<?xml version="1.0" encoding="utf-8"?>
    <rss version="2.0">
      <channel xmlns:content="http://purl.org/rss/1.0/modules/content/">
        <title>Frontiers in Cell and Developmental Biology | Morphogenesis and Patterning section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/cell-and-developmental-biology/sections/morphogenesis-and-patterning</link>
        <description>RSS Feed for Morphogenesis and Patterning section in the Frontiers in Cell and Developmental Biology journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-13T21:06:42.298+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1807574</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1807574</link>
        <title><![CDATA[Reorganization of E-cadherin into apical spot junctions mediates interlineage adhesion between epithelial and germline cells]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Vanessa Weichselberger</author><author>Ramya Balaji</author><author>Marta Rodriguez-Franco</author><author>Anne-Kathrin Classen</author>
        <description><![CDATA[During development, epithelia must coordinate morphogenesis with neighboring cell lineages to drive structural remodeling of organ systems. How adhesion between epithelial and other cell types is established and maintained remains poorly understood. Using the Drosophila ovary as an in vivo model, we show that anterior follicle cells (AFCs) undergo epithelial plasticity to establish and maintain adhesion with germline nurse cells during late oogenesis. As AFCs spread over the nurse-cell compartment, adherens junctions disassemble, and E-cadherin, together with junctional partners, reorganizes into apical “spot junctions.” Formation of these junctions requires E-cadherin in both follicle and germline cells and is promoted by the expansion of the AFC apical surface. Quantitative imaging reveals that spot junctions form a uniformly spaced lattice that remains stable as the AFC-nurse cell interface enlarges. Functionally, these E-cadherin-based junctions are essential to maintain soma–germline adhesion, enabling full envelopment and clearance of nurse cell remnants by AFCs during late oogenesis. Our findings uncover a mechanism by which an epithelium repurposes its apical membrane into a specialized adhesive surface, providing a paradigm for the emergence of interlineage adhesion in developing tissues.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1829891</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1829891</link>
        <title><![CDATA[LRP1 in atherosclerosis: a hierarchical view of regulatory mechanisms and epigenetic knowledge gaps]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Rocio Casale</author><author>Gustavo A. Chiabrando</author><author>Danilo G. Ceschin</author>
        <description><![CDATA[Inflammation is a central driver of vascular dysfunction and plays a pivotal role in the initiation and progression of atherosclerosis. This chronic inflammatory condition arises from complex molecular, cellular, and epigenetic interactions within vascular and immune networks. Monocytes and macrophages act as key mediators of plaque development, integrating lipid handling and inflammatory signaling. Low-density lipoprotein receptor-related protein 1 (LRP1) has emerged as a multifunctional receptor at the interface between lipid metabolism and immune regulation, modulating Toll-like receptor pathways and inflammatory responses in a context-dependent manner. Here, we review current evidence on the regulatory mechanisms controlling LRP1 expression and propose a hierarchical framework in which transcription factor-mediated and non-coding RNA-mediated mechanisms represent the most strongly supported layers of regulation. In contrast, although epigenetic processes broadly influence vascular inflammation, direct chromatin-level interrogation of the LRP1 locus remains limited. Together, this framework highlights key knowledge gaps and provides a conceptual basis for understanding how multi-layered regulation of LRP1 contributes to vascular inflammation and plaque progression.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1806426</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1806426</link>
        <title><![CDATA[Integrated analysis of cell-in-cell related genes and immune microenvironment in heart failure]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Linna Zhao</author><author>Yuepeng Zhou</author><author>Jiahuan Sun</author><author>Shupeng Liu</author><author>Weizhe Liu</author><author>Aiying Li</author>
        <description><![CDATA[BackgroundHeart failure (HF) is a major global public health challenge, and its pathogenesis involves the regulation of a complex immune microenvironment (IME). Cell-in-cell (CIC), as a non-classical form of cell-cell interaction, has been extensively studied in fields like oncology, but its role in HF remains unclear. This study aimed to systematically analyze the expression patterns and functions of CIC-related genes (CRGs) within the HF immune microenvironment.MethodsBased on transcriptomic data from public databases, CIC-related differentially expressed genes (DEGs) between HF and healthy samples were identified. Three machine learning algorithms—Random Forest, LASSO, and SVM-RFE—were employed to screen diagnostic markers and construct a nomogram model. Consensus clustering analysis was used to stratify HF patients into distinct subtypes based on CRG expression, and their immune infiltration characteristics were compared. Single-cell transcriptomic data were utilized to validate the cellular localization of key genes within the HF microenvironment. Experimental validation of key CRGs was performed using a transverse aortic constriction (TAC)-induced HF rat model.ResultsA total of 21 CIC-related DEGs were identified. A diagnostic model comprising 10 core genes demonstrated high predictive performance in both the training and validation sets. Based on CRG expression, HF patients were classified into two subtypes: Subtype A was enriched with regulatory T cells and M2 macrophages, exhibiting an immunosuppressive and fibrotic phenotype; Subtype B was dominated by cytotoxic T cells and NK cell infiltration, displaying an immune-activated phenotype. Single-cell analysis revealed high expression of CTSK in fibroblasts and enrichment of GZMB in T/NK cells. Animal experiments confirmed the upregulation of LPAR2 and GZMB and the downregulation of IL-10 in the TAC model.ConclusionCIC-related genes possess significant diagnostic value in HF and can distinguish HF subtypes with distinct immune microenvironment features. CRGs may participate in HF progression by regulating immune cell infiltration and fibrotic processes, providing a new perspective for understanding HF heterogeneity and developing targeted immunotherapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1762737</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1762737</link>
        <title><![CDATA[Novel mouse line with D277N mutation in the Plau gene displays autism spectrum disorder-like traits]]></title>
        <pubdate>2026-05-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Maxim Karagyaur</author><author>Olga Averina</author><author>Kirill Bozov</author><author>Stalik Dzhauari</author><author>Anastasia Priymak</author><author>Raushana Khaybullina</author><author>Oleg Permyakov</author><author>Vladimir Popov</author><author>Olga Grigorieva</author><author>Maria Illarionova</author><author>Liliia Shkarina</author><author>Mikhail Gulyaev</author><author>Dmitry Lebedev</author><author>Alexandra Primak</author><author>Petr Sergiev</author><author>Ekaterina Semina</author><author>Polina Klimovich</author><author>Larisa Samokhodskaya</author><author>Pavel Malkov</author><author>Yury Pirogov</author><author>Boris Tsygankov</author><author>Yuliya Chaika</author><author>Vsevolod Tkachuk</author><author>Elena Neyfeld</author>
        <description><![CDATA[IntroductionGenetic technologies provide an opportunity to study the molecular basis of a wide range of hereditary pathologies, including mental disorders. Reproducing of potentially pathogenic genomic variants in cellular and animal models allows establishing their functional significance and possible mechanisms of involvement in the pathogenesis of certain disorders.MethodsIn this study, a genetic variant of urokinase type plasminogen activator (uPA, gene Plau) was modeled in mice using CRISPR/Cas genome editing tool, enabling a better understanding of the role of this molecule and its associated pathways in brain development. The protease uPA plays an important role in the directed migration of neural progenitors, glial, endothelial and immune cells, it participates in axon guidance and maturation of synaptic connections, activation of growth factors and degradation of the extracellular matrix. To study the contribution of the catalytic function of uPA to brain development, we have created for the first time a mouse line carrying the D277N (rs1243306395) mutation. We assessed social activity, anxiety, memory, problem-solving ability and stress resistance of these mice, as well as histological features of their brains.ResultsTimely and correct functioning of the Plau gene ensures adequate positioning of crucial cellular components in the developing nervous system. According to bioinformatic calculations, the D277N (corresponds to the human single nucleotide variant rs1243306395) substitution that happens due to C-to-T mutation in the murine Plau gene may impair the catalytic activity of the uPA protein. While retaining their ability to find solutions in the escape test, this mouse line is characterized by high levels of anxiety, impaired social behavior, slowed learning dynamics (spatial memory), and impaired adaptation to stressors. This behavioral pattern can potentially be interpreted as autism spectrum disorder Histological analysis of the brain and cerebral cortex in Plau-D277N mice revealed brain volume enlargement and cortical thickening of approximately 10-15% compared to wild-type mice.DiscussionIn this study, we draw attention for the first time to the genomic variant rs1243306395 in the Plau gene as a potential cause of autism spectrum disorder and propose the genetically modified Plau-D277N mouse line as a model object for studying the pathogenesis of this disorder. These models can also be used for the development and testing of promising therapeutic approaches and pharmacological agents.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1786373</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1786373</link>
        <title><![CDATA[Transcriptomic profiling and RANKL/RANK/OPG-mediated osteoclastogenesis in zebrafish larvae under simulated microgravity conditions]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Juan D. Carvajal-Agudelo</author><author>Tamara A. Franz-Odendaal</author>
        <description><![CDATA[IntroductionMicrogravity is one type of external stimulus that affects bone homeostasis and bone development. This study investigates the molecular drivers of these effects in order to more fully understand the cellular communication network between bone cells when bone homeostasis is perturbed.MethodsThe transcriptional responses of bone-related genes in zebrafish larvae (Danio rerio) when exposed to simulated microgravity (SMG) using a Random Positioning Machine were analysed. Larvae were initially analyzed at 6, 12, 18, and 24 h post-exposure via RT-qPCR with a focus on the RANKL/RANK/OPG pathway.ResultsShort exposures (6–12 h) produced minimal changes, whereas 18–24 h SMG triggered a two-phase response: initial suppression of osteoblast markers (bglap, sp7, alpl, collagens) followed by activation of osteoclast-associated genes (tnfsf11/RANKL, tnfrsf11b/OPG, tnfrsf11a/RANK, nfatc1, ctsk) and stress-adaptive pathways (hsp family). We then conducted a transcriptomic analysis at 18 and 24 h. Transcriptomic and gene–protein interaction network analyses revealed distinct regulatory clusters encompassing extracellular matrix and osteoclast signaling genes, highlighting the coordinated modulation of bone formation and resorption. Functional enrichment analyses confirmed the involvement of WNT, BMP, HIPPO, and MAPK signaling pathways in skeletal regulation under SMG, and activated stress-adaptive pathways while concurrently downregulating apoptosis-related genes reflecting a complex interplay among developmental, metabolic, and disease-associated bone processes.DiscussionThis data highlights a developmental stage-specific protective response. Collectively, these results demonstrate that SMG disrupts the balance between osteoblast and osteoclast activity, promoting bone resorption via the RANKL/RANK/OPG pathway while suppressing matrix deposition. These findings lay the groundwork for designing targeted interventions to mitigate bone loss during spaceflight and in osteoporotic conditions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1845465</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1845465</link>
        <title><![CDATA[Correction: Lmx1a is essential for marginal cell differentiation and stria vascularis formation]]></title>
        <pubdate>2026-04-24T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Justine M. Renauld</author><author>Igor Y. Iskusnykh</author><author>Ebenezer N. Yamoah</author><author>Richard J. H. Smith</author><author>Corentin Affortit</author><author>David Z. He</author><author>Huizhan Liu</author><author>David Nichols</author><author>Judith Bouma</author><author>Mahesh K. Nayak</author><author>Xin Weng</author><author>Tianli Qin</author><author>Mai Har Sham</author><author>Victor V. Chizhikov</author><author>Bernd Fritzsch</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1812941</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1812941</link>
        <title><![CDATA[In vivo CRISPR-mediated activation of cardiogenic genes to reprogram cardiac fibroblasts]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Suchandrima Dutta</author><author>Sophie Chen</author><author>Waqas Ahmad</author><author>Wei Huang</author><author>Yigang Wang</author><author>Jialiang Liang</author>
        <description><![CDATA[BackgroundWe previously demonstrated that fibroblasts can be reprogrammed through a proliferative progenitor stage to drive both cardiomyogenesis and neovascularization. However, it remains to be determined whether cardiac fibroblasts (CFs), the primary mediators of post-injury remodeling, retain the plasticity to be concurrently redirected into cardiovascular lineages within the in vivo environment.MethodsThis study aimed to activate endogenous cardiogenic genes (Gata4, Nkx2.5, Tbx5, Isl1, and Smarcd3, referred to as GNTIS) in CFs using a CRISPR activation (CRISPRa) system. CFs isolated from fibroblast-specific transgenic dCas9 mice were used to validate cardiogenic gene activation mediated by single-guide RNAs and VP64 activators delivered via adeno-associated viral vectors (AAVs). The reprogramming potential of CFs into cardiovascular lineages was further evaluated in dCas9 mice subjected to myocardial infarction followed by administration of pooled AAVs.ResultsIndividual GNTIS sgRNAs effectively upregulated their respective targets in the transfected CFs. The pooled sgRNAGNTIS induced cardiac-like phenotypes in the CFs, as demonstrated by the Nkx2.5 cardiac progenitor reporter and increased cardiac differentiation markers. Subsequently, AAV-sgRNAGNTIS was assessed in vivo in dCas9 mice following myocardial infarction. While global cardiac function did not reach statistical significance, GNTIS activation improved key hemodynamic parameters, effectively preserving cardiac performance compared to controls. Immunostaining further revealed that GNTIS-activated CFs exhibited the potential for transdifferentiation into cardiomyocyte-like or vascular smooth muscle cell-like lineages within the infarcted heart, which was not observed in the control group.ConclusionThis CRISPRa transgenic model provides a foundational proof of concept for in vivo reprogramming of CFs into cardiovascular cells.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1775639</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1775639</link>
        <title><![CDATA[Regulating glial morphogenesis: insights from Drosophila]]></title>
        <pubdate>2026-03-26T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Vrushali Katagade</author><author>Anuradha Ratnaparkhi</author>
        <description><![CDATA[Glia are critical cellular components of the nervous system. Their morphogenesis during development is an important process that ensures formation of a functional nervous system in the adult organism. Drosophila melanogaster has been used extensively as a model to study the cellular and molecular mechanisms underlying glial development primarily because of the presence of different types of glia that are functionally analogous those found in vertebrates. In this review, we summarize and discuss signalling pathways that drive glial morphogenesis in Drosophila with a focus on those that regulate shape during development. We systematically discuss the different types of glia, their origin, function and signalling mechanisms that operate to regulate the ‘form-function’ relationship across development. We conclude by drawing attention to questions that need to be addressed, and the signalling pathways that need to be explored in this context which has implications to both, development and disease.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1751258</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1751258</link>
        <title><![CDATA[Metabolic profiling of a polycystic ovary syndrome-like organoid model reveals the critical role of glutamine in local endometrial dysregulation related to implantation failure]]></title>
        <pubdate>2026-03-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Haoxuan Yang</author><author>Jing Zhang</author><author>Su Long</author><author>Yuhuan Xue</author><author>Jinfeng Tan</author><author>Ge Chen</author><author>Yongqi Luo</author><author>Ricardo Azziz</author><author>Chichiu Wang</author><author>Wenming Xu</author><author>Xiaomiao Zhao</author>
        <description><![CDATA[Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder characterized by reproductive and metabolic disturbances, which causes a chronic lack of ovulation that leads to increased incidence of atypical endometrial hyperplasia and carcinogenesis. Increasing evidence indicates that metabolic changes may play a crucial role in PCOS pathogenesis; however, the metabolic profile of fluid in PCOS-related endometrium has not yet been characterized. In this study, we successfully constructed three cases of endometrial organoids derived from clinically healthy endometrium. We established a high-androgen model by adding different ratios of estradiol and testosterone to simulate PCOS-like characteristics. Through scanning electron microscopy and immunofluorescence detection, we found that extra androgen treatment-induced cellular damage led to cellular fragments and apoptosis. The intra-organoid fluid (IOF) and extra-organoid fluid (EOF) of the organoids were separated and analyzed by high-throughput quantitative metabolomics. The results showed that amino acid metabolism, specifically glutamine metabolic changes, was the major metabolic pathway altered in the EOF; meanwhile, changes in fatty acids were the main metabolites in the IOF among the groups. Specifically, the in vitro model confirmed that glutamine enhances endometrial stromal cell decidualization with altered mitochondrial function during the implantation process, which may provide the basis for metabolic marker screening and for identifying potential metabolic targets for intervention in female infertility related to PCOS.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1740081</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1740081</link>
        <title><![CDATA[Persistent Wnt/β-catenin signaling disables soft palatogenesis and palatal osteogenesis by inducing mesenchymal condensation]]></title>
        <pubdate>2026-03-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Biying Wang</author><author>Junyuan Xue</author><author>Yufan Bian</author><author>Jiamin Deng</author><author>Bo Liu</author><author>Nan Li</author><author>Lei Zhu</author><author>Jing Xiao</author><author>Chao Liu</author><author>Han Liu</author>
        <description><![CDATA[IntroductionMammalian palates are composed of the anterior hard palate and the posterior soft palate. However, the correlation of the genesis, pattern formation, and morphogenesis between the hard and soft palates remains elusive.MethodsIn this study, we explicated the complicated palatal defects in Osr2-creKI;Ctnnb1ex3f mice, in which canonical Wnt activity was persistent due to constitutively active β-catenin in the palatal mesenchyme. Osr2-creKI;Ctnnb1ex3f palates displayed an ectopic mesenchymal condensation extending from the proximal–posterior area to the distal–anterior area, along with impaired osteogenesis and agenesis of soft palate.ResultsImmunohistochemistry showed the overlapping active canonical Wnt domain with the ectopic mesenchymal condensation, indicating that the condensation was induced by persistent canonical Wnt signaling. Wnt5a, a chemokine that induces posterior–anterior migration of palatal mesenchymal cells, was activated in the anterior and middle palatal mesenchyme of Osr2-creKI;Ctnnb1ex3f mice. Exogenous supplementation of Wnt5a into wild-type (WT) palates recapitulated the mesenchymal condensation. These findings indicate that the persistent canonical Wnt signaling in the palatal mesenchyme extended Wnt5a expression, which enforced posterior mesenchymal migration toward the anterior to form the convoluted condensation, thereby impairing the genesis of the soft palate in Osr2-creKI;Ctnnb1ex3f mice. Moreover, the medially osteogenic markers Sox9, Runx2, and Osx; the laterally Shh, Foxf1, and Fgf10; and another Wnt inhibitor, Sfrp2, were significantly reduced or even diminished in Osr2-creKI;Ctnnb1ex3f palatal shelves. In contrast, the condensed Osr2-creKI;Ctnnb1ex3f palatal mesenchyme displayed the medial markers Dlx5 and p-Smad1/5/8, along with the fibrosis/dermal markers ɑ-SMA and Tbx15. The Wnt and TGF-β/BMP inhibitors Ectodin and Noggin were also ectopically activated in the palatal epithelium overlying the condensed mesenchyme Osr2-creKI;Ctnnb1ex3f mice.DiscussionThese findings indicate a transition of palatal mesenchymal cells from an osteogenic fate into fibrosis commitment, along with disrupted mediolateral patterning of the palatal shelves due to persistent canonical Wnt activity. Our study provides molecular clues that fine-tuning the mesenchymal canonical Wnt activity and Wnt5a-directed cell migration correlates with the morphogenesis of hard palates and the genesis of soft palates.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1784707</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1784707</link>
        <title><![CDATA[Iron toxicity undermines microfracture-induced cartilage regeneration by predisposing a pre-ferroptotic niche]]></title>
        <pubdate>2026-03-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Haining Peng</author><author>Zhongkai Ren</author><author>Yingze Zhang</author><author>Tengbo Yu</author><author>Xiaohong Huang</author>
        <description><![CDATA[Microfracture (MF) often yields regenerated cartilage that resembles scar tissue and is prone to rapid deterioration. This outcome may be linked to elevated iron levels, which upregulate sphingolipid (SP) signaling and increase lipid exposure to reactive oxygen species (ROS), thereby heightening cellular sensitivity to iron. In this study, we analyze whether heme-derived iron released during clinical MF undermines cartilage regeneration. We compared regenerated and intact cartilage using histomorphological, proteomic, metabolomic, and transcriptional analyses. Regenerated tissue exhibited disrupted cellular organization and a deficient extracellular matrix. Omics profiling highlighted transferrin-mediated iron transfer, striking SP signaling, and increased oxidized glutathione tripeptide in cartilage regeneration. Integrated analysis further revealed a pre-ferroptotic microenvironment in newborn chondrocytes after MF, which is characterized by extracellular Fe3+ accumulation, moderately increased Fe2+ levels, heterogeneous expression of ferroptotic markers, and altered mitochondrial and lysosomal structures. To assess the role of iron toxicity and iron-dependent oxidative stress, we administered intra-articular injections of the iron chelator deferoxamine (DFO) or the lipid ROS scavenger ferrostatin-1 (FER-1). Both treatments improved joint mobility, increased regenerated tissue thickness, elevated proteoglycan content, reduced sphingomyelin levels, preserved mitochondrial structure, and decreased lysosome abundance. These findings demonstrate that iron toxicity establishes a pre-ferroptotic niche that compromises cartilage regeneration following MF. In this study, we provide new mechanistic insights for developing targeted therapeutic strategies to enhance cartilage restoration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1736159</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1736159</link>
        <title><![CDATA[In vitro assays to monitor membrane fusion]]></title>
        <pubdate>2026-03-10T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Hunter J. Madison</author><author>Adam L. Yokom</author>
        <description><![CDATA[Membrane fusion is essential to maintain eukaryotic life. Fusion is tightly regulated and relies on a complex network of protein tethers and lipid interactions. This inherent complexity makes mechanistic investigation of membrane fusion challenging. Taking a reductionist in vitro approach has established a fundamental paradigm for most SNARE dependent fusion events. Classically, bulk in vitro reconstitution assays leveraging synthetic lipid vesicles can determine the protein assemblies that drive membrane fusion. However, this bulk approach may overlook the heterogeneity of fusion events found within our cells. Recent advancements in single molecule light microscopy and cryo electron tomography enable visualization of individual fusion events at high temporal and spatial resolutions, respectively. In this review we highlight key features of bulk and single fusion assays with a focus on the variables to be considered within each approach. Additionally, we propose potential avenues to expand the in vitro toolbox to dissect membrane fusion intermediates.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1778977</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1778977</link>
        <title><![CDATA[Temporal expression dynamics of glypicans during hiPSC cardiac differentiation]]></title>
        <pubdate>2026-02-25T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Fernanda C. P. Mesquita</author><author>Stephanie J. Kim</author><author>Andreia Z. Chignalia</author><author>Camila Hochman-Mendez</author>
        <description><![CDATA[Human pluripotent stem cells (hPSCs) offer a versatile platform for modeling human cardiac development and generating cardiomyocytes for research and translational applications. Cardiac differentiation protocols are well established and rely on the sequential activation and inhibition of WNT, BMP, and FGF signaling pathways to guide lineage progression. While these intracellular signaling events are well characterized, less attention has been given to the temporal behavior of extracellular components present at the cell surface during differentiation. Glypicans (GPCs) are a family of membrane-bound heparan sulfate proteoglycans within the glycocalyx that are known to interact with morphogens in multiple developmental contexts. In this study, we profiled the expression of GPC1-6 during a standard chemically defined cardiac differentiation protocol, in the absence of targeted interventions. Gene expression analysis across stages revealed distinct, stage-associated patterns: GPC3 and GPC6 were upregulated during the WNT activation phase; GPC4 was suppressed after WNT inhibition and maintained low during cardiac commitment. GPC2 and GPC5 expressions peaked during the formation of cardiac progenitors, and GPC1 expression increased following cardiac specification. These findings provide a temporal map of GPC expression coinciding with established differentiation stages, demonstrating that members of the glypican family are dynamically expressed during human cardiac differentiation. By documenting when specific glypicans are expressed during a commonly used differentiation workflow, this study offers a descriptive reference framework that may inform future mechanistic studies investigating how extracellular components intersect with canonical cardiac signaling pathways.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1737571</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1737571</link>
        <title><![CDATA[Transcriptional coordination in multicellular lineage differentiation during lung organogenesis: deciphering the role of epithelial cells as a microenvironmental regulatory hub]]></title>
        <pubdate>2026-02-20T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Chunyan Zhang</author><author>Jin Liu</author><author>Yanxia Li</author><author>Bing Han</author><author>Min Liu</author><author>Jie Zheng</author><author>Xiaozhi Liu</author>
        <description><![CDATA[Lung development is a complex and precisely regulated process of continuously branching morphogenesis, the core of which lies in the directed differentiation of diverse cell types and the dynamic intercellular interaction network. This review systematically delineates the differentiation pathways of major cellular lineages during pulmonary development, with a particular focus on the dual functions of epithelial cells as the core regulatory hub of the microenvironment. These cells not only dominate the spatial patterning of lung branching morphogenesis but also orchestrate the developmental fates of key cell types through multiple signaling cues. Furthermore, this review discusses the regenerative properties of lung-resident stem cells and the interaction patterns between various cell types and epithelial cells. These insights not only provide an important theoretical framework for elucidating the molecular regulatory network of lung development but also offer novel ideas for the optimization of strategies in lung regenerative medicine and the precision intervention for lung-related diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1724475</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1724475</link>
        <title><![CDATA[Fgf8/18 antagonizes Shh expression in lingual ventral–dorsal patterning]]></title>
        <pubdate>2026-02-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Shuhui Yang</author><author>Junyuan Xue</author><author>Han Liu</author><author>Nan Zhou</author><author>Hui Feng</author><author>Nan Li</author><author>Bo Liu</author><author>Lei Zhu</author><author>Jing Xiao</author><author>Chao Liu</author>
        <description><![CDATA[IntroductionThe cellular and molecular mechanisms in tongue development are still poorly understood. Explicating how the developing tongue is patterned into a dorsally wide and ventrally narrow asymmetry would benefit the pathological interpretation of tongue deformities.MethodsIn this study, we first revealed that the dorsal extension of Fgf8 from the ventral mesenchyme in Osr2-creKI;Rosa26R-Fgf8 mouse embryonic tongues disrupted dorsal–ventral asymmetry by suppressing the cell proliferation and tenogenic differentiation of lingual dorsal mesenchyme. By intersecting the differentially expressed genes (DEGs) in mouse embryonic dorsal tongues with the canonical gene set of dorsal–ventral pattern formation, Shh and Shh-related genes were found to be specifically activated in the embryonic dorsal tongue. The DEGs between WT dorsal and Osr2-creKI;Rosa26R-Fgf8 dorsal tongues showed that the expression of Lhx6, an Fgf8/18-related transcription factor robustly expressed in the WT ventral tongue, was increased in the Osr2-creKI;Rosa26R-Fgf8 dorsal tongue.ResultsHistological assays verified that in both Osr2-creKI;Rosa26R-Fgf8 and Shh-cre;Rosa26R-Fgf8 embryonic tongues, the expression of Shh and Shh-related genes, including goosecoid (Gsc), Foxa2, and Foxf1, was suppressed in the dorsal area, while the transcription of the ventrally located Fgf8/18-related Lhx6 was extended into the dorsal area. FGF8 or FGF18 supplementation in WT tongues recapitulated the suppression of Shh and Shh-related genes. However, exogenous SHH neither suppressed Fgf18 and Lhx6 nor activated the Shh-related gene Foxf1 in the lingual ventral mesenchyme. These results indicate the involvement of Shh and Fgf8/18 in lingual dorsal–ventral patterning, in which ventral Fgf8/18 suppresses the extension of dorsal Shh.DiscussionOur findings not only confirm the existence of dorsal–ventral patterning during tongue development but also identify Shh and Fgf8/18 as key genes defining the lingual dorsal–ventral axis, providing cellular and molecular clues for interpreting the clinical manifestations of congenital lingual deformities.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2025.1664285</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2025.1664285</link>
        <title><![CDATA[Neuron-secreted chemokine-like Orion interacts with the glial receptor Draper during mushroom body neuronal remodeling in Drosophila]]></title>
        <pubdate>2026-01-20T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Clarisse Perron</author><author>Ana Boulanger</author><author>Jean-Maurice Dura</author>
        <description><![CDATA[Across the animal kingdom, neuronal remodeling is a crucial developmental mechanism to refine neurite targeting necessary for both maturation and function of neural circuits. The neuronal chemokine-like Orion is essential for astrocyte infiltration and likely for phagocytosis during mushroom body γ-neuron remodeling during metamorphosis in Drosophila. The Drpr phagocytic receptor is a critical and well-studied regulator of many aspects of neuronal remodeling, where it is required for neurite pruning and cell body removal. In this study, we show a drprnull allele displaying a mushroom body (MB)-pruning phenotype very similar, if not identical, to that of orionnull alleles. Furthermore, when Orion is permanently tethered to the surface of the γ-axons, we show strong genetic interactions between neuronal Orion and glial Drpr. These results strongly suggest that Drpr is the glial receptor for Orion in mushroom body neuronal remodeling.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2025.1724413</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2025.1724413</link>
        <title><![CDATA[De novo assembly and single-molecule study of kinetochore-microtubule interactions]]></title>
        <pubdate>2026-01-12T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Joshua D. Larson</author><author>Lillian R. Worst</author><author>Charles L. Asbury</author>
        <description><![CDATA[Kinetochores are essential molecular machines composed of dozens of protein subcomplexes that assemble onto specialized centromeric nucleosomes during every cell cycle prior to mitosis. During mitosis, the assembled kinetochores are responsible for maintaining load-bearing attachments to dynamic spindle microtubules, and for harnessing the forces generated by attached microtubules to organize and separate sister chromatids. Recent work shows that kinetochores can be reconstituted by assembling them in vitro onto centromeric DNAs in yeast whole cell lysates. By tethering individual centromeric DNAs to the surface of a coverslip, the assembly process and the microtubule-attachment activity of the assembled kinetochores can be studied at the single-molecule level. Kinetochores reconstituted in this manner are able to capture taxol-stabilized microtubules, with a strong intrinsic preference specifically for capturing microtubule plus ends. Super-resolution tracking further shows that the architecture of the assembled kinetochores changes in a microtubule polarity-dependent manner under external load. We anticipate that extensions of these approaches will uncover the molecular basis of the kinetochore’s plus end-preference and, ultimately, will reveal how tension affects the arrangement of core subcomplexes and transient regulatory factors. Here we detail how to study individual kinetochores assembled from yeast whole cell lysate using single-molecule total internal reflection fluorescence microscopy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2025.1685907</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2025.1685907</link>
        <title><![CDATA[From “immune silence” to “immune dialogue”: modification strategies for bone substitutes based on bone immunomodulatory characteristics]]></title>
        <pubdate>2025-10-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jiaming Zhao</author><author>Quan Sun</author><author>Jing Gu</author><author>Xiaofan Xu</author><author>Minghui Xia</author><author>Haibin Xia</author><author>Zifan Zhao</author>
        <description><![CDATA[Traditional bone substitute materials primarily employ a strategy centered on the direct modulation of osteoblast differentiation. However, this strategy, to some extent, overlooks the pivotal regulatory role of the immune microenvironment in the process of bone regeneration. With the continuous advancement of bone biology research, the significant regulatory role of the immune microenvironment in the osteogenic process has gradually been substantiated. Osteoimmunology studies reveal that immune cells dynamically coordinate the osteoblast-osteoclast balance through shared signaling networks. The “immune-silent” characteristic of traditional bone substitute materials often leads to fibrous encapsulation and failure of osseointegration at the surgical site. Conversely, the research focus of the new generation of bone substitute materials is centered on dynamic immune interaction strategies: by optimizing surface topology to guide macrophages toward a reparative polarization; leveraging the temporal release of bioactive ions to precisely regulate the balance between inflammation and regeneration; and integrating intelligent response systems to dynamically adapt to changes in the pathological microenvironment. Through the synergistic effects of these multifaceted approaches, the ultimate goal is to effectively promote bone tissue regeneration. Against this backdrop, this paper proposes a transition strategy from “immune silence” to “immune dialogue,” which emphasizes the active and effective modulation of immune responses through meticulous material design, thereby reshaping the bone microenvironment to create favorable conditions for bone tissue repair and reconstruction. This innovative concept breaks through the limitations of traditional unidirectional osteogenic modulation, successfully establishing a two-way dialogue bridge between bone substitute materials and the immune system, significantly improving the efficiency of clinical bone defect repair, while also greatly enhancing patient satisfaction. This review systematically outlines the latest advancements in the fields of osteoimmunology and biomaterials, focusing on the key scientific issue of “osteogenic differentiation regulated by the osteoimmune microenvironment,” and provides an in-depth analysis of biomaterial design strategies based on the dynamic balance of the immune microenvironment. The aim is to elucidate the immune-metabolic modulation mechanisms mediated by materials, thereby enhancing the clinical translation efficacy of biomaterials, and provide theoretical support and technical pathways for the precise repair of bone defects.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2025.1712557</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2025.1712557</link>
        <title><![CDATA[Editorial: Editors’ showcase 2024: insights in morphogenesis and patterning]]></title>
        <pubdate>2025-10-06T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Glenn S. Edwards</author><author>Shinji Takada</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2025.1685609</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2025.1685609</link>
        <title><![CDATA[Cementum regeneration strategies: Insights from development and periodontal microenvironment]]></title>
        <pubdate>2025-10-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Huiyi Wang</author><author>Liu Yang</author><author>Xin Huang</author><author>Li Ma</author><author>Chuan Wang</author><author>Xiaoxuan Wang</author><author>Zhengguo Cao</author>
        <description><![CDATA[Cementum, a mineralized tissue covering the root surface of the tooth, maintains tooth stability through providing support for the attachment of periodontal ligament fibres, and protects the pulp from external damage via acting as a barrier against microbial invasion and destruction. Notably, both physiological and pathological factors may lead to the destruction of this vulnerable tissue, thus impeding its function. However, the intricate periodontal microenvironment, which consists of host cells, microbial communities, and metabolites, presents challenges to cementum regeneration. In addition, there remains a debate regarding whether the cellular origin of cementum is derived from mesenchymal cells or epithelial cells. Due to the limitations of traditional regenerative surgeries in achieving complete cementum regeneration, researchers are exploring new strategies based on cementum development and the periodontal microenvironment. Our group has revealed the crucial regulatory mechanisms in cementoblast differentiation and developed engineering materials for cementum regeneration. Drawing upon the latest research on cementum development and regeneration, alongside the comprehensive studies undertaken by our research group over the years, this review systematically consolidates current knowledge on cementum development and the regulatory functions of the periodontal microenvironment. It emphasizes mechanisms such as metabolic reprogramming, epigenetic modifications, and immune-stem cell interactions. Furthermore, the review seeks to provide innovative, target-oriented insights for strategies aimed at cementum regeneration, grounded in the understanding of cementum development and the periodontal microenvironment.]]></description>
      </item>
      </channel>
    </rss>