UNSW Embryo- Development of Neural Crest Selected References Back to Neural Crest Notes page 1 / page 2 Page Link: Articles Reviews Books See Also: Links: Page 2 Page 1 PubMed Link About PubMed Note: A Selected List of References for Neural Crest Development from PubMed May 1999. Internet access computers will be able to get abstract directly from PubMed (when available) by clicking Author's name below.

Articles Effects of Shh and Noggin on neural crest formation demonstrate that BMP is required in the neural tube but not ectoderm. Selleck MA, Garcia-Castro MI, Artinger KB, Bronner-Fraser M Development 1998 Dec;125(24):4919-30 Our results suggest three phases of neurulation that relate to neural crest formation: (1) an initial BMP-independent phase that can be prevented by Shh-mediated signals from the notochord (2) an intermediate BMP-dependent phase around the time of neural tube closure, when BMP-4 is expressed in the dorsal neural tube (3) a later pre-migratory phase which is refractory to exogenous Shh and Noggin. Neural crest cell dynamics revealed by time-lapse video microscopy of whole embryo chick explant cultures. Kulesa PM, Fraser SE Dev Biol 1998 Dec 15;204(2):327-44 Excellent recent paper with timelapse videos from Paul Kulesa DiI-labeled cranial neural crest cells were followed in whole embryo chick explant cultures using time-lapse confocal microscopy. Neural crest cells emerged along the dorsal midline of all rhombomeres. There was a small amount of mixing of neural crest cells between adjoining rhombomeres as cells emerged from the dorsal midline; this mixing persisted during their migration out of the neural tube. Neural crest cell-free zones lateral to rhombomere 3 (r3) and r5 resulted from neural crest cells migrating in either rostral or caudal directions to join other neural crest cells exiting adjacent to r2, r4, or r6. Neural crest cells migrated in a wide variety of individual cell behaviors, ranging from rapid unidirectional motion to stationary and even backward movement (toward the neural tube). Neural crest cells also migrated collectively, extending filipodia to form chain-like cell arrangements. In the midbrain and r1 region, many chains stretched from the dorsal midline to just beyond the lateral extent of the neural tube. In the r7 region, cells linked together and stretched laterally from the neural tube to other neural crest cells migrating into the third branchial arch. The unpredictable cell trajectories, the mixing of neural crest cells between adjoining rhombomeres, and the diversity in cell migration behavior within any particular region imply that no single mechanism guides migration. The regional differences in cell migration characteristics suggests that influential factors may vary spatially along the rostrocaudal axis in the head. Copyright 1998 Academic Press. PMID: 9882474, UI: 99102782 Regulation of neural crest cell populations: occurrence, distribution and underlying mechanisms. Vaglia JL, Hall BK Int J Dev Biol 1999 Mar;43(2):95-110 Regulation is a significant developmental event because successful cell proliferation and migration are critical to shaping young embryos. Regulation -- the replacement of undifferentiated embryonic cells by other cells in response to signals received from the environment -- is distinct from wound healing and regeneration. Investigations on regulation of neural crest cells span all vertebrates and have revealed that regulative ability varies both among classes (even species), and spatially and temporally within individuals. In general, there is greatest regulation for cranial neural crest cells, less for trunk, and virtually none forcardiac. Regulation also appears to be more complete at early embryonic stages. Fate-mapping studies have demonstrated that large regions of neural crest cells must be removed to generate missing or morphologically reduced structures. Recent studies reveal that less extensive neural crest cell extirpations result in normal morphology of cartilaginous and neuronal elements in the head, and normal development of pigmentation in the trunk. Ablation of cardiac neural crest cells frequently generates abnormalities of the heart, great vessels and parasympathetic nerve innervation. Decreased cell death, increased division, change in fate and altered migration are possible cellular mechanisms of regulation. In mostcases, the specific mechanisms of regulation are unknown, but a major premise underlying regulation is that cell potential is greater than cell fate. This concept was born from studies which demonstrated that some cells were able to express alternative fates if transplanted to a new environment. Among the potential cellular mechanisms for regulation, cell migration has received the most attention. Following ablation of neural crest cells, replacement neural crest cells migrate into gaps, most frequently from anterior/posterior locations. Cells from surrounding epidermal and neural ectoderm may have limited regulative ability, while compensation by cells from the ventral neural tube has been demonstrated to an even lesser extent. Regulation by such non-crest cells would require their transformation into neural crest cells. The potential for regulation of neural crest by placodal cells supports a closer relationship between neural crest and placodal ectoderm than previously recognized. Decreased cell death has been discussed primarily with reference to (1) cranial ganglia that have dual contributions from neural crest and placodal cells and (2) programmed cell death in rhombomeres three and five. Increased cell division in response to neural crest ablation is likely more common than has been reported, but this mechanism is difficult to interpret without a 3-D context for viewing how patterns of division differ from normal. Lastly, changes in cell fate may be the driving factor in regulation of embryonic cells. It has been repeatedly demonstrated thatcell potential is greaterthan cell fate. Once reliable mechanisms for assessing cell potential are established, we may find that fates are commonly altered in response to environmental signals. Regulation is therefore significant both as a basic developmental mechanism and as a mechanism for evolutionary change. The more labile the fate of embryonic cells, the more potential there is for maintaining existing characters and for generating new ones. According to Ettensohn (1992, p. 50), further analysis of such systems might <<shed light both on the way evolutionary processes act to modify ontogenetic programs and on the cellular and molecular mechanisms of cell interactions during development>>. With regard to the neural crest, studies on regulation of this vital population of cells provide insight to the origin of the neural crest, to embryonic repair, and to the source of many craniofacial malformations, heart and other embryonic defects. PMID: 10235385, UI: 99249464   Determination of the identity of the derivatives of the cephalic neural crest: incompatibility between Hox gene expression and lower jaw development. Couly G, Grapin-Botton A, Coltey P, Ruhin B, Le Douarin NM Development 1998 Sep;125(17):3445-59 Abstract | A signaling cascade involving endothelin-1, dHAND and msx1 regulates development of neural-crest-derived branchial arch mesenchyme. Thomas T, Kurihara H, Yamagishi H, Kurihara Y, Yazaki Y, Olson EN, Srivastava D Development 1998 Aug;125(16):3005-14 Abstract | Identification of dividing, determined sensory neuron precursors in the mammalian neural crest. Greenwood AL, Turner EE, Anderson DJ Development 1999;126(16):3545-3559 Abstract | Reviews Epithelium-mesenchyme transition during neural crest development. Duband JL, Monier F, Delannet M, Newgreen DActa Anat (Basel) 1995;154(1):63-78 Abstract | Books