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1
Trainor, P. A., S. S. Tan, and P. P. Tam. "Cranial paraxial mesoderm: regionalisation of cell fate and impact on craniofacial development in mouse embryos." Development 120, no. 9 (September 1, 1994): 2397–408. http://dx.doi.org/10.1242/dev.120.9.2397.
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A combination of micromanipulative cell grafting and fluorescent cell labelling techniques were used to examine the developmental fate of the cranial paraxial mesoderm of the 8.5-day early-somite-stage mouse embryo. Mesodermal cells isolated from seven regions of the cranial mesoderm, identified on the basis of their topographical association with specific brain segments were assessed for their contribution to craniofacial morphogenesis during 48 hours of in vitro development. The results demonstrate extensive cell mixing between adjacent but not alternate groups of mesodermal cells and a strict cranial-to-caudal distribution of the paraxial mesoderm to craniofacial structures. A two-segment periodicity similar to the origins of the branchial motor neurons and the distribution of the rhombencephalic neural crest cells was observed as the paraxial mesoderm migrates during formation of the first three branchial arches. The paraxial mesoderm colonises the mesenchymal core of the branchial arches, consistent with the location of the muscle plates. A dorsoventral regionalisation of cell fate similar to that of the somitic mesoderm is also found. This suggests evolution has conserved the fate of the murine cranial paraxial mesoderm as a multiprogenitor population which displays a predominantly myogenic fate. Heterotopic transplantation of cells to different regions of the cranial mesoderm revealed no discernible restriction in cell potency in the craniocaudal axis, reflecting considerable plasticity in the developmental fate of the cranial mesoderm at least at the time of experimentation. The distribution of the different groups of cranial mesoderm matches closely with that of the cranial neural crest cells suggesting the two cell populations may share a common segmental origin and similar destination.
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Hacker, A., and S. Guthrie. "A distinct developmental programme for the cranial paraxial mesoderm in the chick embryo." Development 125, no. 17 (September 1, 1998): 3461–72. http://dx.doi.org/10.1242/dev.125.17.3461.
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Cells of the cranial paraxial mesoderm give rise to parts of the skull and muscles of the head. Some mesoderm cells migrate from locations close to the hindbrain into the branchial arches where they undergo muscle differentiation. We have characterised these migratory pathways in chick embryos either by DiI-labelling cells before migration or by grafting quail cranial paraxial mesoderm orthotopically. These experiments demonstrate that depending on their initial rostrocaudal position, cranial paraxial mesoderm cells migrate to fill the core of specific branchial arches. A survey of the expression of myogenic genes showed that the myogenic markers Myf5, MyoD and myogenin were expressed in branchial arch muscle, but at comparatively late stages compared with their expression in the somites. Pax3 was not expressed by myogenic cells that migrate into the branchial arches despite its expression in migrating precursors of limb muscles. In order to test whether segmental plate or somitic mesoderm has the ability to migrate in a cranial location, we grafted quail trunk mesoderm into the cranial paraxial mesoderm region. While segmental plate mesoderm cells did not migrate into the branchial arches, somitic cells were capable of migrating and were incorporated into the branchial arch muscle mass. Grafted somitic cells in the vicinity of the neural tube maintained expression of the somitic markers Pax3, MyoD and Pax1. By contrast, ectopic somitic cells located distal to the neural tube and in the branchial arches did not express Pax3. These data imply that signals in the vicinity of the hindbrain and branchial arches act on migrating myogenic cells to influence their gene expression and developmental pathways.
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Kitajima, S., A. Takagi, T. Inoue, and Y. Saga. "MesP1 and MesP2 are essential for the development of cardiac mesoderm." Development 127, no. 15 (August 1, 2000): 3215–26. http://dx.doi.org/10.1242/dev.127.15.3215.
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The transcription factors, MesP1 and MesP2, sharing an almost identical bHLH motif, have an overlapping expression pattern during gastrulation and somitogenesis. Inactivation of the Mesp1 gene results in abnormal heart morphogenesis due to defective migration of heart precursor cells, but somitogenesis is not disrupted because of normal expression of the Mesp2 gene. To understand the cooperative functions of MesP1 and MesP2, either a deletion or sequential gene targeting strategy was employed to inactivate both genes. The double-knockout (dKO) embryos died around 9.5 days postcoitum (dpc) without developing any posterior structures such as heart, somites or gut. The major defect in this double-knockout embryo was the apparent lack of any mesodermal layer between the endoderm and ectoderm. The abnormal accumulation of cells in the primitive streak indicates a defect in the migratory activity of mesodermal cells. Molecular markers employed to characterize the phenotype revealed a lack of the cranio-cardiac and paraxial mesoderm. However, the axial mesoderm, as indicated by brachyury (T) expression, was initially generated but anterior extension was halted after 8.5 dpc. Interestingly, a headfold-like structure developed with right anterior-posterior polarity; however, the embryos lacked any posterior neural properties. The persistent and widely distributed expression of Cerberus-like-1(Cer1), Lim1 and Otx2 in the anterior endoderm might be responsible for the maintenance of anterior neural marker expression. We also performed a chimera analysis to further study the functions of MesP1 and MesP2 in the development of mesodermal derivatives. In the chimeric embryos, dKO cells were scarcely observed in the anterior-cephalic and heart mesoderm, but they did contribute to the formation of the somites, notochord and gut. These results strongly indicate that the defect in the cranial-cardiac mesoderm is cell-autonomous, whereas the defect in the paraxial mesoderm is a non-cell-autonomous secondary consequence.
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Bildsoe, Heidi, Xiaochen Fan, Emilie E. Wilkie, Ator Ashoti, Vanessa J. Jones, Melinda Power, Jing Qin, Junwen Wang, Patrick P. L. Tam, and David A. F. Loebel. "Dataset of TWIST1-regulated genes in the cranial mesoderm and a transcriptome comparison of cranial mesoderm and cranial neural crest." Data in Brief 9 (December 2016): 372–75. http://dx.doi.org/10.1016/j.dib.2016.09.001.
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Horáček, Ivan, Robert Cerny, and Lennart Olsson. "The Trabecula cranii: development and homology of an enigmatic vertebrate head structure." Animal Biology 56, no. 4 (2006): 503–18. http://dx.doi.org/10.1163/157075606778967801.
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AbstractThe vertebrate cranium consists of three parts: neuro-, viscero- and dermatocranium, which differ in both developmental and phylogenetic origin. Traditionally, developmental origin has been used as a criterion for homology, but this becomes problematic when skull elements such as the parietal bone are now shown, by modern fate-mapping studies, to have different developmental origins in different groups of tetrapods. This indicates a flexibility of developmental programmes and regulatory pathways which has probably been very important in cranial evolution. The trabecula cranii is an intriguing cranial element in the anterior cranial base in vertebrates. It forms a viscerocranial part of the neurocranium and is believed to be neural crest-derived in gnathostomes, but a similarly named structure in lampreys has been shown to have a mesodermal origin. Topographically, this trabecula seems to be homologous to the gnathostome trabecula cranii, and might also have the same function: to form a border between adjacent morphogenetic domains, to constrain and redirect growth of both brain and stomodeum and thus to refine developmental schedules of both. We suggest that such a border zone can recruit cells from either the mesoderm (as in the lamprey) or from the neural crest (as in the gnathostomes investigated), and still retain its homology. In our view, the trabecula is an interface element that integrates the respective divergent morphogenetics programs of the preotic head into a balanced unit; we suggest that such a definition can be used to define "the sameness" of this element throughout vertebrates.
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Kinder, S. J., T. E. Tsang, G. A. Quinlan, A. K. Hadjantonakis, A. Nagy, and P. P. Tam. "The orderly allocation of mesodermal cells to the extraembryonic structures and the anteroposterior axis during gastrulation of the mouse embryo." Development 126, no. 21 (November 1, 1999): 4691–701. http://dx.doi.org/10.1242/dev.126.21.4691.
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The prospective fate of cells in the primitive streak was examined at early, mid and late stages of mouse gastrula development to determine the order of allocation of primitive streak cells to the mesoderm of the extraembryonic membranes and to the fetal tissues. At the early-streak stage, primitive streak cells contribute predominantly to tissues of the extraembryonic mesoderm as previously found. However, a surprising observation is that the erythropoietic precursors of the yolk sac emerge earlier than the bulk of the vitelline endothelium, which is formed continuously throughout gastrula development. This may suggest that the erythropoietic and the endothelial cell lineages may arise independently of one another. Furthermore, the extraembryonic mesoderm that is localized to the anterior and chorionic side of the yolk sac is recruited ahead of that destined for the posterior and amnionic side. For the mesodermal derivatives in the embryo, those destined for the rostral structures such as heart and forebrain mesoderm ingress through the primitive streak early during a narrow window of development. They are then followed by those for the rest of the cranial mesoderm and lastly the paraxial and lateral mesoderm of the trunk. Results of this study, which represent snapshots of the types of precursor cells in the primitive streak, have provided a better delineation of the timing of allocation of the various mesodermal lineages to specific compartments in the extraembryonic membranes and different locations in the embryonic anteroposterior axis.
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Maddin, Hillary C., Nadine Piekarski, Elizabeth M. Sefton, and James Hanken. "Homology of the cranial vault in birds: new insights based on embryonic fate-mapping and character analysis." Royal Society Open Science 3, no. 8 (August 2016): 160356. http://dx.doi.org/10.1098/rsos.160356.
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Bones of the cranial vault appear to be highly conserved among tetrapod vertebrates. Moreover, bones identified with the same name are assumed to be evolutionarily homologous. However, recent developmental studies reveal a key difference in the embryonic origin of cranial vault bones between representatives of two amniote lineages, mammals and birds, thereby challenging this view. In the mouse, the frontal is derived from cranial neural crest (CNC) but the parietal is derived from mesoderm, placing the CNC–mesoderm boundary at the suture between these bones. In the chicken, this boundary is located within the frontal. This difference and related data have led several recent authors to suggest that bones of the avian cranial vault are misidentified and should be renamed. To elucidate this apparent conflict, we fate-mapped CNC and mesoderm in axolotl to reveal the contributions of these two embryonic cell populations to the cranial vault in a urodele amphibian. The CNC–mesoderm boundary in axolotl is located between the frontal and parietal bones, as in the mouse but unlike the chicken. If, however, the avian frontal is regarded instead as a fused frontal and parietal (i.e. frontoparietal) and the parietal as a postparietal, then the cranial vault of birds becomes developmentally and topologically congruent with those of urodeles and mammals. This alternative hypothesis of cranial vault homology is also phylogenetically consistent with data from the tetrapod fossil record, where frontal, parietal and postparietal bones are present in stem lineages of all extant taxa, including birds. It further implies that a postparietal may be present in most non-avian archosaurs, but fused to the parietal or supraoccipital as in many extant mammals.
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Trainor, P. A., and P. P. Tam. "Cranial paraxial mesoderm and neural crest cells of the mouse embryo: co-distribution in the craniofacial mesenchyme but distinct segregation in branchial arches." Development 121, no. 8 (August 1, 1995): 2569–82. http://dx.doi.org/10.1242/dev.121.8.2569.
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The spatial distribution of the cranial paraxial mesoderm and the neural crest cells during craniofacial morphogenesis of the mouse embryo was studied by micromanipulative cell grafting and cell labelling. Results of this study show that the paraxial mesoderm and neural crest cells arising at the same segmental position share common destinations. Mesodermal cells from somitomeres I, III, IV and VI were distributed to the same craniofacial tissues as neural crest cells of the forebrain, the caudal midbrain, and the rostral, middle and caudal hindbrains found respectively next to these mesodermal segments. This finding suggests that a basic meristic pattern is established globally in the neural plate ectoderm and paraxial mesoderm during early mouse development. Cells from these two sources mixed extensively in the peri-ocular, facial, periotic and cervical mesenchyme. However, within the branchial arches a distinct segregation of these two cell populations was discovered. Neural crest cells colonised the periphery of the branchial arches and enveloped the somitomere-derived core tissues on the rostral, lateral and caudal sides of the arch. Such segregation of cell populations in the first three branchial arches is apparent at least until the 10.5-day hindlimb bud stage and could be important for the patterning of the skeletal and myogenic derivatives of the arches.
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Noden, Drew M. "Interactions and fates of avian craniofacial mesenchyme." Development 103, Supplement (September 1, 1988): 121–40. http://dx.doi.org/10.1242/dev.103.supplement.121.
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Craniofacial mesenchyme is composed of three mesodermal populations – prechordal plate, lateral mesoderm and paraxial mesoderm, which includes the segmented occipital somites and the incompletely segmented somitomeres – and the neural crest. This paper outlines the fates of each of these, as determined using quail–chick chimaeras, and presents similarities and differences between these cephalic populations and their counterparts in the trunk. Prechordal and paraxial mesodermal populations are the sources of all voluntary muscles of the head. The latter also provides most of the connective precursors of the calvaria, occipital, otic–parietal and basisphenoid tissues. Lateral mesoderm is the source of peripharyngeal connective tissues; the most rostral skeletal tissues it forms are the laryngeal and tracheal cartilages. When migrating neural crest cells encounter segmented paraxial mesoderm (occipital and trunk somites), most move into the region between the dermamyotome and sclerotome in the cranial half of each somite. In contrast, most cephalic crest cells migrate superficial to somitomeres. There is, however, a small subpopulation of the head crest that invades somitomeric mesoderm. These cells subsequently segregate presumptive myogenic precursors of visceral arch voluntary muscles from underlying mesenchyme. In the neurula-stage avian embryo, all paraxial and lateral mesodermal populations contain precursors of vascular endothelial cells, which can be detected in chimaeric embryos using anti-quail endothelial antibodies. Some of these angioblasts differentiate in situ, contributing directly to pre-existing vessels or forming isolated, nonpatent, cords that subsequently vesiculate and fuse with nearby vessels. Many angioblasts migrate in all directions, invading embryonic mesenchymal and epithelial tissues and participating in new blood vessel formation in distant sites. The interactions leading to proper spatial patterning of craniofacial skeletal, muscular, vascular and peripheral neural tissues has been studied by performing heterotopic transplants of each of these mesodermal and neural crest populations. The results consistently indicate that connective tissue precursors, regardless of their origin, contain spatial information used by the precursors of muscles and blood vessels and by outgrowing peripheral nerves. Some of these connective tissue precursors (e.g. the neural crest, paraxial mesoderm) acquire their spatial programming while in association with the central nervous system or developing sensory epithelia (e.g. otic, optic, nasal epithelia).
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Vyas, Bhakti, Nitya Nandkishore, and Ramkumar Sambasivan. "Vertebrate cranial mesoderm: developmental trajectory and evolutionary origin." Cellular and Molecular Life Sciences 77, no. 10 (November 13, 2019): 1933–45. http://dx.doi.org/10.1007/s00018-019-03373-1.
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Gopalakrishnan, Swetha, Glenda Comai, Ramkumar Sambasivan, Alexandre Francou, Robert G. Kelly, and Shahragim Tajbakhsh. "A Cranial Mesoderm Origin for Esophagus Striated Muscles." Developmental Cell 34, no. 6 (September 2015): 694–704. http://dx.doi.org/10.1016/j.devcel.2015.07.003.
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Lescroart, Fabienne, Wissam Hamou, Alexandre Francou, Magali Théveniau-Ruissy, Robert G. Kelly, and Margaret Buckingham. "Clonal analysis reveals a common origin between nonsomite-derived neck muscles and heart myocardium." Proceedings of the National Academy of Sciences 112, no. 5 (January 20, 2015): 1446–51. http://dx.doi.org/10.1073/pnas.1424538112.
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Neck muscles constitute a transition zone between somite-derived skeletal muscles of the trunk and limbs, and muscles of the head, which derive from cranial mesoderm. The trapezius and sternocleidomastoid neck muscles are formed from progenitor cells that have expressed markers of cranial pharyngeal mesoderm, whereas other muscles in the neck arise from Pax3-expressing cells in the somites. Mef2c-AHF-Cre genetic tracing experiments and Tbx1 mutant analysis show that nonsomitic neck muscles share a gene regulatory network with cardiac progenitor cells in pharyngeal mesoderm of the second heart field (SHF) and branchial arch-derived head muscles. Retrospective clonal analysis shows that this group of neck muscles includes laryngeal muscles and a component of the splenius muscle, of mixed somitic and nonsomitic origin. We demonstrate that the trapezius muscle group is clonally related to myocardium at the venous pole of the heart, which derives from the posterior SHF. The left clonal sublineage includes myocardium of the pulmonary trunk at the arterial pole of the heart. Although muscles derived from the first and second branchial arches also share a clonal relationship with different SHF-derived parts of the heart, neck muscles are clonally distinct from these muscles and define a third clonal population of common skeletal and cardiac muscle progenitor cells within cardiopharyngeal mesoderm. By linking neck muscle and heart development, our findings highlight the importance of cardiopharyngeal mesoderm in the evolution of the vertebrate heart and neck and in the pathophysiology of human congenital disease.
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Melton, K., K. Zueckert-Gaudenz, J. Griffith, and P. Trainor. "Characterizing The Early Cranial Mesoderm: Development of The Endothelium." Pediatric Research 56, no. 4 (October 2004): 668. http://dx.doi.org/10.1203/00006450-200410000-00030.
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Noden, Drew M., and Paul A. Trainor. "Relations and interactions between cranial mesoderm and neural crest populations." Journal of Anatomy 207, no. 5 (November 2, 2005): 575–601. http://dx.doi.org/10.1111/j.1469-7580.2005.00473.x.
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Yoshioka, Kiyoshi, Hiroshi Nagahisa, Fumihito Miura, Hiromitsu Araki, Yasutomi Kamei, Yasuo Kitajima, Daiki Seko, et al. "Hoxa10 mediates positional memory to govern stem cell function in adult skeletal muscle." Science Advances 7, no. 24 (June 2021): eabd7924. http://dx.doi.org/10.1126/sciadv.abd7924.
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Muscle stem cells (satellite cells) are distributed throughout the body and have heterogeneous properties among muscles. However, functional topographical genes in satellite cells of adult muscle remain unidentified. Here, we show that expression of Homeobox-A (Hox-A) cluster genes accompanied with DNA hypermethylation of the Hox-A locus was robustly maintained in both somite-derived muscles and their associated satellite cells in adult mice, which recapitulates their embryonic origin. Somite-derived satellite cells were clearly separated from cells derived from cranial mesoderm in Hoxa10 expression. Hoxa10 inactivation led to genomic instability and mitotic catastrophe in somite-derived satellite cells in mice and human. Satellite cell–specific Hoxa10 ablation in mice resulted in a decline in the regenerative ability of somite-derived muscles, which were unobserved in cranial mesoderm–derived muscles. Thus, our results show that Hox gene expression profiles instill the embryonic history in satellite cells as positional memory, potentially modulating region-specific pathophysiology in adult muscles.
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Anggraeni, Yessy Mulyanur, Bambang Rahardjo, and Indriati Dwi Rahayu. "Pengaruh Pemberian Ekstrak Kulit Buah Manggis (Garcinia mangostana L.) Menghambat Flexi Cranial Embrio Ayam Umur 48 Jam." Journal of Issues in Midwifery 4, no. 3 (December 22, 2020): 122–30. http://dx.doi.org/10.21776/ub.joim.2020.004.03.3.
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Embryonic development forms three layers of germinativum that is endoderm, mesoderm and ectoderm. At the beginning of intrauterine fetus exchange of substances through diffusion, but in line with the development of the embryo, nutrition is not obtained through diffusion alone. Endoderm lining mesoderm cells will then be formed angioblasts as an early sign of vascularity. In the development of flexi cranial can be known from the development of the brain and heart which is characterized by bending the head of the embryo and decreased heart from the cranial down. The development of a normal vascular system will have an effect on organogenesis and morphogesis processes. If there are disturbances in the process of growth and development at that stage can cause congenital abnormalities. Xanthones mangosteen peel is rich in benefits, but in research on the effects of xanthones on embryos is still very limited and has not been able to explain their effects on the condition of the fetus. The study was conducted with the aim to determine the effect of mangosteen peel extract inhibiting the flexi cranial of 48 hours chicken embryos using doses of 100 µg/mL, 150 µg/mL and 200 µg/mL. Mangosteen peel extract is injected into chicken eggs less than 7 days after oviposition then incubated for 48 hours. The results showed that mangosteen peel extract inhibited flexi cranial of chicken embryos with Chi-Square test results (p = 0.002). The conclusion of the study was that exposure to mangosteen peel extract inhibited flexi cranial and gave significant results.
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Ruiz i Altaba, A. "Neural expression of the Xenopus homeobox gene Xhox3: evidence for a patterning neural signal that spreads through the ectoderm." Development 108, no. 4 (April 1, 1990): 595–604. http://dx.doi.org/10.1242/dev.108.4.595.
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The Xenopus laevis homeobox gene Xhox3 is expressed in the axial mesoderm of gastrula and neurula stage embryos. By the late neurula-early tailbud stage, mesodermal expression is no longer detectable and expression appears in the growing tailbud and in neural tissue. In situ hybridization analysis of the expression of Xhox3 in neural tissue shows that it is restricted within the neural tube and the cranial neural crest during the tailbud-early tadpole stages. In late tadpole stages, Xhox3 is only expressed in the mid/hindbrain area and can therefore be considered a marker of anterior neural development. To investigate the mechanism responsible for the anterior-posterior (A-P) regionalization of the neural tissue, the expression of Xhox3 has been analysed in total exogastrula. In situ hybridization analyses of exogastrulated embryos show that Xhox3 is expressed in the apical ectoderm of total exogastrulae, a region that develops in the absence of anterior axial mesoderm. The results provide further support for the existence of a neuralizing signal, which originates from the organizer region and spreads through the ectoderm. Moreover, the data suggest that this neural signal also has a role in A-P patterning the neural ectoderm.
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Hallett, Shawn A., Wanida Ono, Renny T. Franceschi, and Noriaki Ono. "Cranial Base Synchondrosis: Chondrocytes at the Hub." International Journal of Molecular Sciences 23, no. 14 (July 15, 2022): 7817. http://dx.doi.org/10.3390/ijms23147817.
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The cranial base is formed by endochondral ossification and functions as a driver of anteroposterior cranial elongation and overall craniofacial growth. The cranial base contains the synchondroses that are composed of opposite-facing layers of resting, proliferating and hypertrophic chondrocytes with unique developmental origins, both in the neural crest and mesoderm. In humans, premature ossification of the synchondroses causes midfacial hypoplasia, which commonly presents in patients with syndromic craniosynostoses and skeletal Class III malocclusion. Major signaling pathways and transcription factors that regulate the long bone growth plate—PTHrP–Ihh, FGF, Wnt, BMP signaling and Runx2—are also involved in the cranial base synchondrosis. Here, we provide an updated overview of the cranial base synchondrosis and the cell population within, as well as its molecular regulation, and further discuss future research opportunities to understand the unique function of this craniofacial skeletal structure.
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Kinder, Simon J., Tania E. Tsang, Maki Wakamiya, Hiroshi Sasaki, Richard R. Behringer, Andras Nagy, and Patrick P. L. Tam. "The organizer of the mouse gastrula is composed of a dynamic population of progenitor cells for the axial mesoderm." Development 128, no. 18 (September 15, 2001): 3623–34. http://dx.doi.org/10.1242/dev.128.18.3623.
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An organizer population has been identified in the anterior end of the primitive streak of the mid-streak stage embryo, by the expression of Hnf3β, GsclacZ and Chrd, and the ability of these cells to induce a second neural axis in the host embryo. This cell population can therefore be regarded as the mid-gastrula organizer and, together with the early-gastrula organizer and the node, constitute the organizer of the mouse embryo at successive stages of development. The profile of genetic activity and the tissue contribution by cells in the organizer change during gastrulation, suggesting that the organizer may be populated by a succession of cell populations with different fates. Fine mapping of the epiblast in the posterior region of the early-streak stage embryo reveals that although the early-gastrula organizer contains cells that give rise to the axial mesoderm, the bulk of the progenitors of the head process and the notochord are localized outside the early gastrula organizer. In the mid-gastrula organizer, early gastrula organizer derived cells that are fated for the prechordal mesoderm are joined by the progenitors of the head process that are recruited from the epiblast previously anterior to the early gastrula organizer. Cells that are fated for the head process move anteriorly from the mid-gastrula organizer in a tight column along the midline of the embryo. Other mid-gastrula organizer cells join the expanding mesodermal layer and colonize the cranial and heart mesoderm. Progenitors of the trunk notochord that are localized in the anterior primitive streak of the mid-streak stage embryo are later incorporated into the node. The gastrula organizer is therefore composed of a constantly changing population of cells that are allocated to different parts of the axial mesoderm.
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McLennan, Rebecca, Caleb M. Bailey, Linus J. Schumacher, Jessica M. Teddy, Jason A. Morrison, Jennifer C. Kasemeier-Kulesa, Lauren A. Wolfe, et al. "DAN (NBL1) promotes collective neural crest migration by restraining uncontrolled invasion." Journal of Cell Biology 216, no. 10 (August 15, 2017): 3339–54. http://dx.doi.org/10.1083/jcb.201612169.
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Neural crest cells are both highly migratory and significant to vertebrate organogenesis. However, the signals that regulate neural crest cell migration remain unclear. In this study, we test the function of differential screening-selected gene aberrant in neuroblastoma (DAN), a bone morphogenetic protein (BMP) antagonist we detected by analysis of the chick cranial mesoderm. Our analysis shows that, before neural crest cell exit from the hindbrain, DAN is expressed in the mesoderm, and then it becomes absent along cell migratory pathways. Cranial neural crest and metastatic melanoma cells avoid DAN protein stripes in vitro. Addition of DAN reduces the speed of migrating cells in vivo and in vitro, respectively. In vivo loss of function of DAN results in enhanced neural crest cell migration by increasing speed and directionality. Computer model simulations support the hypothesis that DAN restrains cell migration by regulating cell speed. Collectively, our results identify DAN as a novel factor that inhibits uncontrolled neural crest and metastatic melanoma invasion and promotes collective migration in a manner consistent with the inhibition of BMP signaling.
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Dastjerdi, Akbar, Lesley Robson, Rebecca Walker, Julia Hadley, Zhen Zhang, Marc Rodriguez-Niedenführ, Paris Ataliotis, Antonio Baldini, Peter Scambler, and Philippa Francis-West. "Tbx1 regulation of myogenic differentiation in the limb and cranial mesoderm." Developmental Dynamics 236, no. 2 (2007): 353–63. http://dx.doi.org/10.1002/dvdy.21010.
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Kuratani, Shigeru, and Shinichi Aizawa. "Patterning of the cranial nerves in the chick embryo is dependent on cranial mesoderm and rhombomeric metamerism." Development, Growth and Differentiation 37, no. 6 (December 1995): 717–31. http://dx.doi.org/10.1046/j.1440-169x.1995.t01-5-00010.x.
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Jacobson, Antone G. "Somitomeres: mesodermal segments of vertebrate embryos." Development 104, Supplement (October 1, 1988): 209–20. http://dx.doi.org/10.1242/dev.104.supplement.209.
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Well before the somites form, the paraxial mesoderm of vertebrate embryos is segmented into somitomeres. When newly formed, somitomeres are patterned arrays of mesenchymal cells, arranged into squat, bilaminar discs. The dorsal and ventral faces of these discs are composed of concentric rings of cells. Somitomeres are formed along the length of the embryo during gastrulation, and in the segmental plate and tail bud at later stages. They form in strict cranial to caudal order. They appear in bilateral pairs, just lateral to Hensen's node in the chick embryo. When the nervous system begins to form, the brain parts and neuromeres are in a consistent relationship to the somitomeres. Somitomeres first appear in the head, and the cranial somitomeres do not become somites, but disperse to contribute to the head the same cell types contributed by somites in the trunk region. In the trunk and tail, somitomeres gradually condense and epithelialize to become somites. Models of vertebrate segmentation must now take into account the early presence of these new morphological units, the somitomeres. Somitomeres were discovered in the head of the chick embryo (Meier, 1979), with the use of stereo scanning electron microscopy. The old question of whether the heads of the craniates are segmented is now settled, at least for the paraxial mesoderm. Somitomeres have now been identified in the embryos of a chick, quail, mouse, snapping turtle, newt, anuran (Xenopus) and a teleost (the medaka). In all forms studied, the first pair of somitomeres abut the prosencephalon but caudal to that, for each tandem pair of somitomeres in the amniote and teleost, there is but one somitomere in the amphibia. The mesodermal segments of the shark embryo are arranged like those of the amphibia.
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Zovein, Ann C., Kirsten A. Turlo, Ryan M. Ponec, Maureen R. Lynch, Kevin C. Chen, Jennifer J. Hofmann, Timothy C. Cox, Judith C. Gasson, and M. Luisa Iruela-Arispe. "Vascular remodeling of the vitelline artery initiates extravascular emergence of hematopoietic clusters." Blood 116, no. 18 (November 4, 2010): 3435–44. http://dx.doi.org/10.1182/blood-2010-04-279497.
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Abstract The vitelline artery is a temporary structure that undergoes extensive remodeling during midgestation to eventually become the superior mesenteric artery (also called the cranial mesenteric artery, in the mouse). Here we show that, during this remodeling process, large clusters of hematopoietic progenitors emerge via extravascular budding and form structures that resemble previously described mesenteric blood islands. We demonstrate through fate mapping of vascular endothelium that these mesenteric blood islands are derived from the endothelium of the vitelline artery. We further show that the vitelline arterial endothelium and subsequent blood island structures originate from a lateral plate mesodermal population. Lineage tracing of the lateral plate mesoderm demonstrates contribution to all hemogenic vascular beds in the embryo, and eventually, all hematopoietic cells in the adult. The intraembryonic hematopoietic cell clusters contain viable, proliferative cells that exhibit hematopoietic stem cell markers and are able to further differentiate into myeloid and erythroid lineages. Vitelline artery–derived hematopoietic progenitor clusters appear between embryonic day 10 and embryonic day 10.75 in the caudal half of the midgut mesentery, but by embryonic day 11.0 are sporadically found on the cranial side of the midgut, thus suggesting possible extravascular migration aided by midgut rotation.
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Lee, J. E., J. Pintar, and A. Efstratiadis. "Pattern of the insulin-like growth factor II gene expression during early mouse embryogenesis." Development 110, no. 1 (September 1, 1990): 151–59. http://dx.doi.org/10.1242/dev.110.1.151.
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The mouse insulin-like growth factor II (IGF-II) gene encodes a polypeptide that plays a role in embryonic growth. We have examined the temporal and spatial pattern of expression of this gene in sections of the mouse conceptus between embryonic days 4.0 and 8.5 by in situ hybridization. Abundant IGF-II transcripts were detected in all the trophectodermal derivatives, after implantation. Labeling was then observed in primitive endoderm, but was transient and disappeared after formation of the yolk sac. Expression was next detected in extraembryonic mesoderm at the early primitive streak stage. Labeling in the embryo proper appeared first at the late primitive streak/neural plate stage in lateral mesoderm and in anterior-proximal cells located between the visceral endoderm and the most cranial region of the embryonic ectoderm. The position of the latter cells suggests that their descendants are likely to participate in the formation of the heart and the epithelium of the ventral and lateral walls of the foregut, where intense labeling was observed at the neural fold stage. Hybridization was also detected in cranial mesenchyme, including neural crest cells. The intensity of hybridization signal increased progressively in paraxial (presomitic and somitic) mesoderm, while declining in the ectoplacental cone. The neuroectoderm and surface ectoderm did not exhibit hybridization at any stage. Immunohistochemical analysis indicated co-localization of IGF-II transcripts, translated pre-pro-IGF-II, and the cognate IGF-II/mannose-6-phosphate receptor. These correlations are consistent with the hypothesis that IGF-II has an autocrine function.
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Goh, K. L., J. T. Yang, and R. O. Hynes. "Mesodermal defects and cranial neural crest apoptosis in alpha5 integrin-null embryos." Development 124, no. 21 (November 1, 1997): 4309–19. http://dx.doi.org/10.1242/dev.124.21.4309.
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Alpha5beta1 integrin is a cell surface receptor that mediates cell-extracellular matrix adhesions by interacting with fibronectin. Alpha5 subunit-deficient mice die early in gestation and display mesodermal defects; most notably, embryos have a truncated posterior and fail to produce posterior somites. In this study, we report on the in vivo effects of the alpha5-null mutation on cell proliferation and survival, and on mesodermal development. We found no significant differences in the numbers of apoptotic cells or in cell proliferation in the mesoderm of alpha5-null embryos compared to wild-type controls. These results suggest that changes in overall cell death or cell proliferation rates are unlikely to be responsible for the mesodermal deficits seen in the alpha5-null embryos. No increases in cell death were seen in alpha5-null embryonic yolk sac, amnion and allantois compared with wild-type, indicating that the mutant phenotype is not due to changes in apoptosis rates in these extraembryonic tissues. Increased numbers of dying cells were, however, seen in migrating cranial neural crest cells of the hyoid arch and in endodermal cells surrounding the omphalomesenteric artery in alpha5-null embryos, indicating that these subpopulations of cells are dependent on alpha5 integrin function for their survival. Mesodermal markers mox-1, Notch-1, Brachyury (T) and Sonic hedgehog (Shh) were expressed in the mutant embryos in a regionally appropriate fashion. Both T and Shh, however, showed discontinuous expression in the notochords of alpha5-null embryos due to (1) degeneration of the notochordal tissue structure, and (2) non-maintenance of gene expression. Consistent with the disorganization of notochordal signals in the alpha5-null embryos, reduced Pax-1 expression and misexpression of Pax-3 were observed. Anteriorly expressed HoxB genes were expressed normally in the alpha5-null embryos. However, expression of the posteriormost HoxB gene, Hoxb-9, was reduced in alpha5-null embryos. These results suggest that alpha5beta1-fibronectin interactions are not essential for the initial commitment of mesodermal cells, but are crucial for maintenance of mesodermal derivatives during postgastrulation stages and also for the survival of some neural crest cells.
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Begemann, Gerrit, Thomas F. Schilling, Gerd-Jörg Rauch, Robert Geisler, and Phillip W. Ingham. "The zebrafishnecklessmutation reveals a requirement forraldh2in mesodermal signals that pattern the hindbrain." Development 128, no. 16 (August 15, 2001): 3081–94. http://dx.doi.org/10.1242/dev.128.16.3081.
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We describe a new zebrafish mutation, neckless, and present evidence that it inactivates retinaldehyde dehydrogenase type 2, an enzyme involved in retinoic acid biosynthesis. neckless embryos are characterised by a truncation of the anteroposterior axis anterior to the somites, defects in midline mesendodermal tissues and absence of pectoral fins. At a similar anteroposterior level within the nervous system, expression of the retinoic acid receptor α and hoxb4 genes is delayed and significantly reduced. Consistent with a primary defect in retinoic acid signalling, some of these defects in neckless mutants can be rescued by application of exogenous retinoic acid. We use mosaic analysis to show that the reduction in hoxb4 expression in the nervous system is a non-cell autonomous effect, reflecting a requirement for retinoic acid signalling from adjacent paraxial mesoderm. Together, our results demonstrate a conserved role for retinaldehyde dehydrogenase type 2 in patterning the posterior cranial mesoderm of the vertebrate embryo and provide definitive evidence for an involvement of endogenous retinoic acid in signalling between the paraxial mesoderm and neural tube.
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Grenier, Julien, Marie-Aimée Teillet, Raphaëlle Grifone, Robert G. Kelly, and Delphine Duprez. "Relationship between Neural Crest Cells and Cranial Mesoderm during Head Muscle Development." PLoS ONE 4, no. 2 (February 9, 2009): e4381. http://dx.doi.org/10.1371/journal.pone.0004381.
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Tam, P. P. "Regionalisation of the mouse embryonic ectoderm: allocation of prospective ectodermal tissues during gastrulation." Development 107, no. 1 (September 1, 1989): 55–67. http://dx.doi.org/10.1242/dev.107.1.55.
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The regionalisation of cell fate in the embryonic ectoderm was studied by analyzing the distribution of graft-derived cells in the chimaeric embryo following grafting of wheat germ agglutinin—gold-labelled cells and culturing primitive-streak-stage mouse embryos. Embryonic ectoderm in the anterior region of the egg cylinder contributes to the neuroectoderm of the prosencephalon and mesencephalon. Cells in the distal lateral region give rise to the neuroectoderm of the rhombencephalon and the spinal cord. Embryonic ectoderm at the archenteron and adjacent to the middle region of the primitive streak contributes to the neuroepithelium of the spinal cord. The proximal-lateral ectoderm and the ectodermal cells adjacent to the posterior region of the primitive streak produce the surface ectoderm, the epidermal placodes and the cranial neural crest cells. Some labelled cells grafted to the anterior midline are found in the oral ectodermal lining, whereas cells from the archenteron are found in the notochord. With respect to mesodermal tissues, ectoderm at the archenteron and the distal-lateral region of the egg cylinder gives rise to rhombencephalic somitomeres, and the embryonic ectoderm adjacent to the primitive streak contributes to the somitic mesoderm and the lateral mesoderm. Based upon results of this and other grafting studies, a map of prospective ectodermal tissues in the embryonic ectoderm of the full-streak-stage mouse embryo is constructed.
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Clouthier, D. E., K. Hosoda, J. A. Richardson, S. C. Williams, H. Yanagisawa, T. Kuwaki, M. Kumada, R. E. Hammer, and M. Yanagisawa. "Cranial and cardiac neural crest defects in endothelin-A receptor-deficient mice." Development 125, no. 5 (March 1, 1998): 813–24. http://dx.doi.org/10.1242/dev.125.5.813.
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Neural crest cells arise in the dorsal aspect of the neural tube and migrate extensively to differentiate into a variety of neural and non-neural tissues. While interactions between neural crest cells and their local environments are required for the proper development of these tissues, little information is available about the molecular nature of the cell-cell interactions in cephalic neural crest development. Here we demonstrate that mice deficient for one type of endothelin receptor, ETA, mimic the human conditions collectively termed CATCH 22 or velocardiofacial syndrome, which include severe craniofacial deformities and defects in the cardiovascular outflow tract. We show that ETA receptor mRNA is expressed by the neural crest-derived ectomesenchymal cells of pharyngeal arches and cardiac outflow tissues, whereas ET-1 ligand mRNA is expressed by arch epithelium, paraxial mesoderm-derived arch core and the arch vessel endothelium. This suggests that paracrine interaction between neural crest-derived cells and both ectoderm and mesoderm is essential in forming the skeleton and connective tissue of the head. Further, we find that pharyngeal arch expression of goosecoid is absent in ETA receptor-deficient mice, placing the transcription factor as one of the possible downstream signals triggered by activation of the ETA receptor. These observations define a novel genetic pathway for inductive communication between cephalic neural crest cells and their environmental counterparts.
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Tribioli, C., and T. Lufkin. "The murine Bapx1 homeobox gene plays a critical role in embryonic development of the axial skeleton and spleen." Development 126, no. 24 (December 15, 1999): 5699–711. http://dx.doi.org/10.1242/dev.126.24.5699.
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Our previous studies in both mouse and human identified the Bapx1 homeobox gene, a member of the NK gene family, as one of the earliest markers for prechondrogenic cells that will subsequently undergo mesenchymal condensation, cartilage production and, finally, endochondral bone formation. In addition, Bapx1 is an early developmental marker for splanchnic mesoderm, consistent with a role in visceral mesoderm specification, a function performed by its homologue bagpipe, in Drosophila. The human homologue of Bapx1 has been identified and mapped to 4p16.1, a region containing loci for several skeletal diseases. Bapx1 null mice are affected by a perinatal lethal skeletal dysplasia and asplenia, with severe malformation or absence of specific bones of the vertebral column and cranial bones of mesodermal origin, with the most severely affected skeletal elements corresponding to ventral structures associated with the notochord. We provide evidence that the failure of the formation of skeletal elements in Bapx1 null embryos is a consequence of a failure of cartilage development, as demonstrated by downregulation of several molecular markers required for normal chondroblast differentiation (α 1(II) collagen, Fgfr3, Osf2, Indian hedgehog, Sox9), as well as a chondrocyte-specific alpha1 (II) collagen-lacZ transgene. The cartilage defects are correlated with failed differentiation of the sclerotome at the time when these cells are normally initiating chondrogenesis. Loss of Bapx1 is accompanied by an increase in apoptotic cell death in affected tissues, although cell cycling rates are unaltered.
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Siismets, Erica M., and Nan E. Hatch. "Cranial Neural Crest Cells and Their Role in the Pathogenesis of Craniofacial Anomalies and Coronal Craniosynostosis." Journal of Developmental Biology 8, no. 3 (September 9, 2020): 18. http://dx.doi.org/10.3390/jdb8030018.
Full textAbstract:
Craniofacial anomalies are among the most common of birth defects. The pathogenesis of craniofacial anomalies frequently involves defects in the migration, proliferation, and fate of neural crest cells destined for the craniofacial skeleton. Genetic mutations causing deficient cranial neural crest migration and proliferation can result in Treacher Collins syndrome, Pierre Robin sequence, and cleft palate. Defects in post-migratory neural crest cells can result in pre- or post-ossification defects in the developing craniofacial skeleton and craniosynostosis (premature fusion of cranial bones/cranial sutures). The coronal suture is the most frequently fused suture in craniosynostosis syndromes. It exists as a biological boundary between the neural crest-derived frontal bone and paraxial mesoderm-derived parietal bone. The objective of this review is to frame our current understanding of neural crest cells in craniofacial development, craniofacial anomalies, and the pathogenesis of coronal craniosynostosis. We will also discuss novel approaches for advancing our knowledge and developing prevention and/or treatment strategies for craniofacial tissue regeneration and craniosynostosis.
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Nishikawa, Misao, Hiroaki Sakamoto, Akira Hakuba, Naruhiko Nakanishi, and Yuichi Inoue. "Pathogenesis of Chiari malformation: a morphometric study of the posterior cranial fossa." Neurosurgical Focus 1, no. 5 (November 1996): E1. http://dx.doi.org/10.3171/foc.1996.1.5.1.
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To investigate overcrowding in the posterior cranial fossa as the pathogenesis of adult-type Chiari malformation, the authors studied the morphology of the brainstem and cerebellum within the posterior cranial fossa (neural structures consisting of the midbrain, pons, cerebellum, and medulla oblongata) as well as the base of the skull while taking into consideration their embryological development. Thirty patients with Chiari malformation and 50 normal control subjects were prospectively studied using neuroimaging. To estimate overcrowding, the authors used a "volume ratio" in which volume of the posterior fossa brain (consisting of the midbrain, pons, cerebellum, and medulla oblongata within the posterior cranial fossa) was placed in a ratio with the volume of the posterior fossa cranium encircled by bony and tentorial structures. Compared to the control group, in the Chiari group there was a significantly larger volume ratio, the two occipital enchondral parts (the exocciput and supraocciput) were significantly smaller, and the tentorium was pronouncedly steeper. There was no significant difference in the posterior fossa brain volume or in the axial lengths of the hindbrain (the brainstem and cerebellum). In six patients with basilar invagination the medulla oblongata was herniated, all three occipital enchondral parts (the basiocciput, exocciput, and supraocciput) were significantly smaller than in the control group, and the volume ratio was significantly larger than that in the Chiari group without basilar invagination. These results suggest that in adult-type Chiari malformation an underdeveloped occipital bone, possibly due to underdevelopment of the occipital somite originating from the paraxial mesoderm, induces overcrowding in the posterior cranial fossa, which contains the normally developed hindbrain. Basilar invagination is associated with a more severe downward herniation of the hindbrain due to the more severely underdeveloped occipital enchondrium, which further exacerbates overcrowding of the posterior cranial fossa.
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Nishikawa, Misao, Hiroaki Sakamoto, Akira Hakuba, Naruhiko Nakanishi, and Yuichi Inoue. "Pathogenesis of Chiari malformation: a morphometric study of the posterior cranial fossa." Journal of Neurosurgery 86, no. 1 (January 1997): 40–47. http://dx.doi.org/10.3171/jns.1997.86.1.0040.
Full textAbstract:
✓ To investigate overcrowding in the posterior cranial fossa as the pathogenesis of adult-type Chiari malformation, the authors studied the morphology of the brainstem and cerebellum within the posterior cranial fossa (neural structures consisting of the midbrain, pons, cerebellum, and medulla oblongata) as well as the base of the skull while taking into consideration their embryological development. Thirty patients with Chiari malformation and 50 normal control subjects were prospectively studied using neuroimaging. To estimate overcrowding, the authors used a “volume ratio” in which volume of the posterior fossa brain (consisting of the midbrain, pons, cerebellum, and medulla oblongata within the posterior cranial fossa) was placed in a ratio with the volume of the posterior fossa cranium encircled by bony and tentorial structures. Compared to the control group, in the Chiari group there was a significantly larger volume ratio, the two occipital enchondral parts (the exocciput and supraocciput) were significantly smaller, and the tentorium was pronouncedly steeper. There was no significant difference in the posterior fossa brain volume or in the axial lengths of the hindbrain (the brainstem and cerebellum). In six patients with basilar invagination the medulla oblongata was herniated, all three occipital enchondral parts (the basiocciput, exocciput, and supraocciput) were significantly smaller than in the control group, and the volume ratio was significantly larger than that in the Chiari group without basilar invagination. These results suggest that in adult-type Chiari malformation an underdeveloped occipital bone, possibly due to underdevelopment of the occipital somite originating from the paraxial mesoderm, induces overcrowding in the posterior cranial fossa, which contains the normally developed hindbrain. Basilar invagination is associated with a more severe downward herniation of the hindbrain due to the more severely underdeveloped occipital enchondrium, which further exacerbates overcrowding of the posterior cranial fossa.
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Barlow, L. A., and R. G. Northcutt. "Taste buds develop autonomously from endoderm without induction by cephalic neural crest or paraxial mesoderm." Development 124, no. 5 (March 1, 1997): 949–57. http://dx.doi.org/10.1242/dev.124.5.949.
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Although it had long been believed that embryonic taste buds in vertebrates were induced to differentiate by ingrowing nerve fibers, we and others have recently shown that embryonic taste buds can develop normally in the complete absence of innervation. This leads to the question of which tissues, if any, induce the formation of taste buds in oropharyngeal endoderm. We proposed that taste buds, like many specialized epithelial cells, might arise via an inductive interaction between the endodermal epithelial cells that line the oropharynx and the adjacent mesenchyme that is derived from both cephalic neural crest and paraxial mesoderm. Using complementary grafting and explant culture techniques, however, we have now found that well-differentiated taste buds will develop in tissue completely devoid of neural crest and paraxial mesoderm derivatives. When the presumptive oropharyngeal region was removed from salamander embryos prior to the onset of cephalic neural crest migration, taste buds developed in grafts and explants coincident with their appearance in intact control embryos. Similarly, explants from neurulae in which movement of paraxial mesoderm had not yet begun also developed taste buds after 9–12 days in vitro. We conclude that neither cranial neural crest nor paraxial mesoderm is responsible for the induction of embryonic taste buds. Surprisingly, the ability to develop taste buds late in embryonic development seems to be an intrinsic feature of the oropharyngeal endoderm that is determined by the completion of gastrulation.
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Schilling, T. F., C. Walker, and C. B. Kimmel. "The chinless mutation and neural crest cell interactions in zebrafish jaw development." Development 122, no. 5 (May 1, 1996): 1417–26. http://dx.doi.org/10.1242/dev.122.5.1417.
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During vertebrate development, neural crest cells are thought to pattern many aspects of head organization, including the segmented skeleton and musculature of the jaw and gills. Here we describe mutations at the gene chinless, chn, that disrupt the skeletal fates of neural crest cells in the head of the zebrafish and their interactions with muscle precursors. chn mutants lack neural-crest-derived cartilage and mesoderm-derived muscles in all seven pharyngeal arches. Fate mapping and gene expression studies demonstrate the presence of both undifferentiated cartilage and muscle precursors in mutants. However, chn blocks differentiation directly in neural crest, and not in mesoderm, as revealed by mosaic analyses. Neural crest cells taken from wild-type donor embryos can form cartilage when transplanted into chn mutant hosts and rescue some of the patterning defects of mutant pharyngeal arches. In these cases, cartilage only forms if neural crest is transplanted at least one hour before its migration, suggesting that interactions occur transiently in early jaw precursors. In contrast, transplanted cells in paraxial mesoderm behave according to the host genotype; mutant cells form jaw muscles in a wild-type environment. These results suggest that chn is required for the development of pharyngeal cartilages from cranial neural crest cells and subsequent crest signals that pattern mesodermally derived myocytes.
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Cho, Raymond I., and Alon Kahana. "Embryology of the Orbit." Journal of Neurological Surgery Part B: Skull Base 82, no. 01 (February 2021): 002–6. http://dx.doi.org/10.1055/s-0040-1722630.
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AbstractThe orbit houses and protects the ocular globe and the supporting structures, and occupies a strategic position below the anterior skull base and adjacent to the paranasal sinuses. Its embryologic origins are inextricably intertwined with those of the central nervous system, skull base, and face. Although the orbit contains important contributions from four germ cell layers (surface ectoderm, neuroectoderm, neural crest, and mesoderm), a significant majority originate from the neural crest cells. The bones of the orbit, face, and anterior cranial vault are mostly neural crest in origin. The majority of the bones of the skull base are formed through endochondral ossification, whereas the cranial vault is formed through intramembranous ossification. Familiarity with the embryology and fetal development of the orbit can aid in understanding its anatomy, as well as many developmental anomalies and pathologic conditions that affect the orbit.
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Trainor, Paul, and Robb Krumlauf. "Plasticity in mouse neural crest cells reveals a new patterning role for cranial mesoderm." Nature Cell Biology 2, no. 2 (January 14, 2000): 96–102. http://dx.doi.org/10.1038/35000051.
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P L Tam, Patrick, Xiaochen Fan, David A F Loebel, Heidi Bildsoe, Emilie E Wilkie, Jing Qin, and Junwen Wang. "Tissue interactions, cell signaling and transcriptional control in the cranial mesoderm during craniofacial development." AIMS Genetics 3, no. 1 (2016): 74–98. http://dx.doi.org/10.3934/genet.2016.1.74.
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Gillis, J. Andrew, Jens H. Fritzenwanker, and Christopher J. Lowe. "A stem-deuterostome origin of the vertebrate pharyngeal transcriptional network." Proceedings of the Royal Society B: Biological Sciences 279, no. 1727 (June 15, 2011): 237–46. http://dx.doi.org/10.1098/rspb.2011.0599.
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Hemichordate worms possess ciliated gills on their trunk, and the homology of these structures with the pharyngeal gill slits of chordates has long been a topic of debate in the fields of evolutionary biology and comparative anatomy. Here, we show conservation of transcription factor expression between the developing pharyngeal gill pores of the hemichordate Saccoglossus kowalevskii and the pharyngeal gill slit precursors (i.e. pharyngeal endodermal outpockets) of vertebrates. Transcription factors that are expressed in the pharyngeal endoderm, ectoderm and mesenchyme of vertebrates are expressed exclusively in the pharyngeal endoderm of S. kowalevskii . The pharyngeal arches and tongue bars of S. kowalevskii lack Tbx1 -expressing mesoderm, and are supported solely by an acellular collagenous endoskeleton and by compartments of the trunk coelom. Our findings suggest that hemichordate and vertebrate gills are homologous as simple endodermal outpockets from the foregut, and that much vertebrate pharyngeal complexity arose coincident with the incorporation of cranial paraxial mesoderm and neural crest-derived mesenchyme within pharyngeal arches along the chordate and vertebrate stems, respectively.
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Pandya, Manish R., Ghanshyam K. Gorvadiya, and Jeel A. Modesara. "Accessory fallopian tube –A rare anomaly." Indian Journal of Obstetrics and Gynecology Research 10, no. 1 (February 15, 2023): 88–90. http://dx.doi.org/10.18231/j.ijogr.2023.020.
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Accessory fallopian tube is a rare, congenital and developmental mullerian duct anomaly. The documented incidence is around 6-10% in women seeking for infertility treatment. We observed accessory fallopian tube in a patient during routine checking of operative field, ovaries and fallopian tube during caesarean section. Accessory fallopian tube is congenital anomaly which is attached with ampullary part of main fallopian tube. Accessory fallopian tube is common site for pyosalpinx, hydrosalpinx, cystic swelling and torsion which can lead to infertility and other complications. The ovum released by ovary may also captured by accessory fallopian tube which can lead to infertility or ectopic pregnancy. During the embryological development of female urogenital system, development of fallopian tube occurs from cranial un fused portion of mullerian ducts. This duct is derived from mesoderm, the middle layer of germ cell layers in the embryo. Bifurcation of cranial end of mullerian duct results in accessory fallopian tube.
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Bildsoe, Heidi, Xiaochen Fan, Emilie E. Wilkie, Ator Ashoti, Vanessa J. Jones, Melinda Power, Jing Qin, Junwen Wang, Patrick P. L. Tam, and David A. F. Loebel. "Transcriptional targets of TWIST1 in the cranial mesoderm regulate cell-matrix interactions and mesenchyme maintenance." Developmental Biology 418, no. 1 (October 2016): 189–203. http://dx.doi.org/10.1016/j.ydbio.2016.08.016.
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Deckelbaum, R. A., G. Holmes, Z. Zhao, C. Tong, C. Basilico, and C. A. Loomis. "Regulation of cranial morphogenesis and cell fate at the neural crest-mesoderm boundary by engrailed 1." Development 139, no. 7 (March 6, 2012): 1346–58. http://dx.doi.org/10.1242/dev.076729.
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Chan, W. Y., and P. P. Tam. "A morphological and experimental study of the mesencephalic neural crest cells in the mouse embryo using wheat germ agglutinin-gold conjugate as the cell marker." Development 102, no. 2 (February 1, 1988): 427–42. http://dx.doi.org/10.1242/dev.102.2.427.
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The distribution of the mesencephalic neural crest cells in the mouse embryo was studied by mapping the colonization pattern of WGA-gold labelled cells following specific labelling of the neuroectoderm and grafting of presumptive neural crest cells to orthotopic and heterotopic sites. The result showed that (1) there were concomitant changes in the morphology of the neural crest epithelium during the formation of neural crest cells, in the 4- to 7-somite-stage embryos, (2) the neural crest cells were initially confined to the lateral subectodermal region of the cranial mesenchyme and there was minimal mixing with the paraxial mesoderm underneath the neural plate, (3) labelled cells from the presumptive crest region colonized the lateral cranio-facial mesenchyme, the developing trigeminal ganglion and the pharyngeal arch, (4) the formation of neural crest cells was facilitated by the focal disruption of the basal lamina and the cell-cell interaction specific to the neural crest site and (5) the trigeminal ganglion was colonized not only by neural crest cells but also by cells from the ectodermal placode.
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Dmytrenko, R., O. Tsyhykalo, and I. Makarchuk. "EMBRYOLOGICAL PREREQUISITES FOR HUMAN CRANIAL DEVELOPMENTAL DEFFECTS." Bukovinian Medical Herald 28, no. 1 (109) (March 28, 2024): 123–31. http://dx.doi.org/10.24061/2413-0737.28.1.109.2024.20.
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The purpose of the work is to find out the embryological prerequisites and the time of the possible occurrence of malformations and congenital deformations of the human skull.Results. The growth and enlargement of the neurocranium is largely determined by the growth of the brain due to their close syntopy. By the end of the second year, the bones are connected by sutures. The neurocranium is embryologically divided into the vault, which is formed by membranous ossification, and the basis cranii, the bones of which are formed by cartilaginous osteogenesis. The initial development of the neurocranium depends on the formation of the brain and its surrounding membranes. The source of the germ of the outer layer is the mesoderm and ectomesenchyme of the neural crest, soon it is divided into the inner layer – endomeninx and outer – ectomeninx. The latter is further divided into the outer osteogenic layer, in which the ossification centers form the bones of the skull, and the inner layer of the dura mater. The centers of ossification form the frontal, parietal, occipital and temporal bones, and the intermediate areas form fibrous sutures and fontanelles. Usually, the sutures are joined at the end of the second year of life. Conclusions. Congenital deformities of the cerebral part of the skull are morphological manifestations of numerous hereditary syndromes and/or metabolic, teratogenic effects, lysosomal storage diseases, brain malformations, unfavorable factors during the fetal period of development: restriction of the intrauterine environment, weak muscle tone, torticollis, clavicle fracture, cervical spine anomalies, multiple pregnancy and bone mineralization disorders. For the differential diagnosis of congenital defects of the skull, along with the use of diagnostic three-dimensional medical imaging, it is necessary to carry out genetic screening.
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Sechrist, J., G. N. Serbedzija, T. Scherson, S. E. Fraser, and M. Bronner-Fraser. "Segmental migration of the hindbrain neural crest does not arise from its segmental generation." Development 118, no. 3 (July 1, 1993): 691–703. http://dx.doi.org/10.1242/dev.118.3.691.
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The proposed pathways of chick cranial neural crest migration and their relationship to the rhombomeres of the hindbrain have been somewhat controversial, with differing results emerging from grafting and DiI-labelling analyses. To resolve this discrepancy, we have examined cranial neural crest migratory pathways using the combination of neurofilament immunocytochemistry, which recognizes early hindbrain neural crest cells, and labelling with the vital dye, DiI. Neurofilament-positive cells with the appearance of premigratory and early-migrating neural crest cells were noted at all axial levels of the hindbrain. At slightly later stages, neural crest cell migration in this region appeared segmented, with no neural crest cells obvious in the mesenchyme lateral to rhombomere 3 (r3) and between the neural tube and the otic vesicle lateral to r5. Focal injections of DiI at the levels of r3 and r5 demonstrated that both of these rhombomeres generated neural crest cells. The segmental distribution of neural crest cells resulted from the DiI-labelled cells that originated in r3 and r5 deviating rostrally or caudally and failing to enter the adjacent preotic mesoderm or otic vesicle region. The observation that neural crest cells originating from r3 and r5 avoided specific neighboring domains raises the intriguing possibility that, as in the trunk, extrinsic factors play a major role in the axial patterning of the cranial neural crest and the neural crest-derived peripheral nervous system.
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Kalcheim, C., and M. A. Teillet. "Consequences of somite manipulation on the pattern of dorsal root ganglion development." Development 106, no. 1 (May 1, 1989): 85–93. http://dx.doi.org/10.1242/dev.106.1.85.
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We have investigated dorsal root ganglion formation, in the avian embryo, as a function of the composition of the paraxial somitic mesoderm. Three or four contiguous young somites were unilaterally removed from chick embryos and replaced by multiple cranial or caudal half-somites from quail embryos. Migration of neural crest cells and formation of DRG were subsequently visualized both by the HNK-1 antibody and the Feulgen nuclear stain. At advanced migratory stages (as defined by Teillet et al. Devl Biol. 120, 329–347 1987), neural crest cells apposed to the dorsolateral faces of the neural tube were distributed in a continuous, nonsegmented pattern that was indistinguishable on unoperated sides and on sides into which either half of the somites had been grafted. In contrast, ventrolaterally, neural crest cells were distributed segmentally close to the neural tube and within the cranial part of each normal sclerotome, whereas they displayed a nonsegmental distribution when the graft involved multiple cranial half-somites or were virtually absent when multiple caudal half-somites had been implanted. In spite of the identical dorsal distribution of neural crest cells in all embryos, profound differences in the size and segmentation of DRG were observed during gangliogenesis (E4–9) according to the type of graft that had been performed. Thus when the implant consisted of compound cranial half-somites, giant, coalesced ganglia developed, encompassing the entire length of the graft. On the other hand, very small, dorsally located ganglia with irregular segmentation were seen at the level corresponding to the graft of multiple caudal half-somites. We conclude that normal morphogenesis of dorsal root ganglia depends upon the craniocaudal integrity of the somites.
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Mayor, R., R. Morgan, and M. G. Sargent. "Induction of the prospective neural crest of Xenopus." Development 121, no. 3 (March 1, 1995): 767–77. http://dx.doi.org/10.1242/dev.121.3.767.
Full textAbstract:
The earliest sign of the prospective neural crest of Xenopus is the expression of the ectodermal component of Xsna (the Xenopus homologue of snail) in a low arc on the dorsal aspect of stage 11 embryos, which subsequently assumes the horseshoe shape characteristic of the neural folds as the convergence-extension movements shape the neural plate. A related zinc-finger gene called Slug (Xslu) is expressed specifically in this tissue (i.e. the prospective crest) when the convergence extension movements are completed. Subsequently, Xslu is found in pre- and post-migratory cranial and trunk neural crest and also in lateral plate mesoderm after stage 17. Both Xslu and Xsna are induced by mesoderm from the dorsal or lateral marginal zone but not from the ventral marginal zone. From stage 10.5, explants of the prospective neural crest, which is underlain with tissue, are able to express Xslu. However expression of Xsna is not apparently specified until stage 12 and further contact with the inducer is required to raise the level of expression to that seen later in development. Xslu is specified at a later time. Embryos injected with noggin mRNA at the 1-cell stage or with plasmids driving noggin expression after the start of zygotic transcription express Xslu in a ring surrounding the embryo on the ventroposterior side. We suggest this indicates (a) that noggin interacts with another signal that is present throughout the ventral side of the embryo and (b) that Xslu is unable to express in the neural plate either because of the absence of a co-inducer or by a positive prohibition of expression. The ventral co-inducer, in the presence of overexpressed noggin, seems to generate an anterior/posterior pattern in the ventral part of the embryo comparable to that seen in neural crest of normal embryos. We suggest that the prospective neural crest is induced in normal embryos in the ectoderm that overlies the junction of the domains that express noggin and Xwnt-8. In support of this, we show animal cap explants from blastulae and gastrulae, treated with bFGF and noggin express Xslu but not NCAM although the mesoderm marker Xbra is also expressed. Explants treated with noggin alone express NCAM only. An indication that induction of the neural plate border is regulated independently of the neural plate is obtained from experiments using ultraviolet irradiation in the precleavage period. At certain doses, the cranial crest domains are not separated into lateral masses and there is a reduction in the size of the neural plate.
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Tannahill, D., H. V. Isaacs, M. J. Close, G. Peters, and J. M. Slack. "Developmental expression of the Xenopus int-2 (FGF-3) gene: activation by mesodermal and neural induction." Development 115, no. 3 (July 1, 1992): 695–702. http://dx.doi.org/10.1242/dev.115.3.695.
Full textAbstract:
We have used a probe specific for the Xenopus homologue of the mammalian proto-oncogene int-2 (FGF-3) to examine the temporal and spatial expression pattern of the gene during Xenopus development. int-2 is expressed from just before the onset of gastrulation through to prelarval stages. In the early gastrula, it is expressed around the blastopore lip. This is maintained in the posterior third of the prospective mesoderm and neuroectoderm in the neurula. A second expression domain in the anterior third of the neuroectoderm alone appears in the late gastrula, which later resolves into the optic vesicles, hypothalamus and midbrain-hindbrain junction region. Further domains of expression arise in tailbud to prelarval embryos, including the stomodeal mesenchyme, the endoderm of the pharyngeal pouches and the cranial ganglia flanking the otocyst. It is shown, by treatment of blastula ectoderm with bFGF and activin, that int-2 can be expressed in response to mesoderm induction. By heterotypic grafting of gastrula ectoderm into axolotl neural plate, we have also demonstrated that int-2 can be expressed in response to neural induction. These results suggest that int-2 has multiple functions in development, including an early role in patterning of the anteroposterior body axis and a later role in the development of the tail, brain-derived structures and other epithelia.
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Meulemans, Daniel, and Marianne Bronner-Fraser. "Amphioxus and lamprey AP-2 genes: implications for neural crest evolution and migration patterns." Development 129, no. 21 (November 1, 2002): 4953–62. http://dx.doi.org/10.1242/dev.129.21.4953.
Full textAbstract:
The neural crest is a uniquely vertebrate cell type present in the most basal vertebrates, but not in cephalochordates. We have studied differences in regulation of the neural crest marker AP-2 across two evolutionary transitions: invertebrate to vertebrate, and agnathan to gnathostome. Isolation and comparison of amphioxus, lamprey and axolotl AP-2 reveals its extensive expansion in the vertebrate dorsal neural tube and pharyngeal arches, implying co-option of AP-2 genes by neural crest cells early in vertebrate evolution. Expression in non-neural ectoderm is a conserved feature in amphioxus and vertebrates, suggesting an ancient role for AP-2 genes in this tissue. There is also common expression in subsets of ventrolateral neurons in the anterior neural tube, consistent with a primitive role in brain development. Comparison of AP-2 expression in axolotl and lamprey suggests an elaboration of cranial neural crest patterning in gnathostomes. However,migration of AP-2-expressing neural crest cells medial to the pharyngeal arch mesoderm appears to be a primitive feature retained in all vertebrates. Because AP-2 has essential roles in cranial neural crest differentiation and proliferation, the co-option of AP-2 by neural crest cells in the vertebrate lineage was a potentially crucial event in vertebrate evolution.