In Vivo Imaging of Embryonic Vascular Development Using Transgenic Zebrafish

Lawson, Nathan D.; Weinstein, Brant M.

doi:10.1006/dbio.2002.0711

Cited by 1,946 publications

(1,788 citation statements)

References 36 publications

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“…Tg(fli1:EGFP) y1 transgenic embryos express GFP in neural crest cells shortly after the onset of migration, and in the vasculature 41 , while Tg(-4.9sox10:EGFP) ba2 transgenic embryos express GFP in neural crest prior to the onset of migration 3 ; here they are called fli1:EGFP and sox10:EGFP, respectively, through the text. We used heterozygous sox10:EGFP transgenics for our analyses, because homozygous embryos can have craniofacial defects 3 .…”

Section: Zebrafish Care and Usementioning

confidence: 99%

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

et al. 2008

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Disruption of signaling pathways such as those mediated by Shh or Pdgf causes craniofacial disease, including cleft palate. The role that microRNAs play in modulating palatogenesis, however, is completely unknown. We show, in zebrafish, that the microRNA Mirn140 negatively regulates Pdgf signaling during palatal development and we provide a mechanism for how disruption of Pdgf signaling causes palatal clefting. The pdgf-receptor alpha (pdgfra) 3' UTR contains a Mirn140 binding site functioning in the negative regulation of Pdgfra protein levels in vivo. Both pdgfra mutants and Mirn140-injected embryos share panoply of facial defects including clefting of the crestderived cartilages that develop in the roof of the larval mouth. Concomitantly, the oral ectoderm beneath where these cartilages develop loses pitx2 and shha expression. Mirn140 modulates Pdgfmediated attraction of cranial neural crest cells to the oral ectoderm, where crest-derived signals are necessary for oral ectodermal gene expression. Both Mirn140 loss-of-function and pdgfra overexpression alters palatal shape and causes neural crest cells to accumulate around the optic stalk, a source of the ligand Pdgfaa. Conserved molecular genetics and expression patterns of mirn140 and pdgfra suggest that their regulatory interactions are ancient methods of palatogenesis that provide a candidate mechanism for cleft palate.Cleft palate and other craniofacial diseases are common in humans and have complex cellular and genetic etiologies. In amniotes, the palate serves to separate the nasal and oral cavities and is generated through an intricate series of morphogenic events that include early neural crest cell migration and cell-cell signaling during the formation of facial prominences, as well as later generation and fusion of palatal shelves. While later events involving palatal shelves have not been described in zebrafish, palatal precursors migrate both rostral and caudal to the eye to condense upon the oral ectoderm in amniotes 1 as well as zebrafish 2,3 and evidence continues to accumulate that the early signaling environment governing palatogenesis is also largely equivalent [3][4][5][6] . For instance, Hh signaling is crucial for palatogenesis in humans and zebrafish 3,4,7 . Zebrafish and amniotes also share expression patterns of palatogenic genes such as Shh 4,8 , Fgf8 4,9,10 and Pdgf receptor alpha (Pdgfra) [11][12][13] .In mouse, the Pdgf family consists of four soluble ligands, Pdgfa, Pdgfb, Pdgfc, and Pdgfd as well as two receptor tyrosine kinases, Pdgfra and Pdgfrb 14 . Pdgf signaling regulates a myriad of biological processes as demonstrated by analyses of mouse Pdgf ligand and receptor mutants 14 . Mice null for Pdgfra have a facial clefting phenotype that includes cleft palate 12,13 . This facial phenotype is fully recapitulated in mice doubly mutant for Pdgfa and Pdgfc 15. Most Pdgfc mutants have cleft palate 15 MicroRNAs (miRNAs) provide a unique mechanism for modulating signaling pathways [17][18][19][20] . Skeletogenic, including...

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Section: Zebrafish Care and Usementioning

confidence: 99%

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

et al. 2008

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“…PCR was used to amplify fragments from embryonic mRNA samples corresponding to the homeodomain-containing transcription factor dlx2a, and the etsdomain-containing factors fli1 and pea3. In both zebrafish and some cichlids, dlx2a is a marker of post-migratory pharyngeal NC (Yelick and Schilling, 2002;Albertson and Kocher, 2006), fli1 labels pharyngeal NC and mesodermally-derived vascular endothelia (Lawson and Weinstein, 2002), and pea3 marks pp (Miller et al, 2004).…”

Section: Pharyngeal Arch Segmentation In Nile Tilapia Embryosmentioning

confidence: 99%

Embryonic Development and Skeletogenesis of the Pharyngeal Jaw Apparatus in the Cichlid Nile Tilapia (Oreochromis niloticus)

Pabic

Stellwag

Scemama

2009

The Anatomical Record

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The evolution of a specialized pharyngeal jaw apparatus (PJA) has been argued to be the key evolutionary innovation that allowed the explosive adaptive radiation of cichlid fishes in East African lakes. Subsequent studies together with recent molecular phylogenies have shown that similar innovations evolved independently several times within the teleosts, which poses the questions: (1) how similar are the developmental mechanisms responsible for these changes in divergent taxa and (2) how did such complex features arise independently in evolution? A detailed knowledge of PJA development in cichlids and other teleosts is needed to address these questions. Here, we provide a detailed account of the development of the PJA in one species of cichlid, the Nile tilapia (Oreochromis niloticus), from the early segmentation and patterning of its embryonic precursors -pharyngeal arches 3 to 7 -to its ossification. We find that pharyngeal segmentation occurs sequentially from anterior to posterior during early segmentation stages through the mid-pharyngula period. We show a clear combinatorial code of Hox gene expression such that each posterior arch is defined by a distinctive Hox signature. Posterior arch chondrogenesis in tilapia is essentially complete by the end of the hatching period, and most elements become ossified over the next two days. Our results reveal that both the fusion of lower jaw bones and articulation between the neurocranium and upper jaws occur during post-embryonic development. Abstract end data should be: Anat Rec, 292:1780Rec, 292: -1800Rec, 292: , 2009. V V C 2009 Wiley-Liss, Inc.

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“…Advances in microscopic imaging methods and improvements in genetically encoded fluorescent proteins have led to the development of powerful tools for studying cell behavior in live embryos. For example, endothelial-specific green fluorescent protein (GFP) reporters have proven useful for noninvasive observation of vascular development in zebrafish (Isogai et al, 2003;Lawson and Weinstein, 2002;Motoike et al, 2000). The uniform expression of GFP within the endothelial cells of these animals limits their utility in following cell movements: the position of a given cell can be tracked in three dimensions (3D) over time (i.e., in 4D) only if it is present among a group of nonexpressing cells, as in a mosaic or mixed-lineage population (e.g., see Anderson et al, 2000;Bak and Fraser, 2003;Hadjantonakis et al, 2001;Srinivas et al, 2004;Tam and Rossant, 2003).…”

Section: Introductionmentioning

confidence: 99%

Using a histone yellow fluorescent protein fusion for tagging and tracking endothelial cells in ES cells and mice

Fraser

Hadjantonakis

Sahr

et al. 2005

genesis

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SummaryWe report the first endothelial lineage-specific transgenic mouse allowing live imaging at subcellular resolution. We generated an H2B-EYFP fusion protein which can be used for fluorescent labeling of nucleosomes and used it to specifically label endothelial cells in mice and in differentiating embryonic stem (ES) cells. A fusion cDNA encoding a human histone H2B tagged at its C-terminus with enhanced yellow fluorescent protein (EYFP) was expressed under the control of an Flk1 promoter and intronic enhancer. The Flk1::H2B-EYFP transgenic mice are viable and high levels of chromatin-localized reporter expression are maintained in endothelial cells of developing embryos and in adult animals upon breeding. The onset of fluorescence in differentiating ES cells and in embryos corresponds with the beginning of endothelial cell specification. These transgenic lines permit real-time imaging in normal and pathological vasculogenesis and angiogenesis to track individual cells and mitotic events at a level of detail that is unprecedented in the mouse.

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In Vivo Imaging of Embryonic Vascular Development Using Transgenic Zebrafish

Cited by 1,946 publications

References 36 publications

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

MicroRNA Mirn140 modulates Pdgf signaling during palatogenesis

Embryonic Development and Skeletogenesis of the Pharyngeal Jaw Apparatus in the Cichlid Nile Tilapia (Oreochromis niloticus)

Using a histone yellow fluorescent protein fusion for tagging and tracking endothelial cells in ES cells and mice

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