IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-02-09 DOI: 10.1242/dev.204549

Ana R Hernandez-Rodriguez, Yisha Lan, Fengtong Ji, Susannah B P McLaren, Joana M N Vidigueira, Ruoheng Li, Yixin Dai, Emily Holmes, Lauren D Moon, Lakshmi Balasubramaniam, Fengzhu Xiong

{"title":"TiFM2.0 - versatile mechanical measurement and actuation in live embryos.","authors":"Ana R Hernandez-Rodriguez, Yisha Lan, Fengtong Ji, Susannah B P McLaren, Joana M N Vidigueira, Ruoheng Li, Yixin Dai, Emily Holmes, Lauren D Moon, Lakshmi Balasubramaniam, Fengzhu Xiong","doi":"10.1242/dev.204549","DOIUrl":"10.1242/dev.204549","url":null,"abstract":"During development, spatial-temporally patterned tissue-level stresses and mechanical properties create diverse tissue shapes. To understand the mechanics of small-scale embryonic tissues, precisely controlled sensors and actuators are needed. Previously, we reported a control-based approach named tissue force microscopy (TiFM1.0), which combines dynamic positioning and imaging of an inserted cantilever probe to directly measure and impose forces in early avian embryos. Here, we present an upgraded system (TiFM2.0) that uses interferometer positioning to minimise probe holder footprint, enhancing accessibility and imaging signal. This new design enables a double-probe configuration for bidirectional stretching, compression and stress propagation experiments. As proof-of-concept, we showcase a variety of examples of TiFM2.0 applications in chicken and zebrafish embryos, including the characterisation of mechanical heterogeneities important for the morphogenesis of the chicken posterior body axis. We also present simplified designs and protocols for the replication of TiFM systems with minimal custom engineering for developmental biology labs.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146009297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An avidity-driven mechanism of extracellular BMP regulation by Twisted gastrulation. 扭曲原肠胚形成调控细胞外BMP的亲切度驱动机制。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-02-16 DOI: 10.1242/dev.204584

Gareth Moore, Raluca Revici, Lauren Forbes Beadle, Catherine Sutcliffe, Holly Birchenough, Clair Baldock, Hilary L Ashe

{"title":"An avidity-driven mechanism of extracellular BMP regulation by Twisted gastrulation.","authors":"Gareth Moore, Raluca Revici, Lauren Forbes Beadle, Catherine Sutcliffe, Holly Birchenough, Clair Baldock, Hilary L Ashe","doi":"10.1242/dev.204584","DOIUrl":"10.1242/dev.204584","url":null,"abstract":"During dorsoventral patterning of bilaterian embryos, the conserved regulator Twisted gastrulation (Tsg) modulates BMP signalling by binding Chordin/Short gastrulation (Sog). Here, we elucidate the mechanism by which Tsg interacts with Sog/Chordin to promote formation of the inhibitory Tsg-Sog/Chordin-BMP complex and regulate BMP signalling extracellularly. We identify and validate in vitro a hydrophobic interface in the Tsg C-terminal domain that binds Chordin. Mutation of this epitope in Drosophila Tsg (TsgL100A) results in an unexpectedly mild perturbation to embryonic BMP gradient formation. We show that a protostome-specific Tsg C-terminal extension also binds Sog, and the presence of this second binding site allows partial rescue of Sog interaction with TsgL100A in the presence of BMP. Consistent with this, a truncated Tsg protein lacking both Sog binding regions is unable to support BMP gradient formation in vivo. As our data show that disruption of either Sog binding site in Tsg, but not both, can be overcome by Tsg-BMP and Sog-BMP interactions, we present a new avidity-driven mechanism of BMP gradient formation that will be relevant to a broad range of developmental contexts.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BMP signaling regulates dorsal skeletal growth in the sea urchin embryo. BMP信号调控海胆胚胎背部骨骼的生长。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-04-23 DOI: 10.1242/dev.205344

William B Douglas, Charles A Ettensohn

{"title":"BMP signaling regulates dorsal skeletal growth in the sea urchin embryo.","authors":"William B Douglas, Charles A Ettensohn","doi":"10.1242/dev.205344","DOIUrl":"https://doi.org/10.1242/dev.205344","url":null,"abstract":"The development of the elaborate, calcified endoskeleton of sea urchin embryos is a model for understanding the dynamic nature of developmental gene regulatory networks and the control of biomineralization. While several signaling pathways have been shown to regulate gene expression and biomineral formation by sea urchin skeletogenic cells, important gaps in our understanding remain. Here, we focused on signals that regulate skeletogenesis along the dorsal-ventral axis of the late-stage embryo. We used a specific inhibitor of Type I BMP receptors, K02288, to show that BMP signaling regulates skeletal growth selectively in the dorsal region. K02288 treatment led to dorsal skeletal defects and inhibited the expression of genes typically expressed specifically in the dorsal skeletogenic cells, including biomineralization genes. Using RNA sequencing, we identified genes that were uniquely downstream of either the BMP or a ventral signaling pathway (the VEGF pathway) at late developmental stages and genes downstream of both pathways. Our findings establish BMP signaling as a key pathway regulating dorsal skeleton formation and show that BMP signaling functions in concert with VEGF signaling to define the dorsal-ventral axis of the skeleton.","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 16","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hemidesmosomes and Notch signaling regulate epidermal differentiation via delamination. 半粒粒和Notch信号通过分层调节表皮分化。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-04-16 DOI: 10.1242/dev.205210

Juliet S King, Kendall J Lough, Scott E Williams

{"title":"Hemidesmosomes and Notch signaling regulate epidermal differentiation via delamination.","authors":"Juliet S King, Kendall J Lough, Scott E Williams","doi":"10.1242/dev.205210","DOIUrl":"10.1242/dev.205210","url":null,"abstract":"Integrins mediate adhesion of basal keratinocytes to the underlying basement membrane. While high expression of integrins has been correlated with stemness, there is limited direct evidence that integrins mediate keratinocyte retention within the basal layer. Here, we generate mosaic, epidermal-specific loss of integrin-β4 (encoded by Itgb4) or its ligand, laminin-α3β3γ2 (Lama3), in mouse using an in utero lentiviral-mediated approach. Although mutations in these genes cause postnatal skin blistering in mice and humans, we observe no evidence of dermal-epidermal separation embryonically. Despite no obvious alterations to apicobasal polarity, Itgb4-deficient basal cells show mild defects in oriented cell divisions, with increased oblique divisions and altered telophase correction. However, differentiation via delamination, whereby basal keratinocytes lose adhesion to the underlying basement membrane and transit into the suprabasal layer, is elevated upon Itgb4 or Lama3 loss. Notably, hyperactive Notch signaling both decreases integrin-β4 expression and increases delamination, while deletion of the Notch effector Rbpj has the opposite effect. These findings conclusively demonstrate a causal role for hemidesmosomes in regulating epidermal differentiation through both mitotic and non-mitotic mechanisms, and shed additional light on the programs regulating delamination.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147590653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Break to build: fracture as a unifying morphogenetic strategy. 断裂构建：断裂作为一种统一的形态发生策略。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-02-09 DOI: 10.1242/dev.205136

Daniel Santos-Oliván, Christopher J J Chan, Alejandro Torres-Sánchez, Rashmi Priya

引用次数: 0

SLIT2 repellent is cleaved by TLL1 protease and promotes sensory axon fasciculation. SLIT2驱蚊剂被TLL1蛋白酶裂解，促进感觉轴突的束控。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-03-26 DOI: 10.1242/dev.205124

Lauren E Jones, Riley Kellermeyer, Ria Anand, Jayden Watson, Leigh Smith, Xieyi Huang, Zhuqing Wang, Wei Yan, Hua Zhang, Cynthia C Mastick, Thomas Kidd, Grant S Mastick

{"title":"SLIT2 repellent is cleaved by TLL1 protease and promotes sensory axon fasciculation.","authors":"Lauren E Jones, Riley Kellermeyer, Ria Anand, Jayden Watson, Leigh Smith, Xieyi Huang, Zhuqing Wang, Wei Yan, Hua Zhang, Cynthia C Mastick, Thomas Kidd, Grant S Mastick","doi":"10.1242/dev.205124","DOIUrl":"10.1242/dev.205124","url":null,"abstract":"SLIT2 is a secreted protein that repels axons from the CNS midline. Full-length SLIT2 (SLIT2-FL) is proteolytically cleaved into two fragments, SLIT2-N and SLIT2-C. SLIT2-FL and SLIT2-N have opposing biological effects on cultured dorsal root ganglion (DRG) axons. This study identified SLIT2 cleavage mechanisms and functional significance for DRG axon guidance. The Tolloid-related protease TLL1 cleaved SLIT2 in cultured cells, with TLL1 requiring activation by furin/prohormone convertases. We used CRISPR editing in mice to produce a Slit2ΔTLS allele lacking the TLL1 cleavage site. Slit2ΔTLS embryos retained dorsal repulsion of DRG axons, in contrast to DRG midline invasion in Slit2 knockouts. However, DRG axons in Slit2 knockouts and Slit2ΔTLS mutants showed reduced fasciculation of rootlets and longitudinal DRG projections. In vitro, SLIT2-N promoted fasciculation of DRG axons. These results suggest that proteolytic cleavage generates additional SLIT2 biological functions for organizing DRG central axon projections.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13102090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146104131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An essential role for actinotrichia in zebrafish fin patterning and courtship behavior. 放线菌在斑马鱼鳍图案和求偶行为中的重要作用。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-04-14 DOI: 10.1242/dev.204990

Paulina Hanzelova, Connor Baird, Bidemi Keshinro, Reeham Kadhom, Robert L Lalonde, Marie-Andrée Akimenko

{"title":"An essential role for actinotrichia in zebrafish fin patterning and courtship behavior.","authors":"Paulina Hanzelova, Connor Baird, Bidemi Keshinro, Reeham Kadhom, Robert L Lalonde, Marie-Andrée Akimenko","doi":"10.1242/dev.204990","DOIUrl":"10.1242/dev.204990","url":null,"abstract":"A key difference between tetrapod limb buds and teleost fin buds is the presence of rigid actinotrichia fibers that guide the migrating cells contributing to ray formation. Major structural components of actinotrichia are encoded by fish-specific actinodin (And) genes, which were lost in tetrapods. To investigate the consequences of this loss during the fin-to-limb transition, we generated deletions in zebrafish and1 and and2 using CRISPR/Cas9 mutagenesis. Double mutants (and1-/-and2-/-) lack actinotrichia. Embryos and larvae have reduced fin fold size, with disorganized cell migration. In adults, all fin fold-derived skeletal structures are disrupted, including the rays of all fins, as well as the caudal fin endoskeleton. Surprisingly, double mutant males fail to breed, despite being fertile. Video analysis revealed that defects in the fins of males impair their ability to stimulate egg release. Our findings highlight the role of actinotrichia in both fin patterning and zebrafish courtship. We propose that actinodin gene maintenance is under strong selection in fish with similar courtship. We speculate that the loss of actinodin genes and a shift in courtship strategy may have coincided during tetrapod evolution.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13120675/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Axonal defasciculation is restricted to specific branching points during regeneration of the lateral line nerve in zebrafish. 在斑马鱼侧线神经再生过程中，轴突失血仅限于特定的分支点。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-01-08 DOI: 10.1242/dev.205054

Rohan S Roy, A J Hudspeth

{"title":"Axonal defasciculation is restricted to specific branching points during regeneration of the lateral line nerve in zebrafish.","authors":"Rohan S Roy, A J Hudspeth","doi":"10.1242/dev.205054","DOIUrl":"10.1242/dev.205054","url":null,"abstract":"Peripheral nerve regeneration requires precise selection of the appropriate targets of innervation, often in an environment that differs from that during the developmental wiring of the neural circuit. Severed axons of the zebrafish posterior lateral line nerve have the capacity to reinnervate mechanosensory hair cells clustered in neuromast organs. Regeneration represents a balance between fasciculated regrowth of the axonal bundle and defasciculation of individual axons into the epidermis where neuromasts reside. The cues that guide pathfinding during regeneration of the posterior lateral line nerve are unknown. Here, we show that regenerating axons selectively defasciculate through distinct gaps in the epidermal boundary layer. We found that the gene col18a1a, which encodes the secreted heparan sulfate proteoglycan collagen XVIII, is expressed by the neuromast and by a subset of Schwann cells that are located at the points of axonal defasciculation. Furthermore, we observed aberrant axonal branching at inappropriate locations during nerve regeneration in col18a1a mutants. We propose a model in which collagen XVIII patterns the basement membrane to affect the precision of axonal navigation.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12848573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fundamental limits on symmetry breaking by Turing-like activator-inhibitor mechanisms. 类图灵激活-抑制机制对对称破缺的基本限制。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-03-20 DOI: 10.1242/dev.205067

Daniel Muzatko, Bijoy Daga, Tom W Hiscock

{"title":"Fundamental limits on symmetry breaking by Turing-like activator-inhibitor mechanisms.","authors":"Daniel Muzatko, Bijoy Daga, Tom W Hiscock","doi":"10.1242/dev.205067","DOIUrl":"10.1242/dev.205067","url":null,"abstract":"Turing's longstanding reaction-diffusion hypothesis explains how molecular patterns can self-organise de novo in otherwise homogeneous tissues. However, whilst Turing-like activator-inhibitor models can qualitatively recapitulate patterning in silico, they are often highly simplified approximations of the molecular complexity operating in vivo. Here, we investigate significantly more complex reaction-diffusion systems that seek to more directly capture the mechanisms involved in intercellular signalling. By combining large-scale simulations with formal mathematical proofs, we show, rather generally, that symmetry breaking is strongly constrained by the extracellular interactions in the system but is relatively insensitive to the intracellular dynamics assumed. When applied to the activator-inhibitor paradigm, we find a broader repertoire of self-organising circuits than previously recognised, including some which are unexpectedly robust to parameters. Beyond these examples, we have packaged our highly performant numerical methods into a freely available and easy-to-use software pipeline, ReactionDiffusion.jl, that allows arbitrarily complex reaction-diffusion systems to be simulated at scale.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CSF1R+ macrophage and osteoclast depletion impairs neural crest proliferation and craniofacial morphogenesis. CSF1R+巨噬细胞和破骨细胞耗竭损害神经嵴增殖和颅面形态发生。

IF 3.6 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-05-06 DOI: 10.1242/dev.205423

Felix Ma, Rose Ru Jing Zhou, Matthew Rosin, Iris Zhou, Sabrina Ownsworth, Rouzbeh Ostadsharif Memar, Vincent B Wong, Jessica M Rosin

{"title":"CSF1R+ macrophage and osteoclast depletion impairs neural crest proliferation and craniofacial morphogenesis.","authors":"Felix Ma, Rose Ru Jing Zhou, Matthew Rosin, Iris Zhou, Sabrina Ownsworth, Rouzbeh Ostadsharif Memar, Vincent B Wong, Jessica M Rosin","doi":"10.1242/dev.205423","DOIUrl":"10.1242/dev.205423","url":null,"abstract":"Despite a wealth of knowledge about the mechanisms underlying craniofacial morphogenesis during gestation, the roles of fetal macrophages and osteoclasts during this process remain less well characterized. Here, we used the pharmacological inhibitor PLX5622 to disrupt colony stimulating factor 1 receptor (CSF1R) signaling, which is essential for macrophage and osteoclast proliferation, differentiation and survival. Prenatal PLX5622 exposure in mouse resulted in ∼50% depletion of CSF1R+ macrophages, with complete loss of osteoclasts. While there were no notable changes in craniofacial nerve or muscle development, prenatal exposure to PLX5622 resulted in skull doming and cranial suture impairments, in addition to disruptions to development of the premaxilla, mandible, ear ossicles, palate and cranial base. In response to PLX5622 exposure, cytokine and chemokine signaling was altered and neural crest proliferation was impaired. Our data also highlight sex- and strain-specific differences in PLX5622 phenotypes and together demonstrate that CSF1R+ macrophages and osteoclasts are essential for craniofacial morphogenesis.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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