Temporal Notch activation through Notch1a and Notch3 is required for maintaining zebrafish rhombomere boundaries

Qiu, Xuehui; Lim, Chiaw-Hwee; Ho, Soo Yei; Lee, Kian-Hong; Jiang, Yun-Jin

doi:10.1007/s00427-009-0296-6

Cited by 13 publications

(14 citation statements)

References 55 publications

(65 reference statements)

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“…When Notch signaling is disrupted, excess neurons often differentiate at early stages at the expense of later-born cell types, including OPCs (Bingham et al, 2003; Haddon et al, 1998a; Itoh et al, 2003; Park et al, 2000; Shih and Keller, 1992). In the zebrafish embryo, Qiu et al reported that Notch3 and Notch1a have redundant functions in controlling hindbrain patterning and neurogenesis (Qiu et al, 2009). They found that excess neurons developed in notch1a mutants that also had reduced notch3 function (via morpholino injection), and rhombomere boundaries were not maintained.…”

Section: Discussionmentioning

confidence: 99%

notch3is essential for oligodendrocyte development and vascular integrity in zebrafish

Zaucker

Mercurio

Sternheim

et al. 2013

Disease Models &Amp; Mechanisms

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SUMMARYMutations in the human NOTCH3 gene cause CADASIL syndrome (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). CADASIL is an inherited small vessel disease characterized by diverse clinical manifestations including vasculopathy, neurodegeneration and dementia. Here we report two mutations in the zebrafish notch3 gene, one identified in a previous screen for mutations with reduced expression of myelin basic protein (mbp) and another caused by a retroviral insertion. Reduced mbp expression in notch3 mutant embryos is associated with fewer oligodendrocyte precursor cells (OPCs). Despite an early neurogenic phenotype, mbp expression recovered at later developmental stages and some notch3 homozygous mutants survived to adulthood. These mutants, as well as adult zebrafish carrying both mutant alleles together, displayed a striking stress-associated accumulation of blood in the head and fins. Histological analysis of mutant vessels revealed vasculopathy, including: an enlargement (dilation) of vessels in the telencephalon and fin, disorganization of the normal stereotyped arrangement of vessels in the fin, and an apparent loss of arterial morphological structure. Expression of hey1, a well-known transcriptional target of Notch signaling, was greatly reduced in notch3 mutant fins, suggesting that Notch3 acts via a canonical Notch signaling pathway to promote normal vessel structure. Ultrastructural analysis confirmed the presence of dilated vessels in notch3 mutant fins and revealed that the vessel walls of presumed arteries showed signs of deterioration. Gaps in the arterial wall and the presence of blood cells outside of vessels in mutants indicated that compromised vessel structure led to hemorrhage. In notch3 heterozygotes, we found elevated expression of both notch3 itself and target genes, indicating that specific alterations in gene expression due to partial loss of Notch3 function might contribute to the abnormalities observed in heterozygous larvae and adults. Our analysis of zebrafish notch3 mutants indicates that Notch3 regulates OPC development and mbp gene expression in larvae, and maintains vascular integrity in adults.

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Section: Discussionmentioning

confidence: 99%

notch3is essential for oligodendrocyte development and vascular integrity in zebrafish

Zaucker

Mercurio

Sternheim

et al. 2013

Disease Models &Amp; Mechanisms

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“…The Wnt/Wg pathway, for example, separates subdomains of the mesoderm in vertebrates and Drosophila , as well as more ancestral ecdysozoans (Eriksson et al, 2009). Notch signaling plays an essential role in generating boundaries between segmental, as well as intra-segmental, subdomains within the ectoderm and mesoderm (McGrew and Pourquie, 1998; Qiu et al, 2009; Tapanes-Castillo and Baylies, 2004). The FGF signaling pathway predates the appearance of Bilaterians and plays a highly conserved role in early mesoderm patterning (Vasiliauskas and Stern, 2001; Wilson and Leptin, 2000; Böttcher and Niehrs, 2005; Rebscher et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

The convergence of Notch and MAPK signaling specifies the blood progenitor fate in the Drosophila mesoderm

Grigorian

Mandal

Hakimi

et al. 2011

Developmental Biology

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Blood progenitors arise from a pool of pluripotential cells (“hemangioblasts”) within the Drosophila embryonic mesoderm. The fact that the cardiogenic mesoderm consists of only a small number of highly stereotypically patterned cells that can be queried individually regarding their gene expression in normal and mutant embryos, is one of the significant advantages that Drosophila offers to dissect the mechanism specifying the fate of these cells. We show in this paper that the expression of the Notch ligand Delta (Dl) reveals segmentally reiterated mesodermal clusters (“cardiogenic clusters”) that constitute the cardiogenic mesoderm. These clusters give rise to cardioblasts, blood progenitors and nephrocytes. Cardioblasts emerging from the cardiogenic clusters accumulate high levels of Dl, which is required to prevent more cells from adopting the cardioblast fate. In embryos lacking Dl function, all cells of the cardiogenic clusters become cardioblasts, and blood progenitors are lacking. Concomitant activation of the Mitogen Activated Protein Kinase (MAPK) pathway by Epidermal Growth Factor Receptor (EGFR) and Fibroblast Growth Factor Receptor (FGFR) is required for the specification and maintenance of the cardiogenic mesoderm; in addition, the spatially restricted localization of some of the FGFR ligands may be instrumental in controlling the spatial restriction of the Dl ligand to presumptive cardioblasts.

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“…Notch activity at the rhombomere boundaries does not seem to result in a direct regulation of cell adhesion molecules. Rather, the maintenance of a characteristic population of cells in this region happens as a consequence of Notch inhibition of neurogenesis (see section 3; Amoyel et al, 2005;Nikolaou et al, 2009;Qiu et al, 2009).…”

Section: Fate Specification and Morphogenesismentioning

confidence: 99%

Brain regionalization: Of signaling centers and boundaries

Cavodeassi

Houart

2012

Developmental Neurobiology

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Our knowledge of the general mechanisms controlling the formation of the vertebrate central nervous system has advanced tremendously in the last decade. Here, we discuss the impact of the combined use of cell manipulation, in vivo imaging and genetics in the zebrafish on recent progress in understanding how signaling processes progressively control regionalization of the central nervous system. We highlight the unresolved issues and speculate upon the fundamental role the zebrafish will continue having in answering them.

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Temporal Notch activation through Notch1a and Notch3 is required for maintaining zebrafish rhombomere boundaries

Abstract: In vertebrates, hindbrain is subdivided into seven segments termed rhombomeres and the interface between each rhombomere forms the boundary. Similar to the

Cited by 13 publications

References 55 publications

notch3is essential for oligodendrocyte development and vascular integrity in zebrafish

notch3is essential for oligodendrocyte development and vascular integrity in zebrafish

The convergence of Notch and MAPK signaling specifies the blood progenitor fate in the Drosophila mesoderm

Brain regionalization: Of signaling centers and boundaries

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