Maintenance of somite borders in mice requires the Delta homologue Dll1

Angelis, Martin Hrabé de; Mclntyre, Joseph; Gossler, Achim

doi:10.1038/386717a0

Cited by 594 publications

(379 citation statements)

References 20 publications

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“…The present finding of increased neurogenesis induced by lunatic fringe complements those previously observed in the Delta-1-null mice, which have a neural crest phenotype (Hrabe de Angelis et al, 1997). More importantly, lunatic fringe-null mice have severe reduction in sensory ganglia size, which indicates fewer neurons (Evrard et al, 1998;Zhang and Gridley, 1998).…”

Section: Discussionsupporting

confidence: 74%

Lunatic fringe causes expansion and increased neurogenesis of trunk neural tube and neural crest populations

et al. 2007

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Both neurons and glia of the PNS are derived from the neural crest. In this study, we have examined the potential function of lunatic fringe in neural tube and trunk neural crest development by gain-offunction analysis during early stages of nervous system formation. Normally lunatic fringe is expressed in three broad bands within the neural tube, and is most prominent in the dorsal neural tube containing neural crest precursors. Using retrovirally-mediated gene transfer, we find that excess lunatic fringe in the neural tube increases the numbers of neural crest cells in the migratory stream via an apparent increase in cell proliferation. In addition, lunatic fringe augments the numbers of neurons and upregulates Delta-1 expression. The results indicate that, by modulating Notch/Delta signaling, lunatic fringe not only increases cell division of neural crest precursors, but also increases the numbers of neurons in the trunk neural crest.

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Section: Discussionsupporting

confidence: 74%

Lunatic fringe causes expansion and increased neurogenesis of trunk neural tube and neural crest populations

et al. 2007

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“…Activation of Notch signaling caused a general disorganization of somite patterning and border formation, consistent with the phenotypes observed in the somites of Notch pathway mutant mice ( Fig. 4B; Conlon et al, 1995;Oka et al, 1995;Hrabe de Angelis et al, 1997).…”

Section: Responsiveness Of Xhey-1 To Notch Signalingsupporting

confidence: 82%

Isolation and characterization of Xenopus Hey‐1: A downstream mediator of Notch signaling

Rones

Woda

Mercola

et al. 2002

Developmental Dynamics

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Regulation of Notch signaling likely occurs, at least in part, at the level of basic helix-loop-helix (bHLH) transcription factors that function downstream of Suppressor of Hairless (Su(H)) in the Notch pathway. To begin to characterize modulation of Notch signaling during organogenesis, we examined the bHLH transcription factor, XHey-1 (hairy related-1) in early Xenopus laevis embryos. XHey-1 is expressed in numerous tissues during early development including the somites, head, embryonic kidneys, and heart. Importantly, the expression of XHey-1 was significantly altered in response to perturbation of Notch signaling by means of inducible constructs that served to either activate or suppress Notch signaling through Su(H) in a temporally controlled manner.

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“…In addition, Lunatic fringe, encoding a glycosyltransferase that modulates the Notch signaling in the chicken and mouse, and the Notch ligand deltaC in the zebrafish also show an oscillatory expression pattern in the PSM. These cyclic genes, as well as other components of the Notch signaling pathway, were shown to be required for the proper somite segmentation in mice (Hrabe de Angelis et al 1997;Kusumi et al 1998;Bessho et al 2001) and zebrafish (Takke and CamposOrtega 1999;Holley et al 2000Holley et al , 2002Henry et al 2002;Oates and Ho 2002) by mutant analysis or morpholino oligo (MO)-mediated gene-knockdown experiments. Furthermore, the cyclic expression of Hes7, her1, and her7 requires their own activity, suggesting that a negative feedback loop involving these genes is a critical component of the oscillation machinery (Oates and Ho 2002;.…”

mentioning

confidence: 99%

Zebrafish Hairy/Enhancer of split protein links FGF signaling to cyclic gene expression in the periodic segmentation of somites

Kawamura¹,

Koshida²,

Hijikata³

et al. 2005

Genes Dev.

111

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Notch and fibroblast growth factor (FGF) signaling pathways have been implicated in the establishmentSomites are the morphologically distinct segmental units that are transiently formed during early vertebrate development and subsequently give rise to metameric and fundamental structures such as the vertebrae of the axial skeleton, their associated muscles, and tendons. The somites are subdivided from the anterior end of the unsegmented paraxial mesoderm, called the presomitic mesoderm (PSM), and sequentially generated in an anterior to posterior direction in a rhythmic fashion at regular spatiotemporal intervals. The molecular mechanism underlying the periodical formation of somites is coupled to an internal oscillator, referred to as the "segmentation clock", which has been evidenced by the cyclic expression of genes in the PSM (Palmeirim et al. 1997;Maroto and Pourquie 2001). Most genes that exhibit a cyclic expression pattern in the PSM are involved in the Notch signaling pathway . Various hairy/Enhancer of split (Espl)-related basic helix-loop-helix (bHLH) genes (hairy-1, hairy-2, and Hey2 in the chicken; Hes1, Hes5, Hes7, and Hey2 in the mouse; her1 and her7 in the zebrafish) that are transcriptional targets of the Notch signaling are expressed in a dynamic pattern of stripes across the PSM in a posterior to anterior direction. In addition, Lunatic fringe, encoding a glycosyltransferase that modulates the Notch signaling in the chicken and mouse, and the Notch ligand deltaC in the zebrafish also show an oscillatory expression pattern in the PSM. These cyclic genes, as well as other components of the Notch signaling pathway, were shown to be required for the proper somite segmentation in mice ( The oscillating and anteriorly propagating wave of gene expression, which is maintained in the posterior PSM, becomes fixed to cause segmentation in the anterior PSM. Activity gradients of signaling molecules, including fibroblast growth factor (FGF), Wnt, and retinoic acid are proposed to regulate the differentiation of PSM cells along the anteroposterior axis from a state permitting the oscillating gene expression to a state driving the segmentation program (Dubrulle et al. 2001;Sawada et al. 2001;Aulehla et al. 2003;Moreno and Kintner 2004). For instance, FGF signaling is the highest at the posterior end of the PSM with a gradual decrease toward the anterior, suggesting a role for FGF signaling in maintaining the characteristics of the posterior PSM cells (Dubrulle et al. 2001;Sawada et al. 2001). In fact, overexpression of FGF8 in the entire PSM of chick embryos causes an increase in the expression of Brachyury in the posterior PSM and suppresses morphological segmentation (Dubrulle et al. 2001). Furthermore, transient activation or inhibition of FGF signaling results in the formation of smaller or larger somites, respectively. Thus, FGF signaling appears to maintain the posterior characteristics, which allows the cyclic gene expression, and the level of FGF activity regulates the transition of the posterior PSM ...

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Maintenance of somite borders in mice requires the Delta homologue Dll1

Cited by 594 publications

References 20 publications

Lunatic fringe causes expansion and increased neurogenesis of trunk neural tube and neural crest populations

Lunatic fringe causes expansion and increased neurogenesis of trunk neural tube and neural crest populations

Isolation and characterization of Xenopus Hey‐1: A downstream mediator of Notch signaling

Zebrafish Hairy/Enhancer of split protein links FGF signaling to cyclic gene expression in the periodic segmentation of somites

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