{"title":"Cell and nuclear scaling constrains tissue fluidity in a doubly-dense remodeling epithelium.","authors":"Liam J Russell, Rashmi Budhathoki, Hugh D Weber, Dinah Loerke, J Todd Blankenship","doi":"10.1242/dev.205317","DOIUrl":"https://doi.org/10.1242/dev.205317","url":null,"abstract":"<p><p>During epithelial remodeling, tissues exhibit solid- or fluid-like properties depending on developmental constraints. In soft matter systems like foams and colloidal glasses, component size influences material mechanics. Here, we investigated how cell and nuclear size affect tissue mechanics. mh mutant embryos have epithelia with doubled cell densities, creating cells with altered 3D aspect ratios. Nuclear volumes scale non-linearly with cell volumes, adopting rounder shapes and reduced apical-basal heights, suggesting that stiff nuclei deform less than cell cortices. These compacted nuclei resemble a jammed state, reducing tissue fluidity and impairing extension movements. Interestingly, oscillatory amplitudes and frequencies in mh cells are comparable to control despite their reduced size, demonstrating an uncoupling between biochemical oscillation machinery and cell dimensions. Additionally, though planar-polarized magnitudes are dampened, the angular assignment of interfacial behaviors is preserved, suggesting that this planar informational system still operates with high fidelity despite reduced cell dimensions. Thus, these results indicate that development has fine-tuned epithelial dimensions to work at time-scales compatible with embryonic requirements.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 20","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191944","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}
DevelopmentPub Date : 2026-10-15Epub Date: 2026-10-19DOI: 10.1242/dev.206180
{"title":"An interview with Neil Vargesson.","authors":"","doi":"10.1242/dev.206180","DOIUrl":"https://doi.org/10.1242/dev.206180","url":null,"abstract":"<p><p>Neil Vargesson is Professor of Developmental Biology at the University of Aberdeen, with particular expertise in angiogenesis during embryonic development and the impact of pharmaceutical drugs, such as thalidomide, that cause limb and embryonic differences. His advocacy, communication and advisory work around thalidomide embryopathy, Primodos and drug safety has supported affected patients and their families across the globe, as well as influencing government health policies worldwide. A Fellow of the Royal Society of Edinburgh since 2021, Neil is the recipient of the 2026 British Society for Developmental Biology Wolpert Medal, which is awarded in honour of the late Lewis Wolpert for extraordinary contributions to the communication and teaching of developmental biology in the UK. Published to coincide with Lewis's birthday on 19 October, the following interview is a conversation with Neil about what the Wolpert Medal means to him as Lewis's last PhD student, his ethos and advice for doing science communication, as well as his outlook on the future of drug safety.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 20","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220098","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}
DevelopmentPub Date : 2026-10-15DOI: 10.1242/dev.205573
Cecilia E Pellegrini, Peter W Reddien
{"title":"Planarian progenitor responses to injury are not specific to missing tissue identity.","authors":"Cecilia E Pellegrini, Peter W Reddien","doi":"10.1242/dev.205573","DOIUrl":"10.1242/dev.205573","url":null,"abstract":"<p><p>Regeneration is the process by which organisms replace lost body parts. How cell-type production is tailored to match missing-tissue identity is a central problem of regeneration. Here, we have investigated the specificity of planarian stem-cell responses to the identity of missing tissues following injury. Proximal injury not affecting the mature tissue nonetheless drives increased cell incorporation into brain neurons, ventral nerve cords, and pharynx muscle and neurons. Following direct injury, there is spatially imprecise amplification of cell incorporation into peripheral neurons relative to the wound, and decreased cell incorporation into body-wall muscle distally in favor of increased incorporation at the wound. By contrast, essentially no stem-cell division contributes to initial epidermal regeneration, instead post-mitotic progenitors supply the wound. Amplification of epidermal incorporation following injury does occur weeks after injury, including to uninjured regions. These results indicate that missing-tissue identity is not a requisite component for there to be a stem-cell response to injury that amplifies production. We suggest that planarian regeneration specificity involves, in large part, a combination of ongoing cell turnover, wound-associated increased stem cell division and spatially broad neoblast specification zones.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073939","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}
DevelopmentPub Date : 2026-10-15DOI: 10.1242/dev.206148
{"title":"The people behind the papers - Cecilia Pellegrini and Peter Reddien.","authors":"","doi":"10.1242/dev.206148","DOIUrl":"https://doi.org/10.1242/dev.206148","url":null,"abstract":"<p><p>Whilst many animals can regenerate lost or damaged tissues following injury, the mechanisms that allow them to identify which specific cell type needs to be regenerated remains unclear. To address this, Cecilia Pellegrini and Peter Reddien map out the response mechanisms to a multitude of different injuries in the planarian flatworm, demonstrating that a general 'bystander' response in areas near injury sites might be sufficient for robust regeneration without the need for precise identification of missing tissues. To learn more about this paper and the people behind it, we spoke to first author Cecilia Pellegrini and corresponding author Peter Reddien, Professor of Biology at the Massachusetts Institute of Technology, USA.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 20","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191906","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}
DevelopmentPub Date : 2026-10-15Epub Date: 2026-10-14DOI: 10.1242/dev.206147
Jake Cornwall-Scoones
{"title":"In preprints - pushing the limits of morphogen scaling in limb regeneration.","authors":"Jake Cornwall-Scoones","doi":"10.1242/dev.206147","DOIUrl":"https://doi.org/10.1242/dev.206147","url":null,"abstract":"<p><p>This article discusses the preprinted work of Tardivo et al. (2026, preprint). As a preprint, this work has not yet undergone peer review.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 20","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180103","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}
DevelopmentPub Date : 2026-10-15Epub Date: 2026-10-16DOI: 10.1242/dev.206057
Ece Atayeter, Jason Ho, Talon G Blottin, Ilyena B Joe, Ron Sistrunk, Bo Zhang, Lilianna Solnica-Krezel, Andreas Gerstlauer, John B Wallingford, Ryan S Gray
{"title":"CiliaIO: machine learning reveals spatial patterns of cilia beating dynamics in the zebrafish spinal cord.","authors":"Ece Atayeter, Jason Ho, Talon G Blottin, Ilyena B Joe, Ron Sistrunk, Bo Zhang, Lilianna Solnica-Krezel, Andreas Gerstlauer, John B Wallingford, Ryan S Gray","doi":"10.1242/dev.206057","DOIUrl":"10.1242/dev.206057","url":null,"abstract":"<p><p>Motile cilia generate fluid flows that are essential for normal development and physiology. Cilia display diverse beating waveforms, and while pronounced defects are strongly associated with motile ciliopathies, subtler alterations also influence disease manifestations. Finer quantification of ciliary dynamics is therefore crucial for understanding ciliopathies, but the heterogeneity of cilia beating makes accurate and robust characterization challenging. Here, we present CiliaIO, a machine learning-based tool for quantification of motile cilia morphodynamics. Using this platform, we discovered subtle but highly significant regional differences in ciliary waveforms in the zebrafish spinal cord. To demonstrate the efficacy of the tool, we used CiliaIO to capture and quantify subtle ciliary defects in a previously unreported bbs2 allele that causes a late-onset scoliosis phenotype. These results provide a workflow for additional fine-scale analyses of ciliary morphodynamics that will be important for understanding motile ciliopathy.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988582","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}
DevelopmentPub Date : 2026-10-15Epub Date: 2026-10-12DOI: 10.1242/dev.206127
Ishika Jain, Vani Dembla, Sumeet Pal Singh
{"title":"In preprints - emerging role of circadian rhythms in refractive development and early-life immune regulation.","authors":"Ishika Jain, Vani Dembla, Sumeet Pal Singh","doi":"10.1242/dev.206127","DOIUrl":"https://doi.org/10.1242/dev.206127","url":null,"abstract":"<p><p>This article discusses the preprinted work of Palumaa and colleagues (2026 preprint) as well as that of Li and team (2026 preprint). As preprints, these works have not yet undergone peer review.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":"153 20","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165405","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}
DevelopmentPub Date : 2026-10-15Epub Date: 2026-10-19DOI: 10.1242/dev.205737
Jinghong J Tang 唐璟鸿, Alicia Shipley, Roger P White, Elijah Ferreira, Somes Schwinghammer, Michael A Welte
{"title":"Drosophila Heat shock factor (HSF) regulates developmental growth by maintaining the basal expression of HSP83/HSP90.","authors":"Jinghong J Tang 唐璟鸿, Alicia Shipley, Roger P White, Elijah Ferreira, Somes Schwinghammer, Michael A Welte","doi":"10.1242/dev.205737","DOIUrl":"10.1242/dev.205737","url":null,"abstract":"<p><p>The heat shock transcription factor HSF1 is best known as a master regulator of the proteotoxic stress response, yet its functions remain incompletely understood. In Drosophila melanogaster, Heat shock factor (HSF) is essential for viability, but the mechanisms by which it promotes development are unclear. Here, we show that Hsf null larvae arrest at the early 2nd instar stage and exhibit a significant reduction in basal HSP83 levels. Tissue-specific knockdown of Hsf revealed widespread, organ-specific requirements, including defects in endoreplication and cell growth in prothoracic and salivary glands, adult wing defects following imaginal disc perturbation, follicle degeneration in the ovary, and melanotic tumors upon simultaneous hemocyte and fat body depletion. In these tissues, HSF loss typically reduced HSP83 levels, and restoring HSP83 expression partially or fully rescued these defects. These findings identify HSP83 as a crucial downstream effector of HSF and demonstrate that HSF promotes development largely by maintaining basal chaperone expression. Together, our results establish HSF as a key regulator of developmental progression and highlight a central role for proteostasis in supporting tissue growth under non-stress conditions.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024007","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}
DevelopmentPub Date : 2026-10-14DOI: 10.1242/dev.205775
Antigoni Gogolou, Nikolas Stefanidis, Fay Cooper, Guillaume Blin, Stanley E Strawbridge, Alexander G Fletcher, Anestis Tsakiridis
{"title":"Notch signalling governs human enteric nervous system progenitor dynamics.","authors":"Antigoni Gogolou, Nikolas Stefanidis, Fay Cooper, Guillaume Blin, Stanley E Strawbridge, Alexander G Fletcher, Anestis Tsakiridis","doi":"10.1242/dev.205775","DOIUrl":"https://doi.org/10.1242/dev.205775","url":null,"abstract":"<p><p>The enteric nervous system (ENS) is the main branch of the peripheral nervous system that innervates the gastrointestinal tract controlling vital functions. It arises during embryogenesis via migration, proliferation and differentiation of neural crest-derived ENS progenitors. Perturbation of these processes, caused by mutations in key signalling pathway components and transcription factors, prevents progenitor colonisation of the distal gut causing aganglionic phenotypes and enteric neuropathies such as Hirschsprung (HSCR) disease. While animal models implicate Notch signalling in ENS specification, its role in human ENS progenitor cell fate decisions remains unclear. Here, we employ a human pluripotent stem cell-based model to show that Notch signalling is a key regulator of human ENS progenitor dynamics. Quantitative modelling of our in vitro data indicates that Notch inhibition accelerates progenitor differentiation without substantially altering neuronal versus glial lineage bias. Furthermore, we establish that Notch signalling controls human ENS progenitor migration by influencing migration velocity and directionality. Together, these findings provide mechanistic insights into how Notch signalling disruption may contribute to the pathogenesis of human intestinal aganglionosis.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180067","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}
DevelopmentPub Date : 2026-10-14DOI: 10.1242/dev.205635
Farina Aziz, Kiera Savage, Jaehwan Kim, Jason G Knott, Bin Gu, Michael A Halbisen, Amy Ralston
{"title":"SOX21 and SOX2 collaboratively promote blastocyst formation downstream of TFAP2C.","authors":"Farina Aziz, Kiera Savage, Jaehwan Kim, Jason G Knott, Bin Gu, Michael A Halbisen, Amy Ralston","doi":"10.1242/dev.205635","DOIUrl":"https://doi.org/10.1242/dev.205635","url":null,"abstract":"<p><p>In mammals, the first cell fate decisions segregate pluripotent fetal cells from the differentiating extraembryonic lineages. In mouse, pluripotent progenitors can be identified as early as the 16-cell (morula) stage, based on their restricted expression of SOX2. In spite of the unique SOX2 expression pattern, however, the first cell fate decision proceeds normally in the absence of Sox2, suggesting an undiscovered compensatory mechanism. We discovered that the closely related Sox paralogue SOX21 is expressed alongside, and independently of Sox2 prior to blastocyst formation. Embryos lacking both Sox2 and Sox21 exhibit a phenotype more severe than those lacking either gene alone, arresting during the morula-to-blastocyst transition. In fact, embryos lacking any three copies of Sox2 or Sox21 frequently phenocopy double knockouts, consistent with a dose-dependent genetic interaction. Finally, we discovered the mechanism promoting parallel expression of Sox2 and Sox21. We show that, like Sox2, expression of Sox21 depends on TFAP2C, and not NANOG or OCT4, clarifying gene regulatory mechanisms preceding blastocyst formation. Overall, our study reveals a novel Sox-dependent pathway regulating embryonic processes even earlier than previously appreciated.</p>","PeriodicalId":11375,"journal":{"name":"Development","volume":" ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180042","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}