Development最新文献_第10页

A developmental biologist's guide to mechanics. 发育生物学家的力学指南。

IF 4 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-08-26 DOI: 10.1242/dev.205785

Jialing Cao, Alessandro Chiappori, Sylvain Landiech, Raphaël Clément, Pierre-François Lenne

{"title":"A developmental biologist's guide to mechanics.","authors":"Jialing Cao, Alessandro Chiappori, Sylvain Landiech, Raphaël Clément, Pierre-François Lenne","doi":"10.1242/dev.205785","DOIUrl":"https://doi.org/10.1242/dev.205785","url":null,"abstract":"Developmental biology seeks to explain how living systems self-organize into functional, robust forms. While molecular and genetic approaches have revealed how biological information is encoded and processed, they often do not explain how this information is translated into physical shape. Here, we introduce the mechanical principles underlying tissue morphogenesis, aimed at developmental biologists with little background in physics. This Primer is structured around three core pillars. First, force generation describes how active and passive processes within cells and tissues drive deformation and motion. Second, constitutive behavior defines how living matter responds to these forces, spanning elastic, viscous and plastic regimes. Third, geometry and boundary constraints set the spatial constraints that shape mechanical interactions at the tissue and organismal levels. Together, these elements provide a framework for understanding how form emerges from the interplay between forces, material properties and geometry. We illustrate key examples across developmental processes and highlight recent advances and future challenges, integrating mechanical and molecular perspectives to guide the study of morphogenesis.","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 16","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817881","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 4 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":"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":4.0,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13200730/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TiFM2.0 - versatile mechanical measurement and actuation in live embryos. TiFM2.0 -活胚胎的多功能机械测量和驱动。

IF 4 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":4.0,"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

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 4 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":4.0,"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

Brassinosteroid controls leaf air space patterning non-cell autonomously by promoting epidermal growth. 油菜素内酯通过促进表皮生长来自主控制叶片空气空间模式。

IF 4 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-05-19 DOI: 10.1242/dev.205110

James M Fitzsimons, Ana B Rock, Richard L De Falbe, Samantha Fox, Chris D Whitewoods

{"title":"Brassinosteroid controls leaf air space patterning non-cell autonomously by promoting epidermal growth.","authors":"James M Fitzsimons, Ana B Rock, Richard L De Falbe, Samantha Fox, Chris D Whitewoods","doi":"10.1242/dev.205110","DOIUrl":"10.1242/dev.205110","url":null,"abstract":"Plant leaves contain a complex network of intercellular air spaces, which allow efficient photosynthesis. However, how leaf air spaces are patterned is poorly understood. It has been proposed for almost a century that air spaces form by faster-growing epidermal tissue pulling slower growing mesophyll cells apart, but this has never been tested. Here, we characterise air space morphogenesis throughout in the first leaf of Arabidopsis thaliana and show that the plant hormone brassinosteroid is required for air space expansion in the palisade, but not in the spongy mesophyll. We also show that epidermal brassinosteroid perception is sufficient to promote air space expansion in the palisade non-cell autonomously and propose that this non-cell-autonomous effect is due to altered epidermal growth. To test whether epidermal growth affects air space patterning we reduce growth specifically in the epidermis using inducible expression of the growth repressor BIG BROTHER and show that an epidermal growth restriction reduces air space expansion in the palisade mesophyll. Overall, we propose that brassinosteroid signalling promotes growth in the epidermis to pattern air spaces in the palisade mesophyll.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765821","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 4 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

An(other) interview with Rashmi Priya. 对拉什米·普丽娅的另一次采访。

IF 4 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-08-20 DOI: 10.1242/dev.206001

引用次数: 0

The tectum transversum maintains patency of the developing coronal suture. 顶盖横突维持冠状缝的通畅。

IF 4 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-06-17 DOI: 10.1242/dev.205347

Meenakshi Umar, Garrett Bartoletti, Dimitri Sokolowskei, Nathan Janser, Robert J Tower, Fenglei He

{"title":"The tectum transversum maintains patency of the developing coronal suture.","authors":"Meenakshi Umar, Garrett Bartoletti, Dimitri Sokolowskei, Nathan Janser, Robert J Tower, Fenglei He","doi":"10.1242/dev.205347","DOIUrl":"10.1242/dev.205347","url":null,"abstract":"Craniosynostosis, the premature fusion of calvarial bones, is a common congenital defect often attributed to the loss of fibrous sutures or excessive ossification. Recent studies have reported aberrant cartilage formation near affected sutures, suggesting a previously unrecognized role for cartilage in suture morphogenesis and maintenance. The tectum transversum (TTR), a transient cartilage adjacent to the coronal suture, has been considered absent in humans. By analyzing published human embryonic datasets, we demonstrate that the TTR is in fact a conserved structure in humans. We further investigated the developmental dynamics and function of the TTR in mice. Spatial transcriptomic analyses reveal that the TTR mediates critical tissue-tissue interactions and may serve as a physical and molecular barrier restricting BMP signaling activation within the coronal suture, potentially modulated by the underlying dura mater. These findings identify the TTR as a conserved regulator of coronal suture morphogenesis and provide new mechanistic insight into the etiology of coronal craniosynostosis.","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 16","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13523350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263890","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

The developing tendon and enthesis are hypoxic and rely on hypoxia-inducible factor 1a during postnatal development. 在出生后的发育过程中，发育中的肌腱和束骨是缺氧的，依赖于缺氧诱导因子1a。

IF 4 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-06-22 DOI: 10.1242/dev.205458

Stephanie S Steltzer, Nicole Migotsky, Tessa Phillips, Syeda N Lamia, Bachir A Abeid, Kiwon Lee, Seung-Ho Bae, Connor Leek, Sydney Grossman, Moaid Shaik, Allison Risha, Kaitlyn Frey, Claudia Loebel, Jun Hee Lee, Yatrik M Shah, Adam C Abraham, Megan L Killian

{"title":"The developing tendon and enthesis are hypoxic and rely on hypoxia-inducible factor 1a during postnatal development.","authors":"Stephanie S Steltzer, Nicole Migotsky, Tessa Phillips, Syeda N Lamia, Bachir A Abeid, Kiwon Lee, Seung-Ho Bae, Connor Leek, Sydney Grossman, Moaid Shaik, Allison Risha, Kaitlyn Frey, Claudia Loebel, Jun Hee Lee, Yatrik M Shah, Adam C Abraham, Megan L Killian","doi":"10.1242/dev.205458","DOIUrl":"10.1242/dev.205458","url":null,"abstract":"The enthesis is a specialized tissue crucial for transmission of muscle force from tendon to bone, yet its postnatal development is not fully understood. In this study, we investigated if and how hypoxia inducible factor 1 alpha (HIF-1α) regulates enthesis cell adaptation, e.g. cell survival and extracellular matrix (ECM) deposition. We investigated the spatial and temporal dynamics of hypoxia in the murine Achilles tendon enthesis and found that, whereas neonatal tendons rapidly resolve hypoxia after birth, the enthesis maintains a hypoxic niche until postnatal day 5, mirroring a hypoxic gradient observed in growth plates. Genetic disruption of Hif1a in mouse tendon/enthesis-resident cells (cKO) resulted in pronounced deficits in grip strength, abnormal tendon-bone attachment morphology, disrupted calcaneal architecture, impaired mineralization and significant ECM disorganization. We found persistent cell death and loss of collagen organization in cKO entheses. In vitro, Hif1a-deficient tendon fibroblasts exhibited blunted transcriptional responses to hypoxia, altered metabolic gene expression and disrupted ECM deposition. Collectively, our findings illuminate hypoxia as a sustained niche in the postnatal enthesis, with HIF-1α required for cell survival, ECM organization and structural integrity of entheses.","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 16","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13354958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293714","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

Combined HS6ST1 and HS6ST2 loss disrupts the formation and migration of gonadotropin-releasing hormone neurons. HS6ST1和HS6ST2的联合缺失会破坏促性腺激素释放激素神经元的形成和迁移。

IF 4 2区生物学

Development Pub Date : 2026-08-15 Epub Date: 2026-07-31 DOI: 10.1242/dev.204788

Roberto Oleari, Federica Amoruso, Antonella Lettieri, Elena Ioannou, Alyssa J J Paganoni, Jessica Gimmelli, Sara Campinoti, Stefano Manzini, Christiana Ruhrberg, Anna Cariboni

{"title":"Combined HS6ST1 and HS6ST2 loss disrupts the formation and migration of gonadotropin-releasing hormone neurons.","authors":"Roberto Oleari, Federica Amoruso, Antonella Lettieri, Elena Ioannou, Alyssa J J Paganoni, Jessica Gimmelli, Sara Campinoti, Stefano Manzini, Christiana Ruhrberg, Anna Cariboni","doi":"10.1242/dev.204788","DOIUrl":"10.1242/dev.204788","url":null,"abstract":"6-O sulfotransferase (HS6ST) enzymes modify heparan sulphate proteoglycans (HSPGs) to promote growth factor binding to extracellular matrix or receptors. HS6ST1 variants are reported in individuals with GnRH deficiency (GD), which is caused by the defective development of gonadotropin releasing hormone (GnRH) neurons. However, it is unknown whether and how HS6ST family members cooperate in GnRH neuron development. Here, we show that Hs6st1 and Hs6st2 are co-expressed in the mouse nasal neurogenic epithelia, where GnRH neurons and their migratory substrate, the terminal nerve, originate. The combined but not individual disruption of Hs6st1 and Hs6st2 disrupted vomeronasal organ formation with incomplete penetrance, and impaired brain entry of GnRH neurons, similar to observations in mice with loss of the morphogen FGF8 or the axon guidance cue SEMA3A, respectively. In agreement with a role for HS6ST-modified HSPG in regulating SEMA3A signalling, SEMA3A binding to nasal tissues was impaired in the absence of HS6ST1 and HS6ST2. Our results establish a mechanistic role for HS6ST1 in GD and suggest HS6ST2 as an additional susceptibility locus for GD.","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13480955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148327671","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