Turtles hold a unique place in vertebrate evolutionary history, making them critical assets in embryology research. Yet, they remain understudied as potential model organisms in the field. Here, to support experimental manipulations with turtle embryos, we have created a complete normal table of development for comprehensive embryonic staging of Trachemys scripta, one of the most common invasive turtle species worldwide.

Echinoderms are invertebrate deuterostomes closely related to chordates and have become a tractable model for the study of the evolution of mechanisms involved in development, primordial germ cell specification, and regeneration. Sea urchins rely on inherited mechanisms for germline formation while sea stars rely instead on cell-cell inductive signaling mechanisms.

In vertebrate embryogenesis, cranial neural crest cells (CNCCs) migrate along discrete pathways. Analyses in the chick have identified key molecular candidates for the confinement of CNCC migration to stereotypical pathways as Colec12, Trail, and Dan. The effects of these factors on CNCCs in vitro are known, but how they confine migration to discrete streams in vivo remains poorly understood. Here, we propose and test several hypothetical mechanisms by which these factors confine cell streams and maintain coherent migration, simulating an expanded agent-based model for collective CNCC migration.

Neural crest cells are a transient cell population that emerges from the dorsal neural tube during neurulation and migrates extensively throughout the embryo. Among their diverse derivatives, glial cells (such as Schwann and satellite ganglionic cells) and melanocytes represent two major lineages. In vitro studies suggested they share a common progenitor yet follow distinct differentiation pathways. Hence, neural crest cells must choose between glia and melanocyte fates-a decision crucial for forming the peripheral nervous and pigmentary systems. A groundbreaking discovery revealed that Schwann cell precursors along peripheral nerves serve as a secondary source of melanocytes during development. This finding challenged the traditional view that melanocytes arise exclusively from direct neural crest migration and demonstrated remarkable plasticity in the glial lineage. This glia/melanocyte fate choice represents a well-characterized example of binary fate decisions in vertebrate development, involving complex interactions between transcriptional networks, signaling pathways, and environmental cues. Importantly, the glia/melanocyte decision has implications for cancer and injury-induced plasticity, where embryonic pathways may be reactivated. For example, during melanomagenesis, cells can exhibit both melanocytic and glial features. Understanding how neural crest cells decide between glial and melanocyte fates may offer new insights for regenerative medicine and cancer therapy.

The lungs of squamate reptiles (lizards and snakes) are highly diverse, exhibiting single chambers, multiple chambers, transitional forms with two to three chambers, along with a suite of other anatomical features, including finger-like epithelial projections into the body cavity known as diverticulae. During embryonic development of the simple, sac-like lungs of anoles, the epithelium is pushed through the openings of a pulmonary smooth muscle mesh by the forces of luminal fluid pressure. This process of stress ball morphogenesis generates the faveolar epithelium typical of squamate lungs.

Activity of the receptor tyrosine kinase PDGFRα and the tyrosine phosphatase SHP2 is critical for vertebrate craniofacial development. SHP2 has been shown to both positively and negatively regulate PDGFR signaling through the recruitment of Grb2 and dephosphorylation of the receptor, respectively. We sought to determine the effect of SHP2 binding to PDGFRα in the facial mesenchyme via phenotypic and biochemical analyses of an allelic series of mouse embryos with combined loss of both proteins in the neural crest lineage.

Sporadic venous malformation (VM) is associated with the hyperactivating p.L914F mutation in TIE2, a receptor tyrosine kinase essential for vascular development. This mutation is not found in hereditary VM, suggesting incompatibility with life when expressed during early vascular development. Therefore, we utilized a genetic mouse model that expresses TIE2 p.L914F to determine its phenotypical effects during development.

Building and disassembling actin filaments is essential for the remodeling of the actin cytoskeleton. In large structures, like Drosophila bristles, the loss of function of actin disassembly proteins can lead to smaller and misshapen bundled actin. Here we investigate whether mutant alleles of the disassembly genes twinstar (tsr), flare (flr), and twinfilin (twf) show similar phenotypes in smaller embryonic actin-based denticles. We also examined potential genetic interactions between F-actin disassembly proteins and the molecular motor ck/myosin VIIA, a protein necessary for denticle formation.

Integrin is an αβ heterodimeric receptor to the extracellular matrix; its binding to the matrix recruits focal adhesions to two NPxY motifs, the tyrosine phosphorylation sites in the cytoplasmic domain. Studies found that replacing tyrosines (Y) with phenylalanines (F) in the motif of β1 integrin displayed little developmental or behavioral defects. However, the tyrosine-to-alanine (A) caused embryonic lethality.

Knockin mouse models expressing calbindin (Calb1), calretinin (Calb2), and peripherin (Prph) exhibit changes in hair cells (HCs), spiral ganglion neurons (SGN), vestibular ganglion neurons (VGNs), and their central projections.

In an era where the diversity and quality of imaging modalities is rapidly increasing, it may seem counterintuitive to promote classical histology as a critical skill. It is a mistake, however, to assume that the heuristic potential of these high-resolution histological data is stagnant. Deep learning algorithms have emerged as an efficient tool for converting and quantifying the cellular resolution of 2D histology sections as detailed 3D models, capable of being integrated with a diversity of multi-omics data. Such analytical innovation requires large numbers of high-quality slides whose construction faces a variety of technical challenges. These challenges are exaggerated for developmental and evolutionary biologists, for whom ontogeny and phylogeny are critical variables that require additional sampling. Our goal is to provide a protocol optimized for the thin-section histology of vertebrate embryos, detailing best practices for sample collection, processing, and slide preparation. We hope that by: (1) synthesizing a scattered methodological literature that often excludes embryological tissues, and (2) recommending adjustments to common techniques like dehydration, xylene infiltration, and sectioning, other researchers may bypass the frustrating and time-consuming problems we encountered and move quickly to producing the high-quality histological data that modern developmental biology is likely to demand.

Sea urchins have contributed to knowledge of fertilization, embryonic development, and cell physiology for 150 years. Their evolutionary position, as basal deuterostomes, and their long background in developmental biology motivate establishing a genetically enabled sea urchin species. Because of its relatively short generation time of 4-6 months and ease of culture, our lab has focused on the California sea urchin Lytechinus pictus as a multigenerational model and produced knockout and transgenic lines using this species. To ensure that diverse genetic lines can be preserved, methods must be developed to cryopreserve gametes and embryos. We have previously reported methods for cryopreservation of sperm, but robust methods to preserve embryos remain lacking.

Tadpoles of the clawed frog Xenopus laevis can regenerate their tails following partial amputation, replacing the missing spinal cord, muscles, and fin. However, for a brief period of development this response becomes unstable, leading to a proportion of tadpoles that undergo wound healing rather than regenerative programme. Inspired by a growing number of links between the microbiome and human inflammatory disease, we asked how the tadpole skin microbiome and innate immunity influence the regeneration of a complex appendage. We previously showed that tadpoles raised in antibiotics such as gentamicin or penicillin/streptomycin or with reduced Toll-like receptor 4 signaling regenerated tails poorly, while adding exogenous lipopolysaccharide promoted or rescued tail regeneration.

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.

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.

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.

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.

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.

The short-lived African turquoise killifish (Nothobranchius furzeri) is an important emerging model organism for gene expression studies, with limited tools for transcript and protein detection, especially methods that are both cost-effective and high-resolution. Brain tissue is particularly challenging to analyze due to its opacity and structural complexity, making whole-organ imaging techniques valuable. However, various tissue-clearing protocols adapted for N. furzeri are long and require specialized equipment.

5' Hox genes play crucial roles in limb patterning along the proximal-distal and anterior-posterior axes in mice. However, their functional conservation across tetrapods remains unclear. We previously found that newt Hox13 is essential for digit formation during both development and regeneration. In contrast, the functions of other 5' Hox genes (Hox9-Hox12) in newts remain u[WLYJ-108]nknown. Therefore, we generated 5' Hox knockout newts (Pleurodeles waltl) using CRISPR-Cas9.