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Head Development (head + development)
Selected AbstractsCell fate and timing in the evolution of neural crest and mesoderm development in the head region of amphibians and lungfishesACTA ZOOLOGICA, Issue 2009Rolf Ericsson Abstract Our research on the evolution of head development focuses on understanding the developmental origins of morphological innovations and involves asking questions like: How flexible (or conserved) are cell fates, patterns of cell migration or the timing of developmental events (heterochrony)? How do timing changes, or changes in life history affect head development and growth? Our ,model system' is a comparison between lungfishes and representatives from all three extant groups of amphibians. Within anuran amphibians, major changes in life history such as the repeated evolution of larval specializations (e.g. carnivory), or indeed the loss of a free-swimming larva, allows us to test for developmental constraints. Cell migration and cell fate are conserved in cranial neural crest cells in all vertebrates studied so far. Patterning and developmental anatomy of cranial neural crest and head mesoderm cells are conserved within amphibians and even between birds, mammals and amphibians. However, the specific formation of hypobranchial muscles from ventral somitic processes shows variation within tetrapods. The evolution of carnivorous larvae in terminal taxa is correlated with changes in both pattern and timing of head skeletal and muscle development. Sequence-heterochronic changes are correlated with feeding mode in terminal taxa and with phylogenetic relatedness in basal branches of the phylogeny. Eye muscles seem to form a developmental module that can evolve relatively independently from other head muscles, at least in terms of timing of muscle differentiation. [source] Cranial neural crest cell migration in the Australian lungfish, Neoceratodus forsteriEVOLUTION AND DEVELOPMENT, Issue 4 2000Pierre Falck SUMMARY A crucial role for the cranial neural crest in head development has been established for both actinopterygian fishes and tetrapods. It has been claimed, however, that the neural crest is unimportant for head development in the Australian lungfish (Neoceratodus forsteri ,), a member of the group (Dipnoi) which is commonly considered to be the living sister group of the tetrapods. In the present study, we used scanning electron microscopy to study cranial neural crest development in the Australian lungfish. Our results, contrary to those of Kemp, show that cranial neural crest cells do emerge and migrate in the Australian lungfish in the same way as in other vertebrates, forming mandibular, hyoid, and branchial streams. The major difference is in the timing of the onset of cranial neural crest migration. It is delayed in the Australian lungfish in comparison with their living sister group the Lissamphibia. Furthermore, the delay in timing between the emergence of the hyoid and branchial crest streams is very long, indicating a steeper anterior-posterior gradient than in amphibians. We are now extending our work on lungfish head development to include experimental studies (ablation of selected streams of neural crest cells) and fate mapping (using fluoresent tracer dyes such as DiI) to document the normal fate as well as the role in head patterning of the cranial neural crest in the Australian lungfish. [source] P1 Regionalisation of the brain as an evolutionarily conserved developmental mechanism.JOURNAL OF ANATOMY, Issue 1-2 2001E. GALE Comparative studies of chordate neural connectivity and gene families have provided evidence for evolutionary conservation of the patterning mechanisms in brain development (review Holland & Holland, Curr. Opin. Neurobiol.9, 1999). Based on expression patterns of ascidian and amphioxus homologues of the Otx gene and the Hox1 gene and of the ascidian Pax-2/5/8, the chordate brain has been suggested to have tripartite development (Wada et al., Development125, 1998; Kozmik et al., Development126, 1999). Primitively, the chordates have regions homologous to the vertebrate forebrain, anterior midbrain and posterior hindbrain while the posterior midbrain/anterior hindbrain region seems to be a vertebrate innovation. The extent of the homologies within each of these regions between the vertebrates and their ancestors is not fully determined but the similarity of Hox gene expression patterns suggests organisational constants over evolutionary time within the posterior hindbrain region. Identification of the posterior hindbrain region as a developmental unit in vertebrates is demonstrated in the retinoid-deficient quail. Embryos laid by quails fed a retinoid-deficient diet have no posterior hindbrain while the anterior hindbrain is specified normally. Through DiI cell lineage tracing and a temporal analysis of gene expression characteristic of this region (Krox-20, Hoxb-1, mafB, and fgf3), we have followed the development of this region of cells. From the initial formation of the neural plate phenotype in the retinoid-deficient quail, there is no evidence of a posterior hindbrain. This region is never specified and all the cells of the hindbrain participate in an anterior hindbrain fate. A single retinoid injection in ovo during early development completely rescues the posterior hindbrain ensuring that the phenotype was the result of a single stimulus. Therefore cells from the posterior hindbrain respond in a coordinated regional manner to the presence or absence of a single gene inducer, retinoic acid. We present evidence of regionalisation of the vertebrate head that is up stream of segment specification. In combination with data from amphioxus and ascidians, this may represent a common mechanism for head development throughout chordate evolution. Interestingly, regional deletion with enlargement of the adjacent region is very reminiscent of the gap gene phenotype in Drosophila. It would be disregarding millions of years of divergent evolution to suggest that vitamin A is identical to a Drosophila gap gene inducer; nevertheless this data supports the hypothesis of common underlying regulation of axial regionalisation and gene hierarchies. [source] Roles of bone morphogenetic protein signaling and its antagonism in holoprosencephaly,AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 1 2010John Klingensmith Abstract Holoprosencephaly (HPE) is the most common malformation of the forebrain, resulting from a failure to completely septate the left and right hemispheres at the rostral end of the neural tube. Because of the tissue interactions that drive head development, these forebrain defects are typically accompanied by midline deficiencies of craniofacial structures. Early events in setting up tissue precursors of the head, as well as later interactions between these tissues, are critical for normal head formation. Defects in either process can result in HPE. Signaling by bone morphogenetic proteins (BMPs), a family of secreted cytokines, generally plays negative roles in early stages of head formation, and thus must be attenuated in multiple contexts to ensure proper forebrain and craniofacial development. Chordin and Noggin are endogenous, extracellular antagonists of BMP signaling that promote the normal organization of the forebrain and face. Mouse mutants with reduced levels of both factors display mutant phenotypes remarkably analogous to the range of malformations seen in human HPE sequence. Chordin and Noggin function in part by antagonizing the inhibitory effects of BMP signaling on the Sonic hedgehog and Nodal pathways, genetic lesions in each being associated with human HPE. Study of Chordin;Noggin mutant mice is helping us to understand the molecular, cellular, and genetic pathogenesis of HPE and associated malformations. © 2010 Wiley-Liss, Inc. [source] | ||||||||||