Developmental Dynamics[JOURNAL]
Sun
200 papers
Ontogeny of RSPO1, FOXL2, and RUNX1 during ovarian differentiation in the marsupial tammar wallaby.
Paranjpe MR, Chen Y, Shaw G … +1 more , Renfree MB
Dev Dyn · 2026 Mar · PMID 40481762 · Full text
BACKGROUND: RSPO1 and FOXL2 are female sex-determining genes involved in the differentiation and organization of the ovary in some eutherian mammals. Mutations or loss of function of these genes are associated with parti...
BACKGROUND: RSPO1 and FOXL2 are female sex-determining genes involved in the differentiation and organization of the ovary in some eutherian mammals. Mutations or loss of function of these genes are associated with partial to full sex reversal in mice, humans, and goats. RUNX1 may also play a role in ovarian development, but its expression in marsupials has not been examined as yet. We studied the conservation and protein localization of RSPO1, FOXL2, and RUNX1 orthologs in the marsupial tammar wallaby (Notamacropus eugenii) compared to other vertebrates. RESULTS: RSPO1, FOXL2, and RUNX1 were highly conserved in their sequences across all vertebrates examined. The localization of these proteins in the tammar ovary was studied from Day 18 postpartum to adulthood. RSPO1, FOXL2, and RUNX1 were expressed in the granulosa cells of the early ovary and granulosa cells of the mature ovary, while RSPO1 expression was also found in the intra-ovarian rete and cell membrane of germ cells during the period of germ cell meiosis and meiotic arrest. CONCLUSIONS: RSPO1, FOXL2, and RUNX1 are highly conserved in the vertebrate ovary-determining pathway and were expressed in the tammar wallaby in a manner consistent with their role in the ovarian differentiation of eutherian mammals.
Embryonic cerebrospinal fluid pressure in fetal mice in utero: External factors pressurize the intraventricular space.
Tsujikawa K, Muramatsu R, Miyata T
Dev Dyn · 2026 Jun · PMID 40476689 · Full text
BACKGROUND: Previous experiments inducing leakage of embryonic cerebrospinal fluid (CSF) suggest the necessity of intraventricular CSF pressure (P) for brain morphogenesis. Nevertheless, how embryonic P occurs is unclear...
BACKGROUND: Previous experiments inducing leakage of embryonic cerebrospinal fluid (CSF) suggest the necessity of intraventricular CSF pressure (P) for brain morphogenesis. Nevertheless, how embryonic P occurs is unclear, especially in utero. RESULTS: Using a Landis water manometer, we measured P in fetal mice isolated from the amniotic cavity (P) and found that P rose from 20 Pa at embryonic day (E) 10 to 100-110 Pa at E14-16. At E13, intraventricular injections of ≥3 μL of saline elevated P by ~30%, whereas those of inhibitors of CSF secretion decreased P by ~30%. Shh-mediated cerebral wall expansion did not significantly increase P. Removal of the brain-surrounding contractile tissues decreased P by 80%-90%. We then found that the intraamniotic pressure measured in utero (P) declined from 2000 Pa at E10 to 500 Pa at E15-18 but was always much greater than P. Direct measurement of P in utero (P) at E13 and E15 coupled with the measurement of P under hydrostatic pressure loading to mimic P at various embryonic ages revealed the following relationship: P = P + P. CONCLUSIONS: The P of mice in utero is influenced by external factors, most strongly by intraamniotic pressure and less strongly by brain-confining tissues.
DNA repair during embryonic epidermal stratification.
Meguro F, Kawasaki K, Kakihara Y … +14 more , Kawasaki M, Fukushima M, Sari FT, Utama V, Kesuma A, Nihara J, Kudo T, Fujita A, Ichikawa K, Osawa K, Maeda T, Tabeta K, Saeki M, Ohazama A
Dev Dyn · 2026 May · PMID 40439281 · Publisher ↗
BACKGROUND: Genomes are constantly exposed to a myriad of DNA-damaging agents. Robust DNA repair mechanisms protect DNA by removing or tolerating damage. However, it remains unclear whether these mechanisms are required...
BACKGROUND: Genomes are constantly exposed to a myriad of DNA-damaging agents. Robust DNA repair mechanisms protect DNA by removing or tolerating damage. However, it remains unclear whether these mechanisms are required for organogenesis. RESULTS: Multiple epithelial layers are essential for skin function, including body protection. The epidermis is initiated as a single layer and then stratifies in utero. Stratification did not occur in mice with epithelial conditional deletion of the DNA repair molecule Reptin (Reptin;K14Cre). DNA damage was observed in the mutant epidermis but not in the wild-type epidermis. The mutant epidermis also showed reduced cell proliferation and upregulated p53 expression. Stratification was restored when p53 was deleted in the Reptin mutant mice by generating Reptin and p53 double mutant mice (Reptin;K14Cre;p53). CONCLUSION: In the wild-type epidermis, DNA is likely damaged at the initiation of embryonic stratification and promptly repaired by DNA repair mechanisms involving Reptin.
Streamlining asymmetry quantification in fetal mouse imaging: A semi-automated pipeline supported by expert guidance.
Rolfe SM, Mao D, Maga AM
Dev Dyn · 2025 Aug · PMID 40421888 · Full text
BACKGROUND: Asymmetry is a key feature of numerous developmental disorders and in phenotypic screens is often used as a readout for environmental or genetic perturbations. A better understanding of the genetic basis of a...
BACKGROUND: Asymmetry is a key feature of numerous developmental disorders and in phenotypic screens is often used as a readout for environmental or genetic perturbations. A better understanding of the genetic basis of asymmetry and its relationship to disease susceptibility will help unravel the complex genetic and environmental factors and their interactions that increase risk in a range of developmental disorders. Large-scale imaging datasets offer opportunities to work with sample sizes necessary to detect and quantify differences in morphology beyond severe deformities but also pose challenges to manual phenotyping protocols. RESULTS: We introduce a tool for quantifying asymmetry in 3D images and apply it to explore the role of genes contributing to abnormal asymmetry by deep phenotyping 3D fetal microCT images from knockout strains acquired as part of the Knockout Mouse Phenotyping Program. Four knockout strains: Ccdc186, Acvr2a, Nhlh1, and Fam20c were identified with highly significant asymmetry in craniofacial regions, making them good candidates for further analysis. CONCLUSION: In this work, we demonstrate an open-source, semi-automated tool to quantify the asymmetry of craniofacial structures that integrates expert anatomical knowledge. This tool can detect abnormally asymmetric phenotypes in fetal mice to explore the relationship between facial asymmetry, perturbed development, and developmental instability.
Differences in palatal shelf epithelial stiffness between the lingual/nasal and buccal/oral surfaces during palatal shelf elevation in developing mice.
Nagasaka A, Bando Y, Toda-Fujii M … +4 more , Onozawa G, Suzuki K, Miyata T, Amano O
Dev Dyn · 2026 May · PMID 40408552 · Publisher ↗
BACKGROUND: During secondary palate formation, bilateral palatal shelves grow vertically to a horizontal position. This morphological change of the palatal shelves, defined as the palatal shelf elevation, occurs from emb...
BACKGROUND: During secondary palate formation, bilateral palatal shelves grow vertically to a horizontal position. This morphological change of the palatal shelves, defined as the palatal shelf elevation, occurs from embryonic day (E)-13.5 to E14 in mice. Palatal shelves show regional differences in elevation patterns along the anterior-posterior (AP) axis; however, the underlying mechanisms remain unclear. Material properties of the lingual/nasal and buccal/oral surfaces, especially stiffness, possibly contribute to different elevation patterns. RESULTS: Indentation test using atomic force microscopy was performed to measure the stiffness at the epithelial surface of the palatal shelf. Measurement of palatal shelf stiffness along the AP axis before and after elevation revealed that the lingual/nasal surface was softer than the buccal/oral surface in the posterior region before elevation and that the palatal shelf was stiffer after elevation than before elevation. Moreover, the thickness of epithelial cells on the lingual/nasal side was lower than that on the buccal/oral side before elevation. CONCLUSION: Overall, our results suggest that epithelial cell thickness affects epithelial surface stiffness, causing regional differences in elevation patterns.
Pss knockdown in the midgut causes growth retardation in Drosophila similar to that in human LMHD.
Kim KY, Hwang YL, Yeom S … +2 more , Kwon SH, Jeon SH
Dev Dyn · 2026 May · PMID 40401988 · Full text
BACKGROUND: Phosphatidylserine synthase (PSS), localized in the mitochondrial membrane, synthesizes phosphatidylserine. In humans, mutations in Pss lead to Lenz-Majewski hyperostotic dwarfism, a disorder affecting growth...
BACKGROUND: Phosphatidylserine synthase (PSS), localized in the mitochondrial membrane, synthesizes phosphatidylserine. In humans, mutations in Pss lead to Lenz-Majewski hyperostotic dwarfism, a disorder affecting growth and development. The effects of Pss mutations on the growth of Drosophila melanogaster are not fully known. Hence, this study was conducted to investigate the effects of Pss knockdown on the growth and development of D. melanogaster. RESULTS: Enterocyte (EC)-specific Pss knockdown resulted in reduced cell size in the gut via reduced Akt signaling. EC-specific Pss knockdown was associated with a decrease in gut size, a change in gut pH, and reduced food intake. These abnormalities affected normal nutrient metabolism in larvae, leading to decreased secretion of Drosophila insulin-like peptides. Consequently, the reduced systemic Akt signaling at the organismal level resulted not only in impaired gut growth but also in abnormal organismal growth and development. CONCLUSION: These findings highlight the significant role of the Pss gene in the growth and development of D. melanogaster.
Protein turnover downstream of the Nipbl/CRL4 axis contributes to abnormal development in zebrafish embryos.
Sanchez AC, Banoukh N, Mensching F … +2 more , Skibbens RV, Iovine MK
Dev Dyn · 2026 Apr · PMID 40396618 · Full text
BACKGROUND: Mutations in cohesins cause cohesinopathies such as Cornelia de Lange Syndrome (CdLS) and Roberts Syndrome (RBS). Prior findings demonstrate that Esco2 (a cohesin activator) and Smc3 (a core cohesin subunit)...
BACKGROUND: Mutations in cohesins cause cohesinopathies such as Cornelia de Lange Syndrome (CdLS) and Roberts Syndrome (RBS). Prior findings demonstrate that Esco2 (a cohesin activator) and Smc3 (a core cohesin subunit) regulate the CRL4 E3 ubiquitin ligase. SMC3 mutations, however, account for a small percentage of CdLS. Here, we test whether NIPBL, which when mutated is responsible for 65% of CdLS cases, also regulates CRL4. RESULTS: We report that Nipbl knockdown in zebrafish embryos produces developmental abnormalities and reduces the transcription of ddb1, which encodes a key component of CRL4 E3 ligase. The severity of phenotypes in Nipbl knockdown embryos is partially rescued by exogenous ddb1 mRNA, demonstrating that CRL4 ligase function is downstream of Nipbl. These findings suggest that aberrant accumulation of CRL4 ligase substrates contributes to developmental abnormalities. To test this model, we identified candidate CRL4 substrates in zebrafish embryos by LC-MS. The results reveal that elevated expression of one of these candidates, pparαa, is sufficient to produce developmental defects in zebrafish embryos. CONCLUSIONS: Nipbl impacts CRL4 ligase activity via regulation of ddb1 expression. We provide evidence that the aberrant accumulation of substrates is sufficient to produce developmental abnormalities consistent with those observed in RBS and CdLS models.
Downstream branches of receptor tyrosine kinase signaling act interdependently to shape the face.
Hanne N, Hu D, Vidal-García M … +5 more , Allen C, Shakir MB, Liu W, Hallgrímsson B, Marcucio R
Dev Dyn · 2025 Aug · PMID 40391979 · Full text
BACKGROUND: Previously we found that increasing fibroblast growth factor (FGF) signaling in the neural crest cells within the frontonasal process (FNP) of the chicken embryo caused dysmorphology that was correlated with...
BACKGROUND: Previously we found that increasing fibroblast growth factor (FGF) signaling in the neural crest cells within the frontonasal process (FNP) of the chicken embryo caused dysmorphology that was correlated with reduced proliferation, disrupted cellular orientation, and lower MAPK activation but no change in PLCγ and PI3K activation. This suggests RTK signaling may drive craniofacial morphogenesis through specific downstream effectors that affect cellular activities. In this study we inhibited three downstream branches of RTK signaling to determine their role in regulating cellular activities and how these changes affect morphogenesis of the FNP. RESULTS: Small molecule inhibitors of MEK1/2, PI3K, and PLCγ were delivered individually and in tandem to the right FNP of chicken embryos. All treatments caused asymmetric proximodistal truncation on the treated side and a mild expansion on the untreated side compared to DMSO control treated FNPs. Inhibiting each pathway caused similar decreased proliferation and disrupted cellular orientation, and only mildly increased apoptosis. CONCLUSIONS: Since RTK signaling is a ubiquitous and tightly regulated biochemical system, we conclude that the downstream pathways are robust to developmental perturbation through redundant signaling systems.
The endocannabinoid system regulates both ependymoglial and neuronal cell responses to a tail amputation in the axolotl.
Tolentino M, Walker SE, Spencer GE … +1 more , Carlone R
Dev Dyn · 2026 Mar · PMID 40377265 · Full text
BACKGROUND: The endocannabinoid system is a neuromodulatory system implicated in cellular processes during both development and regeneration. The Mexican axolotl, one of only a few vertebrates capable of central nervous...
BACKGROUND: The endocannabinoid system is a neuromodulatory system implicated in cellular processes during both development and regeneration. The Mexican axolotl, one of only a few vertebrates capable of central nervous system regeneration, was used to examine the role of the endocannabinoid system in the regeneration of the tail and spinal cord following amputation. RESULTS: The endocannabinoid receptor CB1 was upregulated in the regenerating axolotl spinal cord by 4 hours following tail amputation, and this upregulation persisted for at least 14 days. The endocannabinoid receptor CB2 was upregulated later, between 7 and 14 days after tail amputation. Both CB1 and CB2 were located in ependymoglia and neurons within the regenerating spinal cord. Treatment with inverse agonists to inhibit CB1 (AM251) or CB2 (AM630) inhibited spinal cord and tail regeneration. During the first 7 days after injury, CB1 and CB2 expression was also necessary for the proliferation of ependymoglial cells and the regeneration of axons into the newly regenerated tail tissue. However, only CB1 was necessary for the differentiation of ependymoglia into immature neurons. CONCLUSIONS: These studies are the first to examine the role of the endocannabinoid system during spinal cord regeneration in a regeneration-competent vertebrate.
Advances in culturing of the sea star Patiria miniata.
Barone V, Coronado L, Ismail D … +2 more , Fiaz S, Lyons DC
Dev Dyn · 2026 Feb · PMID 40372060 · Publisher ↗
BACKGROUND: The use of the sea star Patiria miniata as a model system has produced groundbreaking advances in a disparate set of biomedical research fields, including embryology, immunology, regeneration, cell biology, a...
BACKGROUND: The use of the sea star Patiria miniata as a model system has produced groundbreaking advances in a disparate set of biomedical research fields, including embryology, immunology, regeneration, cell biology, and evolution of development. Nonetheless, the life cycle of P. miniata has not yet been closed in the laboratory, precluding the generation of stable transgenic and mutant lines, which would greatly expand the toolset for experimentation with this model system. Rearing P. miniata in the laboratory has been challenging due to limited knowledge about metamorphosis cues, feeding habits of juveniles, and their relatively long generation time. RESULTS: Here we report protocols to rear P. miniata embryos through sexual maturity in a laboratory setting. We provide detailed staging of early embryonic development at different temperatures, and show that larvae can be raised to competence in as little as 15 days. We find that retinoic acid induces metamorphosis effectively and present methods to rear juveniles on commercially available foods. We show that in a flow-through system, juveniles double in size every 2 months and reach sexual maturity in approximately 2 years. CONCLUSIONS: We report the first example of P. miniata raised through sexual maturity in a laboratory setting, paving the way for the generation of stable mutant sea star lines.
Therapeutic potential of stem cells in colorectal cancer management: Current trends and future prospects.
Desai MD, Parmar NB, Shah IT … +3 more , Parekh PS, Patel R, Chorawala MR
Dev Dyn · 2025 Dec · PMID 40359344 · Publisher ↗
Colorectal cancer (CRC) ranks among the leading causes of cancer-related morbidity and mortality worldwide. Despite progress in understanding its molecular intricacies, the management of CRC, especially in advanced stage...
Colorectal cancer (CRC) ranks among the leading causes of cancer-related morbidity and mortality worldwide. Despite progress in understanding its molecular intricacies, the management of CRC, especially in advanced stages, remains a significant clinical hurdle. This review delves into the evolving landscape of stem cell-based therapeutic strategies in CRC, with a specific focus on the interplay between cancer stem cells (CSCs) and CRC pathogenesis and treatment resistance. Highlighting the pivotal roles of CSCs in tumor initiation, progression, metastasis, and recurrence, the review comprehensively examines their involvement in CRC, ranging from normal colonic tissue to cancer initiation. The potential of stem cells for medicinal purposes in CRC management is explored, encompassing diverse modalities such as transplantation, differentiation therapy, immunotherapy, and gene/cell-based approaches. Challenges and opportunities associated with these strategies are also evaluated, providing insights into their clinical potential and limitations. The review also appraises preclinical investigations contributing to the understanding of CRC and stem cells. Current clinical trials, patient stratification strategies, and regulatory considerations related to stem cell-based therapies in CRC are scrutinized. Furthermore, the review explores emerging trends and future directions, including developments in stem cell technologies and ethical considerations. It highlights the transformative potential of stem cell-based therapeutic strategies in CRC.
Dynamics of postnatal bone development and epiphyseal synostosis in the caprine autopod.
Panebianco CJ, Essaidi M, Barnes E … +6 more , Williams A, Vancíková K, Labberté MC, Brama P, Nowlan NC, Boerckel JD
Dev Dyn · 2026 Apr · PMID 40359336 · Full text
BACKGROUND: Bones develop to structurally balance strength and mobility. Bone developmental dynamics are influenced by whether an animal is ambulatory at birth. Precocial species, which are ambulatory at birth, develop a...
BACKGROUND: Bones develop to structurally balance strength and mobility. Bone developmental dynamics are influenced by whether an animal is ambulatory at birth. Precocial species, which are ambulatory at birth, develop advanced skeletal maturity in utero and experience postnatal development under mechanical loading. Here, we characterized postnatal bone development in the lower forelimbs of precocial goats using microcomputed tomography and histology. Our analysis focused on the two phalanges 1 (P1) bones and the partially fused metacarpal bone of the goat autopod from birth through adulthood. RESULTS: P1 cortical bone densified rapidly after birth, but cortical thickness increased continually through adulthood. Upon normalization by body mass, the P1 normalized polar moment of inertia was constant over time, suggestive of changes correlating with ambulatory loading. P1 trabecular bone increased in trabecular number and thickness until sexual maturity (12 months), while metacarpal trabeculae grew primarily through trabecular thickening. Unlike prenatal synostosis (i.e., bone fusion) of the metacarpal diaphysis, synostosis of the epiphyses occurred postnatally, prior to growth plate closure, through a unique fibrocartilaginous endochondral ossification. CONCLUSIONS: These findings implicate ambulatory loading in postnatal bone development of precocial goats and identify a novel postnatal synostosis event in the caprine metacarpal epiphysis.
Rodent monocyte-derived macrophages do not express CD163: Comparative analysis using macrophages from living boreoeutherians.
Saito Y, Fujiwara Y, Yamaguchi YL … +7 more , Tanaka SS, Miura K, Hizukuri Y, Yamashiro K, Hayashi Y, Nakashima Y, Komohara Y
Dev Dyn · 2026 Apr · PMID 40355384 · Full text
BACKGROUND: CD163 is a scavenger receptor predominantly expressed on the surfaces of macrophages in various mammalian species and is a marker of anti-inflammatory (M2-like) macrophages. High density of CD163-positive tum...
BACKGROUND: CD163 is a scavenger receptor predominantly expressed on the surfaces of macrophages in various mammalian species and is a marker of anti-inflammatory (M2-like) macrophages. High density of CD163-positive tumor-associated macrophages (TAMs) is associated with worse prognosis in various patient tumors. Interestingly, studies on mice have shown that CD163-positive TAMs only infiltrate the margins of tumor tissues, not the center. Based on these observations, we hypothesized that circulating monocyte-derived macrophages (MDMs), which are the origin of most TAMs, do not express CD163 in mice. RESULTS: We examined CD163 expression in MDMs, differentiated from healthy animals in vitro, and in normal, pathogenic, and tumorigenic macrophages infiltrating various tumors and organs across multiple species including primates, rodents, cetartiodactylans, and carnivores. We found that MDMs, including TAMs, do not express CD163 in mice. Our findings also suggest that murine CD163-positive macrophages likely originate from a specific subset of resident macrophages, namely fetal liver monocytes/macrophages, as indicated by fetal analysis. Furthermore, we revealed that the CD163-negative expression pattern in MDMs is a trait shared by the rodent clade. CONCLUSIONS: Rodent MDMs do not express CD163, a phenotype not shared with MDMs of other mammals. Our findings caution against the extrapolation of rodent experimental results to other animal models.
Myomaker and Myomixer are required for craniofacial myoblast fusion in zebrafish.
Zhang Z, Yong P, Hu Q … +1 more , Du S
Dev Dyn · 2026 Mar · PMID 40317819 · Full text
BACKGROUND: Craniofacial and trunk skeletal muscles are derived from different progenitor populations during development. Trunk skeletal muscles contain mostly multinucleated myofibers that are formed through myoblast fu...
BACKGROUND: Craniofacial and trunk skeletal muscles are derived from different progenitor populations during development. Trunk skeletal muscles contain mostly multinucleated myofibers that are formed through myoblast fusion. However, myoblast fusion in craniofacial muscles and its molecular regulation are not well understood. Recent studies revealed that genetic mutations in MYOMAKER and MYOMIXER fusogens in humans cause Carey-Fineman-Ziter Syndrome (CFZS), characterized by facial weakness and lower jaw deformity. RESULTS: Previous studies in zebrafish revealed that knockout of myomaker and myomixer resulted in deformed craniofacial formation. To establish the causal connection between loss of fusogen function and craniofacial deformities, we characterized myoblast fusion in zebrafish craniofacial muscles. Our results demonstrate that myomaker and myomixer are expressed in both slow and fast craniofacial muscles, and loss of these fusogens results in defects in craniofacial myoblast fusion. Interestingly, unlike trunk muscles of early embryos and larvae that show fast-fiber-specific fusogen expression and fusion while slow muscle fusion only occurs at 3 weeks post-fertilization, both slow and fast craniofacial muscles fuse as early as 3 days post-fertilization. CONCLUSIONS: Collectively, this study demonstrates that myomaker and myomixer are expressed in both slow and fast-twitch craniofacial muscles and are essential for myoblast fusion and the development of craniofacial muscles.
Tissue-specific requirement of Polr1D in the prothoracic gland for ecdysone-mediated developmental transitions in Drosophila melanogaster.
Walker BM, Palumbo RJ, Knutson BA
Dev Dyn · 2026 Feb · PMID 40317818 · Publisher ↗
BACKGROUND: POLR1D is a shared subunit of RNA Polymerases I and III, which transcribe the rRNA incorporated into ribosomes. Mutations in POLR1D cause Treacher Collins syndrome, a craniofacial disorder that arises from im...
BACKGROUND: POLR1D is a shared subunit of RNA Polymerases I and III, which transcribe the rRNA incorporated into ribosomes. Mutations in POLR1D cause Treacher Collins syndrome, a craniofacial disorder that arises from impaired ribosome biogenesis in neural crest cells. Previously, we found that RNAi knockdown of Polr1D in several non-neural Drosophila tissues caused developmental defects that phenocopy mutations affecting ecdysone signaling. Ecdysone is a steroid hormone produced in the prothoracic gland (PG) of insects that triggers developmental transitions. Here, we show that Polr1D is required for PG development and ecdysone production to facilitate larval developmental transitions. RESULTS: We found that Polr1D RNAi in the PG causes larval developmental arrest due to defective peripheral ecdysone signaling. We also found that Polr1D is required for the growth of PG cells and for maintaining nucleolar structure. We found that Polr1D is required for the synthesis of mature ribosomes and the production of the Pol III-transcribed 7SK RNA. Furthermore, developmental arrest of Polr1D RNAi larvae and Polr1D mutant (G30R) larvae was partially rescued by treatment with exogenous ecdysone. CONCLUSION: These results demonstrate a role for Drosophila Polr1D in PG development and suggest that disruptions in human Polr1D might impact additional cell types during development.
Pre-oviposition development of the brown anole (Anolis sagrei).
Weberling A, Shylo NA, Kircher BK … +7 more , Wilson H, McClain M, Marchini M, Starr KB, Sanger TJ, Hollfelder F, Trainor PA
Dev Dyn · 2026 Feb · PMID 40243194 · Full text
BACKGROUND: The brown anole, Anolis sagrei, has emerged as a representative squamate species for developmental studies during the past decades. Novel functional tools have been established to manipulate embryogenesis thr...
BACKGROUND: The brown anole, Anolis sagrei, has emerged as a representative squamate species for developmental studies during the past decades. Novel functional tools have been established to manipulate embryogenesis through genome editing or the introduction of small molecule inhibitors, and their effective use requires a thorough understanding of early anole embryogenesis. To enable precise and reproducible staging of anole embryos, we need knowledge of the progression of anole embryogenesis and morphogenesis. While post-oviposition development has been described, the pre-oviposition period remains to be explored. RESULTS: We provide the first staging series of pre-oviposition development for the brown anole. Analyzing the follicles and embryos through brightfield imaging, SEM, STEM, histology, and DAPI staining, we define 26 distinct developmental stages. Furthermore, we followed heart development, neural crest cell migration, and central nervous system development using immunofluorescence analyses and provide new comparative insights into the morphogenesis of each of these organ systems. CONCLUSIONS: Our dataset reveals that peri-gastrulation morphogenesis up to the initiation of neurulation diverges significantly from chick, the common representative model of reptile embryogenesis. With this study, we establish the brown anole as a squamate model organism for cross-clade evolutionary studies of early embryogenesis.
Dynamic expression of lamin B1 during adult neurogenesis in the vertebrate brain.
Zhilina D, Bolaños Castro LA, Eguiguren JS … +10 more , Zocher S, Karasinsky A, Widmer D, Espinós A, Borrell V, Brand M, Miura K, Zierau O, Yun MH, Toda T
Dev Dyn · 2026 Feb · PMID 40214400 · Full text
BACKGROUND: In mammals, specific brain regions such as the dentate gyrus (DG) of the hippocampus and the subventricular zone (SVZ) of the lateral ventricles harbor adult neural stem/progenitor cells (ANSPCs) that give ri...
BACKGROUND: In mammals, specific brain regions such as the dentate gyrus (DG) of the hippocampus and the subventricular zone (SVZ) of the lateral ventricles harbor adult neural stem/progenitor cells (ANSPCs) that give rise to new neurons and contribute to structural and functional brain plasticity. In contrast, other vertebrates such as salamanders and zebrafish exhibit a widely distributed neurogenic niches throughout the brain, suggesting a greater neurogenic capacity in adulthood. However, the mechanisms underlying this divergence in neurogenic potential among vertebrates remain elusive. To address this, we examined the expression dynamics of a critical epigenetic regulator for the long-term maintenance of murine ANSPCs, lamin B1, during adult neurogenesis across the vertebrate spectrum. RESULTS: Lamin B1 expression patterns during adult neurogenesis are conserved among mammals including mouse, naked mole-rat, and ferret. However, these patterns differ between mammals and anamniotes. In mammals, neural stem cells and neuroblasts exhibited higher lamin B1 levels, and differentiated neurons possessed lower lamin B1 levels. On the other hand, anamniotes showed the opposite patterns of lamin B1 expression, with higher levels in neurons compared to stem cells. CONCLUSIONS: Our study shows that the lamin B1 expression pattern during adult neurogenesis differs between species, and that changes in lamin B1 protein sequence may contribute to the differences in lamin B1 expression patterns. This study highlights potential differences in cell-autonomous epigenetic regulation in the maintenance of ANSPC pools in the adult brain among species.
Comprehensive observation of histone lysine lactylation during gametogenesis of Drosophila melanogaster.
Hayashi Y, Sato B, Kageyama R … +4 more , Miyado K, Saito D, Kobayashi S, Kawano N
Dev Dyn · 2025 Nov · PMID 40152687 · Publisher ↗
BACKGROUND: Histone post-translational modification (PTM) is an important epigenomic regulation content and an essential process regulating gene expression. Histone lysine lactylation is the newly identified histone PTM...
BACKGROUND: Histone post-translational modification (PTM) is an important epigenomic regulation content and an essential process regulating gene expression. Histone lysine lactylation is the newly identified histone PTM that utilizes the lactyl moiety for its modification. Although histone lysine lactylation is considered an essential outcome of the Wardburg effects and the interconnection between cellular metabolism and gene regulation, the developmental contexts involving this PTM are largely unknown. In this study, we comprehensively observed histone lysine lactylation during Drosophila oogenesis, one of the developmental contexts in which chromatin regulation plays crucial roles. RESULTS: Our study revealed that lactylation on the specific histone lysine mainly occurs in the oocyte karyosome and condensed meiotic chromosome, suggesting histone lysine lactylation has a vital role in female meiosis. Interestingly, one of the histone lysine lactylations, lactylation of lysine 14 of histone H3, is intensively observed in the meiotic germline in the mouse ovary, suggesting that lactylation has an evolutionarily conserved role. CONCLUSIONS: Our results revealed that histone lysine lactylation is predominantly present in transcriptionally repressive meiotic chromatin, which contradicts the previously reported function of histone lactylation in transcriptional activation. This study, therefore, provides the first fundamental information to understand the role of histone lysine lactylation in the germline and repressive chromatin.
Lineage labeling with zebrafish hand2 Cre and CreERT2 recombinase CRISPR knock-ins.
Ming Z, Liu F, Moran HR … +12 more , Lalonde RL, Adams M, Restrepo NK, Joshi P, Ekker SC, Clark KJ, Friedberg I, Sumanas S, Yin C, Mosimann C, Essner JJ, McGrail M
Dev Dyn · 2026 Jan · PMID 40135929 · Full text
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 traje...
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.
Gfi1 in the inner ear: A retrospective review.
Li Z, Chen H, Feng H
Dev Dyn · 2025 Nov · PMID 40135914 · Publisher ↗
Gfi1 plays an important role in the development of hair cells (HCs), as indicated by its ability to regulate the expression of HC-related genes while the organ of Corti is developing. Given that the HCs and the supportin...
Gfi1 plays an important role in the development of hair cells (HCs), as indicated by its ability to regulate the expression of HC-related genes while the organ of Corti is developing. Given that the HCs and the supporting cells (SCs) are coming from a common stem/progenitor cell pool, it is conceivable to regenerate HCs from SCs that ectopically express Gfi1. The focus of this review was to elucidate the role of Gfi1 in controlling the development of HCs by dissecting the phenotypes of the inner ear in Gfi1-mutated mouse lines. In addition, we reviewed studies of regeneration in the mammalian inner ear, by which we discussed the novel function of Gfi1 as an essential factor in guiding non-HCs toward an HC destiny in coordination with Atoh1 and Pou4f3. Finally, we summarized the known Gfi1-specific Cre/CreER/reporter mouse lines and highlighted the pros and cons of each line, with the aim of providing insights for use in future studies. In summary, a better understanding of Gfi1 and its diverse roles is beneficial for advancing studies of HC regeneration in the inner ear.
About
- Frequency
- Sun
- Papers found
- 200
- RSS feed
- Subscribe