Developmental Dynamics[JOURNAL]
Sun
200 papers
Pathogenesis and potential therapeutic targets of trichorhinophalangeal syndrome; lessons obtained from animal studies.
Saeki N, Kanai R, Tatsuta S … +4 more , Kawaguchi S, Itoh M, Ohba S, Abe M
Dev Dyn · 2026 Mar · PMID 40995872 · Full text
Trichorhinophalangeal syndrome (TRPS) is a rare genetic disease inherited in an autosomal dominant manner. It occurs in 1 in 100,000 people globally and is caused by several types of mutations of the TRPS1 gene. Since th...
Trichorhinophalangeal syndrome (TRPS) is a rare genetic disease inherited in an autosomal dominant manner. It occurs in 1 in 100,000 people globally and is caused by several types of mutations of the TRPS1 gene. Since the first human patient was reported in 1966, typical and atypical pathologies, disease courses, and treatment case presentations have been reported. TRPS is characterized by sparse slow-growing fine hair, a bulbous nose with tented nares, and brachydactyly with cone-shaped epiphyses on the hands and feet. Growth retardation and hip dysplasia are also frequently observed, suggesting that hair and skeletal phenotypes are the major pathologies of TRPS. Several animal models have been established and studied intensively to address this rare disease. However, comprehensive treatment strategies for TRPS have not been established. In this review, we summarize TRPS pathologies and the characteristics of TRPS1 as an atypical GATA-type transcription factor. We review rodent strains that have contributed to our understanding of the in vivo roles of Trps1 and discuss their validity as animal models of TRPS. We also summarize diseases that demonstrate pathologies similar to TRPS and findings in their animal models.
Thyroid hormone receptor blockade by amiodarone disrupts angiogenesis via VEGFα, WNT7A, BMP, and PI3K/AKT pathways in chick embryo vascular development.
Vaishnav J, Balakrishnan S
Dev Dyn · 2025 Sep · PMID 40944523 · Publisher ↗
BACKGROUND: Thyroid hormones (TH) play critical roles in embryonic vascular development, yet their precise molecular contributions remain inadequately defined. This study investigates how pharmacological blockade of thyr...
BACKGROUND: Thyroid hormones (TH) play critical roles in embryonic vascular development, yet their precise molecular contributions remain inadequately defined. This study investigates how pharmacological blockade of thyroid hormone receptors (TR) by amiodarone disrupts angiogenesis and associated molecular signaling pathways in chick embryos. RESULTS: Amiodarone-treated embryos exhibited notable morphological defects, including hematomas, anophthalmia, ventral wall defects, and limb anomalies, primarily affecting lateral plate mesoderm-derived tissues. Chorioallantoic membrane analysis revealed significant reductions in vessel density, branching, and total vessel length, along with increased lacunarity, indicating impaired angiogenesis. Molecular profiling showed consistent down-regulation of key angiogenic regulators such as VEGFα, WNT7A, BMP2/6, and phosphatidylinositol 3-kinase/ Ak strain transforming (PI3K/AKT) at both transcript and protein levels. In silico docking confirmed strong TRα and TRβ binding, while deiodinase activity assays and western blotting demonstrated impaired thyroxine-to-triiodothyronine (T3) conversion and reduced T3 levels, confirming systemic hypothyroidism and disrupted thyroid hormone signaling. CONCLUSION: Our findings underscore the essential role of thyroid hormone signaling in embryonic angiogenesis. Disruption of TR activation by amiodarone significantly impairs vascular formation through coordinated suppression of Vascular endothelial growth factor alpha (VEGFα), WNT7A, bone morphogenetic proteins, and PI3K/AKT pathways. These insights enhance our understanding of TH-related developmental disorders and may guide therapeutic strategies for managing vascular dysfunctions associated with impaired thyroid signaling.
Role of p53 family members during development of striated muscle, with focus on p63.
Ziermann-Canabarro JM, Boughner JC, McPike KN
Dev Dyn · 2026 Feb · PMID 40937686 · Publisher ↗
BACKGROUND: During vertebrate development, p53 family members (p53, p63, and p73) play both discrete and redundant roles. While p63 gene mutations lead to various skeletal and organ birth defects, p63's role in muscle de...
BACKGROUND: During vertebrate development, p53 family members (p53, p63, and p73) play both discrete and redundant roles. While p63 gene mutations lead to various skeletal and organ birth defects, p63's role in muscle development is less considered. Muscles derive from embryonic mesoderm. However, head and heart muscle differentiation also depends on intrinsic cues and signals from adjacent epithelia. In p63 mutant mice, ectoderm- and endoderm-derived epithelia are defective, implying defective myogenesis. We review the evidence that p63 is important for the differentiation of striated muscles, including cardiopharyngeal field-derived head and heart musculature. RESULTS: Several p63 isoforms act during mesoderm induction, myoblast proliferation, cell cycle exit, and cell differentiation. Of particular interest, TAp63γ is expressed in embryonic myoblasts and endoderm. In striated muscles, TAp63γ functions in myogenic proliferation and differentiation and participates in sarcomere development and myofibril assembly. CONCLUSIONS: p63 is active during all muscle development stages, from mesoderm induction to myocyte differentiation. Different p53 family members, including several p63 isoforms, have overlapping functions. This redundancy could explain the limited myopathies described in p63 mouse mutants. As these defects may be subtler and more age/stage-dependent than appreciated, they warrant further study.
Easily adaptable Fiji macro for mean linear intercept measurement of peripheral respiratory airspace.
Patlin B, Yin Y, Li L … +1 more , Ornitz DM
Dev Dyn · 2025 Sep · PMID 40937540 · Publisher ↗
BACKGROUND: Mean linear intercept (MLI) is a method of evaluating lung structure and pathology that is widely used in clinical and research settings. Unfortunately, no widely available software for automation of this pro...
BACKGROUND: Mean linear intercept (MLI) is a method of evaluating lung structure and pathology that is widely used in clinical and research settings. Unfortunately, no widely available software for automation of this process is available, and many clinicians and scientists still perform these measurements manually. RESULTS: To increase the speed and accuracy of obtaining MLI measurements, we have developed a macro for Fiji is just ImageJ (Fiji) to semi-automate the acquisition of these measurements. Twenty to 25 images from each of 43 mouse lungs, a total of 1042 images, were analyzed manually and by macro (automated) to validate the accuracy of the MLI macro. No significant difference was recorded between the manual and automated methods in mouse lung tissue of either different age (P14, P21, 8 weeks) or different condition (healthy vs. emphysema). Optimization of MLI macro parameters showed that additional measurements beyond three lines per image did not further improve accuracy. We also provide an Excel macro that summarizes the airspace data for each image and averages all the image data in a given batch of images. CONCLUSION: This Fiji macro can be used to automate MLI measurement in histological sections of lung tissue faster and with lower variance.
Heterozygous Med13l mice recapitulate a developmental growth delay and craniofacial anomalies seen in MED13L syndrome.
Leinheiser AK, Nguyen TT, Henry KM … +3 more , Rosales M, Van Otterloo E, Grueter CE
Dev Dyn · 2025 Sep · PMID 40919805 · Full text
BACKGROUND: Gene transcription is crucial for embryo and postnatal development and is regulated by the Mediator complex. Mediator is comprised of four submodules, including the kinase submodule (CKM). The CKM consists of...
BACKGROUND: Gene transcription is crucial for embryo and postnatal development and is regulated by the Mediator complex. Mediator is comprised of four submodules, including the kinase submodule (CKM). The CKM consists of MED13, MED12, CDK8, and CCNC. In mammals, there are paralogs for CKM components, including MED13L, MED12L, and CDK19. Neurological disorders have been associated with mutations in CKM genes including MED13L syndrome. MED13L syndrome is generally characterized as a haploinsufficiency of MED13L with a broad phenotypic response due in part to a wide range of de novo mutations. RESULTS: We developed a Med13l heterozygous (HET) mouse model with an exon 11 deletion to evaluate whether Med13l HET mice are a viable research tool to study human phenotypes. We characterized our mouse model using growth, cardiovascular, and skeletal readouts. We observed Med13l HET mice are smaller than wildtype (WT) littermates, and over 60% of them exhibited one of two craniofacial anomalies: a pug snout with midface hypoplasia or a crooked snout. We also observed discontinuous squamosal sutures in a subset of our Med13l HETs. CONCLUSIONS: Med13l HET mice recapitulate MED13L syndrome phenotypes including a developmental growth delay and craniofacial anomalies. Med13l HET mice represent a novel research tool for MED13L syndrome.
Single-cell sequencing reveals potential novel insights into appendage-patterning and joint-development in a spider.
Medina-Jiménez BI, Budd GE, Janssen R
Dev Dyn · 2025 Aug · PMID 40772585 · Publisher ↗
BACKGROUND: Jointed appendages represent one of the key innovations of arthropods, and thus understanding the development and evolution of these structures is important for the understanding of the evolutionary success o...
BACKGROUND: Jointed appendages represent one of the key innovations of arthropods, and thus understanding the development and evolution of these structures is important for the understanding of the evolutionary success of Arthropoda. In this paper, we analyze a cell cluster that was identified in a previous single-cell sequencing (SCS) experiment on embryos of the spider Parasteatoda tepidariorum. This cell cluster is characterized by marker genes that suggest a role in appendage patterning and joint development. RESULTS: We analyzed the expression profiles of these marker genes showing that they are expressed in the developing appendages and in a pattern that suggests a potential function during joint development. Several of the investigated genes represent new and unexpected factors such as dysfusion (dysf), spätzle3 (spz3), seven-up (svp). In order to study their evolutionary origin, we also investigated orthologs of the identified appendage-patterning genes in the harvestman Phalangium opilio, a distantly related chelicerate. CONCLUSION: Our work highlights the usefulness of SCS experiments for the identification of potential new genetic factors that are involved in specific developmental processes. The current data provide potential new insights into the gene regulatory networks that underlie arthropod joint development.
The establishment, maintenance, and breaking of symmetry.
Trainor PA
Dev Dyn · 2025 Aug · PMID 40771088 · Publisher ↗
Abstract loading — click title to view on PubMed.
Possible role of microtubules in vesicular transport of matrix protein during sea urchin larval biomineralization.
Qassem A, Gildor T, de-Leon SB
Dev Dyn · 2026 Jun · PMID 40757679 · Full text
BACKGROUND: Biomineralization is a vital biological process through which organisms produce mineralized structures such as shells, skeletons, and teeth. Microtubules are essential for biomineralization in various eukaryo...
BACKGROUND: Biomineralization is a vital biological process through which organisms produce mineralized structures such as shells, skeletons, and teeth. Microtubules are essential for biomineralization in various eukaryotic species; however, their specific roles in this process remain unclear. RESULTS: Here, we investigated the structure and function of microtubule filaments and their co-localization with matrix and focal adhesion proteins during the elongation of the calcite spicules of the sea urchin larva. First, we show that inhibiting microtubule polymerization using Nocodazole in whole embryos and isolated skeletogenic cell cultures results in a significant reduction of skeletal growth and affects skeletal morphology. Next, we demonstrate that microtubule filaments elongate from around the skeletogenic nuclei to the biomineralization compartment where they overlap with active focal adhesion kinase. The expression of spicule matrix proteins overlaps with microtubule filaments around the nuclei and with microtubule filaments that elongate to the spicule cavity. CONCLUSIONS: We propose that vesicles bearing matrix proteins are trafficked on microtubules to the spicule cavity where their exocytosis is assisted by focal adhesions. The role of microtubules in biomineralization from unicellular algae to human bones suggests that the proposed microtubule-guided vesicle transport into the biomineralization compartment could be a common mechanism in Eukaryotes' biomineralization.
Identification of novel genes regulating the development of the palate.
Bhaskar A, Astrof S
Dev Dyn · 2025 Aug · PMID 40751508 · Full text
BACKGROUND: The International Mouse Phenotyping Consortium (IMPC) has generated thousands of knockout mouse lines, many of which exhibit embryonic or perinatal lethality. Using micro-computed tomography (micro-CT), the I...
BACKGROUND: The International Mouse Phenotyping Consortium (IMPC) has generated thousands of knockout mouse lines, many of which exhibit embryonic or perinatal lethality. Using micro-computed tomography (micro-CT), the IMPC has created and publicly released three-dimensional image data sets of embryos from these lethal and subviable lines. In this study, we leveraged this data set to screen homozygous null mutants for anomalies in secondary palate development. We analyzed optical sections from 2987 embryos at embryonic days E15.5 and E18.5, representing 484 homozygous mutant lines. RESULTS AND CONCLUSIONS: Our analysis identified 44 novel genes implicated in palatogenesis. Gene set enrichment analysis highlighted biological processes and pathways relevant to palate development and uncovered 18 genes jointly regulating the development of the eye and the palate. These findings present a valuable resource for further research, offer novel insights into the molecular mechanisms underlying palatogenesis, and provide important context for understanding the etiology of rare human congenital disorders involving malformations of the palate and other organs.
Whole tissue imaging of cellular boundaries at sub-micron resolutions for deep learning cell segmentation: Applications in the analysis of epithelial bending of ectoderm.
Norris SCP, Hu JK, Shubin NH
Dev Dyn · 2026 May · PMID 40716088 · Full text
BACKGROUND: To understand cellular morphology, biologists have relied on traditional optical microscopy of tissues combined with tissue clearing protocols to image structures deep within tissues. Unfortunately, these pro...
BACKGROUND: To understand cellular morphology, biologists have relied on traditional optical microscopy of tissues combined with tissue clearing protocols to image structures deep within tissues. Unfortunately, these protocols often struggle to retain cell boundary markers, especially at high enough resolutions necessary for precise cell segmentation. This limitation affects the ability to study changes in cell shape during major developmental events. RESULTS: We introduce a method that preserves cell boundary markers and matches the refractive index of tissues with water. This technique enables the use of high-magnification, long working distance water-dipping objectives that provide sub-micron resolution images. We subsequently segment individual cells using a trained neural network segmentation model. These segmented images facilitate quantification of cell properties of the entire three-dimensional tissue. As a demonstration, we examine mandibles of transgenic mice that express fluorescent proteins in their cell membranes and extend this technique to a non-model animal, the catshark, investigating its dental lamina and dermal denticles-invaginating and evaginating ectodermal structures, respectively. This technique provides insight into the mechanical environment that cells experience during developmental transitions. CONCLUSIONS: This pipeline, named MORPHOVIEW, provides a powerful tool to quantify in high throughput the 3D structures of cells and tissues during organ morphogenesis.
Streptozotocin induced hyperglycemia in the axolotl.
Sørensen PL, Dittrich A, Lauridsen H
Dev Dyn · 2026 Jun · PMID 40698726 · Full text
BACKGROUND: Diabetes is a group of diseases characterized by loss of β cell mass and/or function, resulting in hyperglycemia. With no established curative treatment, this has initiated research in β cell regeneration. Cu...
BACKGROUND: Diabetes is a group of diseases characterized by loss of β cell mass and/or function, resulting in hyperglycemia. With no established curative treatment, this has initiated research in β cell regeneration. Current animal models have either limited regenerative capacity (mice) or small size and evolutionary distance from humans (zebrafish). There is a need for new models to study endogenous regeneration pathways. This study proposes the axolotl salamander (Ambystoma mexicanum) as a model for studying the regeneration of β cells and aims to establish a protocol for STZ-induced hyperglycemia to mimic a diabetic state. RESULTS: In this pilot study, five streptozotocin (STZ) protocols were tested, and the most effective one was identified on the basis of glucose tolerance tests. Blood glucose levels were monitored to track both disease progression and remission. Histological examination of the pancreas and systemic effects of STZ treatment were also evaluated. CONCLUSION: Induction of a diabetes-like state (hyperglycemia) in axolotls was possible with STZ, but variability among animals suggests the need for a higher degree of normalization or larger sample sizes. Histological regeneration was not observed, though blood glucose levels normalized over time. Some STZ-treated animals developed edema, but its cause remains unknown.
Pancreatic injury induces β-cell regeneration in axolotl.
Powell CJ, Singer HD, Juarez AR … +12 more , Kim RT, Kim E, Payzin-Dogru D, Savage AM, Lopez NJ, Thornton K, Blair SJ, Abouelela A, Dittrich A, Akeson SG, Jain M, Whited JL
Dev Dyn · 2025 Jul · PMID 40679186 · Full text
BACKGROUND: Diabetes is a condition characterized by a loss of pancreatic β-cell function, which results in the dysregulation of insulin homeostasis. Using a partial pancreatectomy model in axolotl, we aimed to observe t...
BACKGROUND: Diabetes is a condition characterized by a loss of pancreatic β-cell function, which results in the dysregulation of insulin homeostasis. Using a partial pancreatectomy model in axolotl, we aimed to observe the pancreatic response to injury. RESULTS: Here we show a comprehensive histological characterization of pancreatic islets in axolotl. Following pancreatic injury, no apparent blastema-like structure was observed. We found a significant, organ-wide increase in cellular proliferation post-resection in the pancreas compared to sham-operated controls. This proliferative response was most robust at the site of injury. Further, an increase in nuclear density was observed, suggesting compensatory congestion as a mechanism of regeneration. We found that β-cells actively contributed to the increased rates of proliferation upon injury. β-Cell proliferation manifested in increased β-cell mass in injured tissue at 2 weeks post-injury. At 4 weeks post-injury, we found organ-wide proliferation to be extinguished while proliferation at the injury site persisted, corresponding to pancreatic tissue recovery. Similarly, total β-cell mass was comparable to sham after 4 weeks. CONCLUSIONS: Our findings suggest a non-blastema-mediated regeneration process takes place in the pancreas, by which pancreatic resection induces whole-organ β-cell proliferation without the formation of a blastemal structure. This process is analogous to other models of compensatory congestion in axolotl.
Anatomy connected 2025: American Association for Anatomy's annual meeting scientific research abstracts.
Dev Dyn · 2025 Jul · PMID 40676863 · Publisher ↗
Abstract loading — click title to view on PubMed.
Identification of neural crest and melanoma cancer cell invasion and migration genes using high-throughput screening and deep attention networks.
Kasemeier-Kulesa JC, Martina Perez S, Baker RE … +1 more , Kulesa PM
Dev Dyn · 2026 Jan · PMID 40637615 · Full text
BACKGROUND: Cell migration and invasion are well-coordinated in development and disease but remain poorly understood. We previously showed that the neural crest (NC) cell migratory wavefront shares a 45-gene panel with o...
BACKGROUND: Cell migration and invasion are well-coordinated in development and disease but remain poorly understood. We previously showed that the neural crest (NC) cell migratory wavefront shares a 45-gene panel with other cell invasion phenomena. To rapidly and systematically identify critical genes, we performed a high-throughput siRNA screen and statistical and deep learning analyses to determine changes in NC- versus non-NC-derived human cell line behaviors. RESULTS: We find 14 out of 45 genes significantly reduced c8161 melanoma cell migration; four of the 14 genes altered leader cell motility (BMP4, ITGB1, KCNE3, and RASGRP1). Deep learning identified marked disruptions in cell-neighbor interactions after BMP4 or RASGRP1 knockdown in c8161 cells. Recombinant proteins added to the culture media revealed five out of the 11 known secreted molecules stimulated c8161 cell migration. BMP4 knockdown severely reduced c8161 in vivo invasion in a chick embryo transplant model. Addition of BMP4 protein to the culture media of BMP4-siRNA-treated c8161 cells rescued cell migratory ability. CONCLUSION: High-throughput screening and deep learning distilled a 45-gene panel to a small subset of genes critical to melanoma and warrant deeper in vivo functional analysis for their role and potential synergies in driving NC cell migration and invasion.
Robinow syndrome DVL1 variants disrupt morphogenesis and appendage formation in a Drosophila disease model.
Akarsu G, MacCharles KR, Wong KKL … +2 more , Richman JM, Verheyen EM
Dev Dyn · 2025 Jul · PMID 40600289 · Publisher ↗
BACKGROUND: Robinow syndrome is a rare developmental syndrome caused by variants in genes in Wnt signaling pathways. We previously showed that expression of patient variants in Dishevelled 1 (DVL1) in Drosophila and chic...
BACKGROUND: Robinow syndrome is a rare developmental syndrome caused by variants in genes in Wnt signaling pathways. We previously showed that expression of patient variants in Dishevelled 1 (DVL1) in Drosophila and chicken models disrupts the balance of canonical and non-canonical Wnt signaling. RESULTS: In this study, we further examine morphological changes that occur due to expression of DVL1, which serves as a prototype for other pathogenic variants. We show that epithelial imaginal disc development is disrupted in legs and wings and accompanied by increased cell death, without changes in cell proliferation. By inhibiting caspase-dependent cell death, we show that the altered epithelial morphology is not solely due to variant-induced cell death. Furthermore, we find alterations of basement membrane components and modulators. Notably we find ectopic Mmp1 expression and tissue distortion, which is dependent on JNK signaling. We also find an abnormal abundance of Drosophila collagen IV (Viking) in pupal wing development. Due to the complex nature of appendage development, we also examined the Bone Morphogenetic Protein pathway and found elevated signaling activity via the transcriptional readout dad-lacZ. CONCLUSIONS: Through these studies, we have gained more insight into the developmental consequences of DVL1 variants implicated in autosomal dominant Robinow syndrome.
Endoderm differentiates into a transient epidermis in the mouse perineum.
Larkins CE, Grunberg DM, Daniels GM … +2 more , Feldtmann EJ, Cohn MJ
Dev Dyn · 2026 Apr · PMID 40557929 · Full text
BACKGROUND: In eutherian mammals, the embryonic cloaca is partitioned into genitourinary and anorectal canals by the urorectal septum. In the mouse embryo, the urorectal septum contributes to the perineum, which separate...
BACKGROUND: In eutherian mammals, the embryonic cloaca is partitioned into genitourinary and anorectal canals by the urorectal septum. In the mouse embryo, the urorectal septum contributes to the perineum, which separates the anus from the external genitalia. During the growth of the urorectal septum, endodermal epithelium of the cloaca is displaced to the surface of the perineum, where endodermal cells are integrated into the developing skin. However, it is unknown whether the endodermal lineage of the perineum acquires true epidermal identity, an enigmatic fate for endodermal cells. RESULTS: We find that endodermal cells that reach the surface of the perineum express markers of basal, spinous, and granular epidermis. During postnatal development, the endodermal lineage of the perineum epidermis undergoes terminal differentiation and desquamation and is replaced by adjacent ectoderm. Live imaging and single-cell tracking show that ectodermal cells move at a faster velocity in a lateral-to-medial direction, indicating convergence toward the narrow band of endoderm that lies between the anus and external genitalia. CONCLUSIONS: Cloacal endoderm differentiates into a non-renewing, transient epidermis at the midline of the perineum. Differences in directionality and velocity of cell movement patterns between endodermal and ectodermal cells suggest that the perineum epidermis develops by convergent extension.
Combinatorial expression of glial transcription factors induces Schwann cell-specific gene expression in mouse embryonic fibroblasts.
Belfiore L, Balakrishnan A, Touahri Y … +5 more , Zinyk D, Noman H, Okawa S, Biernaskie J, Schuurmans C
Dev Dyn · 2026 Jun · PMID 40538023 · Full text
BACKGROUND: Schwann cells provide peripheral nerve trophic support, myelinate axons, and assist in repair. However, Schwann cell repair capacity is limited by chronic injury, disease, and aging. Schwann cell reprogrammin...
BACKGROUND: Schwann cells provide peripheral nerve trophic support, myelinate axons, and assist in repair. However, Schwann cell repair capacity is limited by chronic injury, disease, and aging. Schwann cell reprogramming is a cellular conversion strategy that could provide a renewable cell supply to repair injured nerves. Here, we developed a plasmid-based approach to test the Schwann cell conversion potential of four glial transcription factors. RESULTS: We employed four transcription factors implicated in Schwann cell differentiation and repair: Sox10, Sox2, Jun, and Pax3. Expression vectors were generated for Sox10 alone and two triple transcription factor combinations: Jun-Pax3-Sox2 (triple 1, T1) and Sox10-Jun-Sox2 (triple 2, T2). Mouse embryonic fibroblasts (MEFs) were transfected with these vectors, transferred to glial inductive media, and Schwann cell-marker expression was in assessed by immunostaining, flow cytometry, and qPCR. All expression vectors repressed fibroblast-specific gene expression. However, T2 was most efficient at generating O4 Schwann cell-like cells, which had some capacity to myelinate denervated axons from explanted dorsal root ganglia. In comparison, T1 more efficiently induced repair Schwann cell-marker expression in converted O4 cells. CONCLUSIONS: T1 and T2 convert MEFs to Schwann cells with different efficacies and gene expression profiles, and may provide cell-based therapies for peripheral nerve repair.
Dental development in the tropical gar (Atractosteus tropicus) and the evolution of vertebrate dentitions.
Pospisilova A, Stundl J, Arias-Rodriguez L … +2 more , Cerny R, Soukup V
Dev Dyn · 2025 Jun · PMID 40538022 · Publisher ↗
BACKGROUND: Dentitions have diversified enormously during vertebrate evolution, involving reductions, modifications, or allocations to prey seizing and processing regions. A combination of ancient and novel features rela...
BACKGROUND: Dentitions have diversified enormously during vertebrate evolution, involving reductions, modifications, or allocations to prey seizing and processing regions. A combination of ancient and novel features related to dental and oropharyngeal apparatuses is found in extant lineages of non-teleost fishes, such as the gars. While relevant to evolutionary-developmental studies, gars have largely been overlooked regarding how their dentition arises, thus leaving our comprehension of the evolutionary history of vertebrate dentitions incomplete. RESULTS: Here, we complement this knowledge gap by studying dental development in the tropical gar, Atractosteus tropicus. We follow ontogenetic changes from the initiation, tooth germ addition to the establishment of the larval replacing dentition. We pay attention to the progressive appearance of tooth fields, the emergence of dental patterns, the development of folded dentin morphology, and features related to tooth resorption and replacement. Furthermore, we identify snout elongation as the critical period when the general dentition layout becomes established. CONCLUSIONS: Our study depicts the gar oropharyngeal apparatus as a system that is established based on patterned initiation, differential growth, replacement, and complex shaping of teeth. These features form a reference standpoint for the likely developmental processes employed in dentitions of fossil stem and crown bony vertebrates, including ray-finned fishes and tetrapods.
Genomic evolution of EGF-CFC genes in deuterostomes.
Shylo NA, Trainor PA
Dev Dyn · 2025 Aug · PMID 40536408 · Publisher ↗
BACKGROUND: EGF-CFC proteins are a bilaterian innovation, but they are best known for their roles in Nodal signaling during gastrulation and left-right patterning in vertebrates. Species with multiple family members show...
BACKGROUND: EGF-CFC proteins are a bilaterian innovation, but they are best known for their roles in Nodal signaling during gastrulation and left-right patterning in vertebrates. Species with multiple family members show evidence of functional specialization. For example, in mouse, Cripto is required for gastrulation, whereas CFC1 is involved in left-right patterning. However, members of the EGF-CFC family across model organisms exhibit limited sequence conservation beyond the EGF-CFC domain, posing challenges for determining their evolutionary history and functional conservation. RESULTS: In this study, we describe the evolutionary history of the EGF-CFC family of proteins across several branches of deuterostomes, with a particular focus on vertebrates. We trace the EGF-CFC gene family from a single gene in the deuterostome ancestor through its expansion and functional specialization in tetrapods, and subsequent gene loss and translocation in eutherian mammals. Mouse Cripto and CFC1, zebrafish Tdgf1, and each Xenopus EGF-CFC gene (Tdgf1, Tdgf1.2 and Cripto.3) are all descendants of the ancestral deuterostome Tdgf1 gene. CONCLUSIONS: We propose that subsequent to EGF-CFC family expansion in tetrapods, Tdgf1B (Xenopus Tdgf1.2) acquired specialization in the left-right patterning cascade, and then after its translocation in eutherians to a different chromosomal location, CFC1 has maintained that specialization.
Differential sensitivity of midline development to mitosis during and after primitive streak extension.
Zhao Z, Asai R, Mikawa T
Dev Dyn · 2026 May · PMID 40503790 · Full text
BACKGROUND: Midline establishment is a fundamental process during early embryogenesis for Bilaterians. Midline morphogenesis in non-amniotes can occur without mitosis, through Planar Cell Polarity (PCP) signaling. By con...
BACKGROUND: Midline establishment is a fundamental process during early embryogenesis for Bilaterians. Midline morphogenesis in non-amniotes can occur without mitosis, through Planar Cell Polarity (PCP) signaling. By contrast, amniotes utilize both cellular processes for developing the early midline landmark, the primitive streak (PS). This study focused on the role of cell proliferation for midline development at pre- and post-PS-extension stages and analyzed PCP signaling components at post-PS-extension stages. RESULTS: In contrast to pre-PS-extension stages, embryos under mitotic arrest during the post-PS-extension preserved notochord (NC) extension and Hensen's node (HN)/PS regression judged by both morphology and marker genes; although they became shorter, their lengths remained proportional to the embryo length. Laterality and segmentation of paraxial mesoderm were lost upon mitotic arrest. Accompanied by mitotic arrest-induced embryonic size reduction, cells including midline tissue displayed hypertrophy. CONCLUSION: This study has identified at least two distinct mitosis sensitivity phases during early midline development: One is PS extension that requires both mitosis and PCP, and the other is mitotic arrest-resistant midline development at post-PS-extension stages, with a still undefined influence by PCP signaling components.
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