Developmental Dynamics最新文献

The arthropod head problem has been puzzling scientists for more than a century. Key to this conceptual dispute is the question if the anterior of the arthropod head is serially homologous with the rest of the arthropod body, is unsegmented, or is built of non-homologous segments. Recent work revived the latter hypothesis which would, if taken for true, provide a simple solution to most aspects of the arthropod head problem, thus being of significant importance for our understanding of structural homology and arthropod evolution. One of the key arguments supporting this hypothesis is that the segment-polarity gene (SPG) network is highly conserved in posterior segments, but varies significantly in anterior head segments. Defining the SPG network as a character-identity network (CHiN) for the arthropod segment, the anterior variability would strongly indicate a different origin of the anterior versus the posterior head segments in arthropods. Here I discuss the arthropod head problem with respect to the proposed CHiN. I come to the conclusion that careful literature analysis shows that the SPG network is more flexible than claimed, in both anterior and posterior segments, and that the CHiN argument is therefore not supporting the so-called "Non-Homology-Hypothesis."

The Japanese medaka, Oryzias latipes, has become an important vertebrate model organism for addressing research questions across a broad range of disciplines, including developmental and evolutionary biology, stem cells, gene–environment interactions, behavioral neuroscience, disease modeling, and drug discovery. The medaka community took advantage of the successful completion of the ERC Synergy Grant project IndiGene to gather once again in the beautiful Heidelberg (July 22–25, 2025). Building on the opportunities created by the IndiGene project, which leverages the medaka inbreed panel Medaka Inbred Kiyosu–Karlsruhe as a unique resource for dissecting complex phenotype–genotype relationships, the meeting offered an outstanding update on emerging concepts, technologies, and community resources. By summarizing the content of each session, this report provides an overview of a vibrant and highly productive event that highlights the continued growth and vitality of medaka research.

Facial morphogenesis relies on the coordinated regulation of cellular behaviors that sculpt the face from simple facial prominences to the fully confluent lip and nose. Disruptions to migration of cranial neural crest cells and/or the directed growth of the prominences will lead to abnormalities such as orofacial clefts. Here we review what is known about the roles of the actin cytoskeleton and its key regulators, the small RHO GTPases, during neural crest cell migration and facial development. Although small RHO GTPase signaling has been studied in the context of cancer and vascular pathologies, their role in facial development has received limited attention. In this review, we review the experimental data that connects changes in the function of small Rho GTPases to cytoskeletal dynamics and ultimately to facial morphogenesis. We also highlight human craniofacial disorders resulting from germline or somatic variants of small Rho GTPase pathway genes as well as associations between variants in GTPase-activating proteins (GAPs) and guanidine nucleotide exchange factors (GEFs) and the complex trait, non-syndromic cleft lip with or without cleft palate. The review points to a model where the gain or loss of RHO GTPase pathway components could be centrally involved in many craniofacial disorders and that the Rho GTPases are major regulators of homeostasis during normal development.

Background: The brown anole is a model species of the genus Anolis, a squamate (encompassing lizards and snakes) group widely studied in evolutionary, behavioral, and developmental biology. Full genome annotation, the establishment of gene editing techniques, and comprehensive description of reproductive tract morphology and embryogenesis in this species have laid the foundation for functional studies. However, analysis of brown anole oogenesis is still required and vital to optimize genome modification, mutant line establishment, and analyses of the evolution of reproductive developmental mechanisms.

Results: Here, we characterize ovary morphology and gametogenesis in the female brown anole, Anolis sagrei, using brightfield imaging, microCT, histology staining, electron microscopy, and confocal imaging. We define 10 stages of oocyte maturation, which commences inside the oogonial nest within the germinal bed and concludes with the mature follicle ready to ovulate based on follicle size, yolk acquisition, and follicular, cellular, and basement membrane architecture.

Conclusions: We describe the complete oogenesis of the brown anole in 10 stages and report that oogenesis is highly conserved within iguanians, a suborder of lizards. With our staging framework, we lay the foundation for functional studies of oogenesis and optimized gene-editing.

Background: Many maternal mRNAs in Drosophila primordial germ cells (PGCs) are degraded in concert with the synthesis of new transcripts from the zygotic genome during gastrulation and germ band elongation (3-5 h after egg laying [AEL]). However, few studies have focused on maternal mRNA destabilization in PGCs at the blastoderm stage that is prior to zygotic genome activation (ZGA). Thus, the stability of maternal mRNAs at this stage and regulation of their degradation remain poorly understood. To address this gap, we examined the role of Nanos, an RNA-binding protein known to promote mRNA degradation, in blastoderm-stage PGCs.

Results: By combining flow cytometry and RNA-sequencing (RNA-seq) analysis of PGCs, we identified the transcripts of 898 genes that were increased in nanos^- PGCs. Among them, 298 genes encode maternal transcripts that were downregulated by Nanos in PGCs.

Conclusions: Our results show that Nanos downregulates maternal mRNA expression in PGCs before ZGA in Drosophila. As Nanos in C. elegans PGCs has also been reported to promote maternal-to-zygotic transition (MZT) via maternal mRNA downregulation during a transcriptionally silent state, our findings highlight the importance of investigating the function of Nanos for understanding the MZT in PGCs across various animal species.

Background: Endocytosis constitutes a fundamental cellular process governing development through coordinated regulation of plasma membrane remodeling and ciliogenesis, processes essential for cell shape changes and tissue development. Although Twist1 null embryos display complete cranial neural tube (NT) closure defects and conditional knockout in neuroectoderm disrupts cranial neural crest cell fate determination and delamination, the function of TWIST1 in NT morphogenesis remains unknown. We investigated the basis underlying neuroectodermal morphological abnormalities in TWIST1 mutant embryos, specifically the formation of ectopic lateral bending points and cellular disorganization, by examining Twist1's role in cilia formation, adherens junction integrity, and endocytic vesicle dynamics.

Results: Immunofluorescence analysis revealed that cytosolic TWIST1 colocalizes with β-catenin and endocytic regulators LRP2 and RAB11B along the apical surface of cranial neuroectoderm. Twist1 knockout resulted in reduced ciliary length and number. Quantitative polymerase chain reaction (PCR) and Western blot analyses demonstrated upregulation of RAB11B and β-catenin at mRNA and protein levels in Twist1 mutants. This molecular dysregulation coincided with increased accumulation of apical endocytic vesicles and altered expression profiles of endocytic component genes, ultimately modifying the apical neuroectodermal cell-cell junctions.

Conclusion: Our findings establish TWIST1 as a crucial factor for neuroectodermal morphology, demonstrating its importance in ciliogenesis, endocytic vesicle dynamics, and cell-cell integrity.

Developmental psychobiology (DPB) is a sub-discipline of developmental biology investigating the roles of physiology, biomechanics, and the environment on behavioral development. Regenerative biology is also a sub-discipline of developmental biology, studying how tissues and organs heal and regenerate after injury. One aspect of healing and regeneration is the behavioral recovery of the whole organism, involving the nervous system and coordinated movements in three-dimensional space. Behavioral recovery is often a secondary measure in many regeneration studies, primarily focusing on molecular and cellular mechanisms involved in structural recovery. Studies and frameworks in DPB, however, suggest that behaviors may have an active role in the regeneration process, and integrating regenerative biology with DPB would provide a basis for behavioral research on regenerative systems as a separate biological question to increase our understanding of behavioral recovery. Here, I introduce the probabilistic epigenesis framework from DPB and elaborate on how it reveals gaps in our knowledge concerning regeneration and behavioral recovery. I close with an initial regenerative history framework to guide regenerative biologists and bioengineers studying behavioral recovery to address these gaps and optimize behavioral recovery with regenerating tissue.

Background: The ability to generate endogenous Cre recombinase drivers using CRISPR-Cas9 knock-in technology allows lineage tracing, cell type-specific gene studies, and in vivo validation of inferred developmental trajectories from phenotypic and gene expression analyses. This report describes endogenous zebrafish hand2 Cre and CreERT2 drivers generated with GeneWeld CRISPR-Cas9 precision targeted integration.

Results: hand2-2A-cre and hand2-2A-creERT2 knock-ins crossed with ubiquitous loxP-based Switch reporters led to broad labeling in expected mesodermal and neural crest-derived lineages in branchial arches, cardiac, fin, liver, intestine, and mesothelial tissues, as well as enteric neurons. Novel patterns of hand2 lineage tracing appeared in venous blood vessels. CreERT2 induction at 24 h reveals hand2-expressing cells in the 24- to 48-h embryo contribute to the venous and intestinal vasculature. Induction in 3 dpf larvae restricts hand2 lineage labeling to mesoderm-derived components of the branchial arches, heart, liver, and enteric neurons.

Conclusions: hand2 progenitors from the lateral plate mesoderm and ectoderm contribute to numerous lineages in the developing embryo. At later stages, hand2-expressing cells are restricted to a subset of lineages in the larva. The endogenous hand2 Cre and CreERT2 drivers establish critical new tools to investigate hand2 lineages in zebrafish embryogenesis and larval organogenesis.