Pub Date : 2026-01-10DOI: 10.1016/j.ydbio.2026.01.007
Punam Bala , Viswadica Prakki , Rohit Joshi
SWI-SNF ATPase Brahma and Notch signalling are known to interact during development, but how this interaction is executed at the molecular level is not fully understood. We have investigated the molecular mechanism of Brm-Notch interaction in the context of Hox-dependent neural stem cell (NSC) apoptosis in the developing Central Nervous System (CNS) of Drosophila. Our results suggest a multi-tier regulation of NSC apoptosis by Brahma, first by regulating the expression of Drosophila CBP/p300 (Nejire) and the molecular triggers of cell death (Hox, bHLH factor Grainyhead, and Notch signalling pathway). The second mode of regulation is by direct binding of Brahma to the apoptotic enhancer and its collaboration with Notch signalling pathway to regulate the RHG family of apoptotic genes, grim and reaper. Our data support a model where, upon activation of Notch signalling, Brahma and CSL-Su(H)/Mastermind complex recruit CBP/p300 onto the apoptotic enhancer. This increases the H3K27ac marks on the nucleosomes to open up the chromatin and facilitate apoptotic gene transcription in Abd-B and Grh dependent manner.
{"title":"SWI/SNF ATPase Brahma and Notch signalling collaborate with CBP/p300 to regulate neural stem cell apoptosis in Drosophila larval central nervous system","authors":"Punam Bala , Viswadica Prakki , Rohit Joshi","doi":"10.1016/j.ydbio.2026.01.007","DOIUrl":"10.1016/j.ydbio.2026.01.007","url":null,"abstract":"<div><div>SWI-SNF ATPase Brahma and Notch signalling are known to interact during development, but how this interaction is executed at the molecular level is not fully understood. We have investigated the molecular mechanism of Brm-Notch interaction in the context of Hox-dependent neural stem cell (NSC) apoptosis in the developing Central Nervous System (CNS) of <em>Drosophila</em>. Our results suggest a multi-tier regulation of NSC apoptosis by Brahma, first by regulating the expression of Drosophila CBP/p300 (Nejire) and the molecular triggers of cell death (Hox, bHLH factor Grainyhead, and Notch signalling pathway). The second mode of regulation is by direct binding of Brahma to the apoptotic enhancer and its collaboration with Notch signalling pathway to regulate the <em>RHG</em> family of apoptotic genes, <em>grim and reaper</em>. Our data support a model where, upon activation of Notch signalling, Brahma and CSL-Su(H)/Mastermind complex recruit CBP/p300 onto the apoptotic enhancer. This increases the H3K27ac marks on the nucleosomes to open up the chromatin and facilitate apoptotic gene transcription in Abd-B and Grh dependent manner.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 60-72"},"PeriodicalIF":2.1,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145958938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-07DOI: 10.1016/j.ydbio.2026.01.004
Manaswini Sarangi
{"title":"Introducing DevBioConnect: A new author webinar series from developmental biology","authors":"Manaswini Sarangi","doi":"10.1016/j.ydbio.2026.01.004","DOIUrl":"10.1016/j.ydbio.2026.01.004","url":null,"abstract":"","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 32-34"},"PeriodicalIF":2.1,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-07DOI: 10.1016/j.ydbio.2026.01.002
Kathryn M. Brewer , Katlyn K. Brewer , Nicholas C. Richardson , Jeremy F. Reiter , Nicolas F. Berbari , Mia J. Konjikusic
Primary cilia orchestrate several signaling pathways, and their disruption results in pleiotropic disorders called ciliopathies. Bardet-Beidl syndrome (BBS), one ciliopathy, provides insights into cilia function in many tissues. Using a mouse model of BBS, Bbs4 knockout (Bbs4−/−), we found that adult Bbs4−/− pituitaries are hypoplastic and have increased gonadotroph populations. Similarly, pituitary deletion of IFT88, required for ciliogenesis, attenuated growth and increased gonadotrophs. The developing Bbs4−/− pituitary experienced mildly reduced Hedgehog (HH) signaling. Isolated Bbs4−/− pituitary stem cells exhibited reduced HH signal responsiveness and expression of stem cell markers. These data demonstrate that cilia and BBS function are necessary for pituitary growth. We propose that altered cilia-mediated patterning of the pituitary contribute to physiological features of ciliopathies such as BBS.
{"title":"Primary cilia and BBS4 are required for postnatal pituitary development","authors":"Kathryn M. Brewer , Katlyn K. Brewer , Nicholas C. Richardson , Jeremy F. Reiter , Nicolas F. Berbari , Mia J. Konjikusic","doi":"10.1016/j.ydbio.2026.01.002","DOIUrl":"10.1016/j.ydbio.2026.01.002","url":null,"abstract":"<div><div>Primary cilia orchestrate several signaling pathways, and their disruption results in pleiotropic disorders called ciliopathies. Bardet-Beidl syndrome (BBS), one ciliopathy, provides insights into cilia function in many tissues. Using a mouse model of BBS, <em>Bbs4</em> knockout (<em>Bbs4</em><sup><em>−/−</em></sup>), we found that adult <em>Bbs4</em><sup><em>−/−</em></sup> pituitaries are hypoplastic and have increased gonadotroph populations. Similarly, pituitary deletion of IFT88, required for ciliogenesis, attenuated growth and increased gonadotrophs. The developing <em>Bbs4</em><sup>−/−</sup> pituitary experienced mildly reduced Hedgehog (HH) signaling. Isolated <em>Bbs4</em><sup>−/−</sup> pituitary stem cells exhibited reduced HH signal responsiveness and expression of stem cell markers. These data demonstrate that cilia and BBS function are necessary for pituitary growth. We propose that altered cilia-mediated patterning of the pituitary contribute to physiological features of ciliopathies such as BBS.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 20-31"},"PeriodicalIF":2.1,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145923441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-07DOI: 10.1016/j.ydbio.2026.01.005
Edward Farrow , Smitha Rao , Simon J.Y. Han , Xuyao Chang , Cindy Huynh , Samantha A. Brugmann , Hee-Woong Lim , Jason Tchieu , Kenneth Campbell , Brian Gebelein
Animal models have demonstrated a critical role of the homeodomain transcription factor Genetic-Screened Homeobox 2 (Gsx2) in the developing basal ganglia. Moreover, recent clinical genetic studies have shown that GSX2 patient variants are associated with severe neurological symptoms and basal ganglia dysgenesis. Unfortunately, technical limitations with existing animal models, such as progenitor heterogeneity and limited temporal control, have impeded the investigation of direct regulatory targets. In this study, we engineered a Dox-inducible human embryonic stem cell (hESC) line to investigate the function of GSX2 in directed differentiation cultures that model developing lateral ganglionic eminence-like (LGE-like) progenitors. Transcriptomic, chromatin accessibility, and genomic binding studies revealed that GSX2: (1) binds both high- and low-accessibility chromatin using varying binding site preferences; (2) alters chromatin accessibility largely through indirect mechanisms; (3) functions primarily as a transcriptional repressor; and (4) regulates key conserved target genes that impact both neuronal progenitor maturation and regional specification. These results provide insight into the key regulatory roles and targets of GSX2, thereby establishing a new tractable experimental system to investigate basal ganglia development.
{"title":"An inducible system to study the regulatory functions of GSX2 in human lateral ganglionic eminence-like progenitors","authors":"Edward Farrow , Smitha Rao , Simon J.Y. Han , Xuyao Chang , Cindy Huynh , Samantha A. Brugmann , Hee-Woong Lim , Jason Tchieu , Kenneth Campbell , Brian Gebelein","doi":"10.1016/j.ydbio.2026.01.005","DOIUrl":"10.1016/j.ydbio.2026.01.005","url":null,"abstract":"<div><div>Animal models have demonstrated a critical role of the homeodomain transcription factor Genetic-Screened Homeobox 2 (Gsx2) in the developing basal ganglia. Moreover, recent clinical genetic studies have shown that GSX2 patient variants are associated with severe neurological symptoms and basal ganglia dysgenesis. Unfortunately, technical limitations with existing animal models, such as progenitor heterogeneity and limited temporal control, have impeded the investigation of direct regulatory targets. In this study, we engineered a Dox-inducible human embryonic stem cell (hESC) line to investigate the function of GSX2 in directed differentiation cultures that model developing lateral ganglionic eminence-like (LGE-like) progenitors. Transcriptomic, chromatin accessibility, and genomic binding studies revealed that GSX2: (1) binds both high- and low-accessibility chromatin using varying binding site preferences; (2) alters chromatin accessibility largely through indirect mechanisms; (3) functions primarily as a transcriptional repressor; and (4) regulates key conserved target genes that impact both neuronal progenitor maturation and regional specification. These results provide insight into the key regulatory roles and targets of GSX2, thereby establishing a new tractable experimental system to investigate basal ganglia development.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 35-51"},"PeriodicalIF":2.1,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-06DOI: 10.1016/j.ydbio.2026.01.003
Jinxia Wang , Yue Li , Yutong Zhang , Yu Zhao , Huili Tong , Shufeng Li
Insulin-like growth factor 1 (IGF-1) is a key regulator of skeletal muscle growth and regeneration. In this study, we demonstrate that IGF-1 promotes C2C12 myoblast proliferation in a dose- and time-dependent manner. Mechanistically, IGF-1 induces the expression of early growth response 1 (Egr1), a transcription factor that directly binds to the promoter region of platelet endothelial aggregation receptor 1 (PEAR1) and enhances its transcription. Upregulation of PEAR1 subsequently facilitates myoblast proliferation by activating the Notch signaling pathway. Furthermore, IGF-1-induced activation of the Egr1-PEAR1 cascade enhances muscle stem cell (MuSC) proliferation and accelerates skeletal muscle regeneration following injury in vivo. Collectively, this study reveals the critical role of the IGF-1-Egr1-PEAR1 regulatory axis in skeletal muscle regeneration, providing novel mechanistic insight into IGF-1-mediated muscle repair.
{"title":"IGF-1 regulates PEAR1 through Egr1 to promote skeletal muscle post-injury regeneration","authors":"Jinxia Wang , Yue Li , Yutong Zhang , Yu Zhao , Huili Tong , Shufeng Li","doi":"10.1016/j.ydbio.2026.01.003","DOIUrl":"10.1016/j.ydbio.2026.01.003","url":null,"abstract":"<div><div>Insulin-like growth factor 1 (IGF-1) is a key regulator of skeletal muscle growth and regeneration. In this study, we demonstrate that IGF-1 promotes C2C12 myoblast proliferation in a dose- and time-dependent manner. Mechanistically, IGF-1 induces the expression of early growth response 1 (Egr1), a transcription factor that directly binds to the promoter region of platelet endothelial aggregation receptor 1 (PEAR1) and enhances its transcription. Upregulation of PEAR1 subsequently facilitates myoblast proliferation by activating the Notch signaling pathway. Furthermore, IGF-1-induced activation of the Egr1-PEAR1 cascade enhances muscle stem cell (MuSC) proliferation and accelerates skeletal muscle regeneration following injury in vivo. Collectively, this study reveals the critical role of the IGF-1-Egr1-PEAR1 regulatory axis in skeletal muscle regeneration, providing novel mechanistic insight into IGF-1-mediated muscle repair.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"532 ","pages":"Pages 52-59"},"PeriodicalIF":2.1,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-03DOI: 10.1016/S0012-1606(25)00359-8
{"title":"Outside Back Cover - Graphical abstract TOC/TOC in double column/Cover image legend if applicable, Bar code, Abstracting and Indexing information","authors":"","doi":"10.1016/S0012-1606(25)00359-8","DOIUrl":"10.1016/S0012-1606(25)00359-8","url":null,"abstract":"","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"530 ","pages":"Page OBC"},"PeriodicalIF":2.1,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145880305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-03DOI: 10.1016/j.ydbio.2026.01.001
Kimberly A. Arena, Christina A. Kearns, Mohamoud Ahmed, Rebecca O'Rourke, Charles G. Sagerström, Santos J. Franco, Bruce Appel
Nervous system development relies on sequential and coordinated formation of diverse neurons and glia from neural progenitor cells (NPCs). In the spinal cord, NPCs of the pMN domain produce neurons early in development followed by oligodendrocyte precursor cells (OPCs), which subsequently differentiate as oligodendrocytes (OLs), the myelinating glia of the central nervous system. The mechanisms that specify neural progenitor cells to the OL lineage are not yet well understood. Using zebrafish as an experimental model system, we generated single-cell RNA sequencing and single-nuclei ATAC sequencing data that identified a subpopulation of NPCs, called pre-OPCs, that appeared fated to produce OPCs. pre-OPCs uniquely express several genes that encode transcription factors specific to the OL lineage, including Gsx2, which regulates OPC formation in the mouse forebrain. To investigate Gsx2 function in zebrafish OPC specification, we used CRISPR/Cas9 genome editing to create gsx2 loss-of-function alleles. gsx2 homozygous mutant embryos initiated OPC formation prematurely and produced excess OPCs without altering OL differentiation. Using our single-nuclei multi-omics dataset, we predicted a gene regulatory network centered around gsx2 and identified genes that might be transcriptionally regulated by Gsx2. Taken together, our studies suggest that Gsx2 expression in pre-OPCs contributes to the timing of OPC specification.
{"title":"Gsx2 regulates oligodendrocyte precursor formation in the zebrafish spinal cord","authors":"Kimberly A. Arena, Christina A. Kearns, Mohamoud Ahmed, Rebecca O'Rourke, Charles G. Sagerström, Santos J. Franco, Bruce Appel","doi":"10.1016/j.ydbio.2026.01.001","DOIUrl":"10.1016/j.ydbio.2026.01.001","url":null,"abstract":"<div><div>Nervous system development relies on sequential and coordinated formation of diverse neurons and glia from neural progenitor cells (NPCs). In the spinal cord, NPCs of the pMN domain produce neurons early in development followed by oligodendrocyte precursor cells (OPCs), which subsequently differentiate as oligodendrocytes (OLs), the myelinating glia of the central nervous system. The mechanisms that specify neural progenitor cells to the OL lineage are not yet well understood. Using zebrafish as an experimental model system, we generated single-cell RNA sequencing and single-nuclei ATAC sequencing data that identified a subpopulation of NPCs, called pre-OPCs, that appeared fated to produce OPCs. pre-OPCs uniquely express several genes that encode transcription factors specific to the OL lineage, including Gsx2, which regulates OPC formation in the mouse forebrain. To investigate Gsx2 function in zebrafish OPC specification, we used CRISPR/Cas9 genome editing to create <em>gsx2</em> loss-of-function alleles. <em>gsx2</em> homozygous mutant embryos initiated OPC formation prematurely and produced excess OPCs without altering OL differentiation. Using our single-nuclei multi-omics dataset, we predicted a gene regulatory network centered around <em>gsx2</em> and identified genes that might be transcriptionally regulated by Gsx2. Taken together, our studies suggest that Gsx2 expression in pre-OPCs contributes to the timing of OPC specification.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"531 ","pages":"Pages 30-44"},"PeriodicalIF":2.1,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145905608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-02DOI: 10.1016/j.ydbio.2025.12.022
A.C. Maia-Fernandes , T. Pais de Azevedo , N. Borralho-Martins , S. Ramalhete , G.G. Martins , I. Palmeirim , I. Duarte , A. Marreiros , P.J. Martel , R.P. Andrade
The chicken embryo has long been a pivotal model system to understand the cellular and molecular mechanisms driving amniote embryo development. Its easy access for in vivo experimentation, together with the development of ex ovo culture techniques, has made it a choice model system for elaborate experimental manipulations. Temporal progression of chick embryo development is classically categorized using the Hamburger and Hamilton staging system (Hamburger, V., & Hamilton, 1951). However, this offers limited temporal resolution when comparing embryos within the same developmental stage and may further be hindered by experimental conditions that directly impact the morphological structures used for stage identification. Here, we performed time-lapse imaging of early chick embryonic stages HH4 to HH10 and obtained quantitative elongation data of multiple embryonic portions, yielding two valuable and freely accessible data resources for the chick research community. We identified length measurements capable of describing developmental time, thus enabling the alignment of independent embryos with temporal resolution. Notably, the head-fold (C-HF) showed a strong time correlation, even though it elongates above the primary embryonic axis. A morphometric characterization of HH stages further showed that C-HF length can discriminate HH stages of development, albeit with limited resolution. Finally, we present ChEEQ: Chicken Embryo Elongation Quantification (https://colab.research.google.com/github/EmbryoClock/ChickElong/blob/main/ChEEQ/ChEEQ.ipynb), a new morphometric tool describing HH4-HH10 embryo elongation, that allows the comparison of user-input data with our reference dataset and is capable of inferring quantitative alterations to embryo developmental time using length measurements alone. Together, these resources open new avenues for investigating vertebrate embryo elongation and quantitatively assessing the effects of experimental interventions on development.
{"title":"A morphometric characterization of early CHICK embryo elongation","authors":"A.C. Maia-Fernandes , T. Pais de Azevedo , N. Borralho-Martins , S. Ramalhete , G.G. Martins , I. Palmeirim , I. Duarte , A. Marreiros , P.J. Martel , R.P. Andrade","doi":"10.1016/j.ydbio.2025.12.022","DOIUrl":"10.1016/j.ydbio.2025.12.022","url":null,"abstract":"<div><div>The chicken embryo has long been a pivotal model system to understand the cellular and molecular mechanisms driving amniote embryo development. Its easy access for <em>in vivo</em> experimentation, together with the development of <em>ex ovo</em> culture techniques, has made it a choice model system for elaborate experimental manipulations. Temporal progression of chick embryo development is classically categorized using the Hamburger and Hamilton staging system (Hamburger, V., & Hamilton, 1951). However, this offers limited temporal resolution when comparing embryos within the same developmental stage and may further be hindered by experimental conditions that directly impact the morphological structures used for stage identification. Here, we performed time-lapse imaging of early chick embryonic stages HH4 to HH10 and obtained quantitative elongation data of multiple embryonic portions, yielding two valuable and freely accessible data resources for the chick research community. We identified length measurements capable of describing developmental time, thus enabling the alignment of independent embryos with temporal resolution. Notably, the head-fold (C-HF) showed a strong time correlation, even though it elongates above the primary embryonic axis. A morphometric characterization of HH stages further showed that C-HF length can discriminate HH stages of development, albeit with limited resolution. Finally, we present <strong>ChEEQ</strong>: <strong>Ch</strong>icken <strong>E</strong>mbryo <strong>E</strong>longation <strong>Q</strong>uantification (<span><span>https://colab.research.google.com/github/EmbryoClock/ChickElong/blob/main/ChEEQ/ChEEQ.ipynb</span><svg><path></path></svg></span>), a new morphometric tool describing HH4-HH10 embryo elongation, that allows the comparison of user-input data with our reference dataset and is capable of inferring quantitative alterations to embryo developmental time using length measurements alone. Together, these resources open new avenues for investigating vertebrate embryo elongation and quantitatively assessing the effects of experimental interventions on development.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"531 ","pages":"Pages 19-29"},"PeriodicalIF":2.1,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-31DOI: 10.1016/j.ydbio.2025.12.021
Kari Price, Lindsay Lewellyn
Intercellular bridges connect cells within tissues and organs across the animal kingdom, where they play important roles in cell-cell communication and coordination. Some of the most well-studied intercellular bridges are the ring canals that connect germline cells within the developing Drosophila egg chamber. The genetic, imaging, and biochemical tools available within this model system have generated a wealth of information about the proteins, pathways, and structures that regulate ring canal formation, stability, and expansion. In this review, we describe the important contributions that have been made to our understanding of ring canal biology, with an emphasis on the mechanisms that promote ring canal expansion. We describe accessible and reliable tools available to study these structures as well as ways in which more modern genetic, imaging, biochemical, and bioinformatics-based approaches could be applied to the study of ring canals within the egg chamber or in other tissues or organisms.
{"title":"Bridges under construction: the dynamics of ring canal expansion during Drosophila oogenesis.","authors":"Kari Price, Lindsay Lewellyn","doi":"10.1016/j.ydbio.2025.12.021","DOIUrl":"https://doi.org/10.1016/j.ydbio.2025.12.021","url":null,"abstract":"<p><p>Intercellular bridges connect cells within tissues and organs across the animal kingdom, where they play important roles in cell-cell communication and coordination. Some of the most well-studied intercellular bridges are the ring canals that connect germline cells within the developing Drosophila egg chamber. The genetic, imaging, and biochemical tools available within this model system have generated a wealth of information about the proteins, pathways, and structures that regulate ring canal formation, stability, and expansion. In this review, we describe the important contributions that have been made to our understanding of ring canal biology, with an emphasis on the mechanisms that promote ring canal expansion. We describe accessible and reliable tools available to study these structures as well as ways in which more modern genetic, imaging, biochemical, and bioinformatics-based approaches could be applied to the study of ring canals within the egg chamber or in other tissues or organisms.</p>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145891982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-25DOI: 10.1016/j.ydbio.2025.12.016
Nicole A. Theodosiou, Anyerys Diaz
The left-right positioning of organs and subsequent formation of asymmetric organ shapes are vital for function and conserved in all vertebrates. Breaking symmetry is linked to Nodal-directed changes in endodermal cell behavior, but no evidence exists to date for differential cell proliferation in mesenchyme prior to asymmetry. Here we use the ancestral shape of the gut tube, the spiral valve intestine, as a model to study the evolution of how symmetry is broken. The spiral intestine is present in all basal fishes and is named after its shape; a short tube with an inner fold that rotates to create a spiral-shaped lumen. In the skate, Nodal signaling is necessary for initiating asymmetry by changes in cell behavior that lead to an expansion of the left endoderm wall. In contrast to previous studies, we also observe a significant increase in cell proliferation in left-sided mesenchymal cells prior to the break in symmetry. Thus, the skate spiral intestine is unique in combining evolutionary conserved mechanisms that change cell architecture with differential cell proliferation during initiation of gut organ morphogenesis.
{"title":"Nodal-directed endodermal cell changes are preceded by differential cell proliferation in the mesenchyme to break symmetry in the Leucoraja erinacea spiral intestine","authors":"Nicole A. Theodosiou, Anyerys Diaz","doi":"10.1016/j.ydbio.2025.12.016","DOIUrl":"10.1016/j.ydbio.2025.12.016","url":null,"abstract":"<div><div>The left-right positioning of organs and subsequent formation of asymmetric organ shapes are vital for function and conserved in all vertebrates. Breaking symmetry is linked to Nodal-directed changes in endodermal cell behavior, but no evidence exists to date for differential cell proliferation in mesenchyme prior to asymmetry. Here we use the ancestral shape of the gut tube, the spiral valve intestine, as a model to study the evolution of how symmetry is broken. The spiral intestine is present in all basal fishes and is named after its shape; a short tube with an inner fold that rotates to create a spiral-shaped lumen. In the skate, Nodal signaling is necessary for initiating asymmetry by changes in cell behavior that lead to an expansion of the left endoderm wall. In contrast to previous studies, we also observe a significant increase in cell proliferation in left-sided mesenchymal cells prior to the break in symmetry. Thus, the skate spiral intestine is unique in combining evolutionary conserved mechanisms that change cell architecture with differential cell proliferation during initiation of gut organ morphogenesis.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"531 ","pages":"Pages 10-18"},"PeriodicalIF":2.1,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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