cell type. In the zebrafish embryo, Notch signaling is utilized at least three times during development of the intestinal epithelium. The first two Notch signaling events are involved in the choice between enterocytes and secretory cells, while the third involves differentiation of a unique cell type that we previously called Notch Receiving Secretory Cells (NRSCs). While we have identified the times when Notch signaling is active, the individual Notch receptors used in each signaling event have not been previously identified. Here we used loss of function mutants in the four Notch receptors (notch1a, 1b, 2, and 3) to identify which are used in the each of the Notch signaling events. We find redundant use of Notch receptors in the choice between enterocytes and secretory cells with loss of combinations of either notch2 and notch3 or notch2 and notch1b but not loss of individual receptors resulting in changes to secretory cell numbers. During the Notch signaling event following the choice between secretory and enterocytes, we identify NRSCs as Bestrophin4 (Best4+) cells. In contrast to the choice between secretory and enterocyte cells, we find that loss of individual Notch receptors result in differing numbers of Best4+ cells. Even though loss of individual receptors affect Best4+ numbers we suggest that combinations of Notch receptors play a role in differentiation of different Best4+ subtypes.