Genes dependent on zebrafishcyclops function identified by AFLP differential gene expression screen

Rubinstein, Amy L.; Lee, Danny; Luo, Rushu; Henion, Paul D.; Halpern, Marnie E.

doi:10.1002/(sici)1526-968x(200001)26:1<86::aid-gene11>3.0.co;2-q

Cited by 108 publications

(82 citation statements)

References 75 publications

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“…6A-F). One exception is crestin, a multicopy retroelement expressed in premigratory and migratory neural crest (Rubinstein et al, 2000), which is absent in the cranial neural crest, while it is only reduced in the mos m188 trunk NC (Fig. 6G,H).…”

Section: Proper Development Of Cranial Neural Crest Progenitors Requimentioning

confidence: 85%

The mother superior mutation ablates foxd3 activity in neural crest progenitor cells and depletes neural crest derivatives in zebrafish

Montero-Balaguer

Lang

Sachdev

et al. 2006

Developmental Dynamics

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The zebrafish mutation mother superior (mos m188 ) leads to a depletion of neural crest (NC) derivatives including the craniofacial cartilage skeleton, the peripheral nervous system (sympathetic neurons, dorsal root ganglia, enteric neurons), and pigment cells. The loss of derivatives is preceded by a reduction in NC-expressed transcription factors, snail1b, sox9b, sox10, and a specific loss of foxd3 expression in NC progenitor cells. We employed genetic linkage analysis and physical mapping to place the mos m188 mutation on zebrafish chromosome 6 in the vicinity of the foxd3 gene. Furthermore, we found that mos m188 does not complement the sym1/foxd3 mutation, indicating that mos m188 resides within the foxd3 locus. Injection of PAC clones containing the foxd3 gene into mos m188 embryos restored foxd3 expression in NC progenitors and suppressed the mos m188 phenotype. However, sequencing the foxd3 transcribed area in mos m188 embryos did not reveal nucleotide changes segregating with the mos m188 phenotype, implying that the mutation most likely resides outside the foxd3-coding region. Based on these findings, we propose that the mos m188 mutation perturbs a NC-specific foxd3 regulatory element. Further analysis of mos m188 mutants and foxd3 morphants revealed that NC cells are initially formed, suggesting that foxd3 function is required to maintain the pool of NC progenitors. Developmental Dynamics 235:3199 -3212, 2006.

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Section: Proper Development Of Cranial Neural Crest Progenitors Requimentioning

confidence: 85%

The mother superior mutation ablates foxd3 activity in neural crest progenitor cells and depletes neural crest derivatives in zebrafish

Montero-Balaguer

Lang

Sachdev

et al. 2006

Developmental Dynamics

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“…It can be observed ( Fig. 2 e-l) that foxd3͞fkd6, crestin, and sox10 (15)(16)(17) are expressed at considerably higher levels in olig3 morphants compared with siblings injected with a mismatched olig3MO. Moreover, in the morphants, these markers are expressed ectopically and along the dorsal midline ( Fig.…”

Section: Resultsmentioning

confidence: 99%

The basic helix–loop–helix olig3 establishes the neural plate boundary of the trunk and is necessary for development of the dorsal spinal cord

Filippi

Tiso

Deflorian

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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olig genes encode a previously unrecognized group of vertebratespecific basic helix-loop-helix transcription factors. As shown in mice, chickens, and zebrafish, two members of this group, olig1 and olig2, are involved in the differentiation of motoneurons and oligodendrocytes, but nothing is known about the role of the third member, olig3. Here, we show that olig3 plays an essential role in the establishment of the neural crest-lateral neural plate boundary. In zebrafish embryos, morpholino-induced olig3 inactivation dramatically increases the number of neural crest cells, but lateral neural plate fates (interneurons and astrocytes) are missing. Zebrafish swirl mutants that have impaired bone morphogenetic protein signaling and lack neural crest cells display an expanded olig3 expression domain. Moreover, olig3 is up-regulated in mindbomb mutants lacking the neural crest because of an impaired notch signaling, and olig3 repression in such mutants rescues the neural crest. In addition, olig3 regulates ngn1 and deltaA expression in interneuron precursors. Our results indicate that olig3 has an essential proneural activity in the dorsal spinal cord and cooperates with the Delta͞Notch regulatory loop to establish the boundary between the neural crest and the lateral neural plate. Thus, a proper regulation of the olig gene family is essential for the formation of three cell types (oligodendrocytes, astrocytes, and neural crest) that are unique to vertebrates.T he spinal cord of vertebrates is originated by remodeling of the neural plate. Its general plan comprises motoneurons located ventrally and interneurons in a more dorsal position. In zebrafish, Rohon-Beard (RB) cells (primary sensory neurons) are generated at the outer border of the neural plate (within the neural crest domain) and migrate in the dorsal spinal cord, whereas cells of the dorsal root ganglia (also originated in the neural crest) migrate ventrally without entering the spinal cord. Two main signaling pathways are thought to establish the dorsoventral patterning of the embryonic neural tissue: bone morphogenetic protein (BMP) and Hedgehog (Hh). Hh signaling regionalizes the ventral neural tube and restricts the expression of some genes to dorsal regions (1). In parallel, BMP signaling determines a gradient of positional information throughout the entire neural plate that defines the establishment of dorsal and intermediate neuronal cell types of the spinal cord (2). The current view is that BMP and Hh morphogenetic activities generate zones of competence within which other factors will subsequently establish different cell fates. In this regard, components of the Delta͞Notch signaling pathway are involved in the generation of different neuronal and glial subtypes with a mechanism called lateral specification. Components of the Delta͞Notch genetic loops are often members of the basic helix-loop-helix (bHLH) family of transcription factors. The Neurogenin (Ngn) subfamily of bHLH is critical to establish the neurogenic program and maintain the Delta͞No...

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“…Digoxigenin-labeled riboprobes for crestin (Rubinstein et al, 2000) and neurog1 (Korzh et al, 1998) were generated as previously described. A 2.1 kb fragment of reck was subcloned into pBluescript II SK, linearized with EcoRV and transcribed with T7 polymerase (Invitrogen) to generate digoxigenin-labeled riboprobe.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

The metalloproteinase inhibitor Reck is essential for zebrafish DRG development

et al. 2012

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SUMMARYThe neural crest is a migratory, multipotent cell lineage that contributes to myriad tissues, including sensory neurons and glia of the dorsal root ganglia (DRG). To identify genes affecting cell fate specification in neural crest, we performed a forward genetic screen for mutations causing DRG deficiencies in zebrafish. This screen yielded a mutant lacking all DRG, which we named sensory deprived (sdp). We identified a total of four alleles of sdp, all of which possess lesions in the gene coding for reversion-inducing cysteine-rich protein containing Kazal motifs (Reck). Reck is an inhibitor of metalloproteinases previously shown to regulate cell motility. We found reck function to be both necessary for DRG formation and sufficient to rescue the sdp phenotype. reck is expressed in neural crest cells and is required in a cell-autonomous fashion for appropriate sensory neuron formation. In the absence of reck function, sensory neuron precursors fail to migrate to the position of the DRG, suggesting that this molecule is crucial for proper migration and differentiation. KEY WORDS: reck, Neural crest, Neurogenesis, ZebrafishThe metalloproteinase inhibitor Reck is essential for zebrafish DRG development MATERIALS AND METHODS Zebrafish husbandryZebrafish were maintained at 28.5°C on a 14-hour/10-hour light/dark cycle following established methods and Institutional Animal Care and Use Committee standards (Westerfield, 2007). Embryos were maintained in E2 medium, and staged according to Kimmel et al. (Kimmel et al., 1995). DRG were identified using Tg(neurog1:egfp) w61 (McGraw et al., 2008). Transgenic linesThe 4.9 kb sox10 promoter (Carney et al., 2006), fluorescent protein Eos (Wiedenmann et al., 2004) (Evrogen) or nls-Eos, and a polyadenylation sequence (Kwan et al., 2007) were Gateway cloned (Invitrogen) to generate pSox10:Eos/pSox10nls-Eos; clones were microinjected with Tol2 transposase to generate germline transgenics Tg(sox10:eos) w9 and Tg(sox10:nlseos) w18 as previously described (Fisher et al., 2006). ImmunohistochemistryEmbryos were stained with the antibodies mouse anti-Elavl1 (Invitrogen), 1:500; rabbit anti-GFP (Invitrogen) 1:1000; mouse anti-acetylated tubulin (Sigma; 1:5000), mouse anti-MF20 (Developmental Studies Hybridoma Bank, University of Iowa; 1:100), rabbit anti-Sox10 (gift of Sarah Kucenas, University of Virginia; 1:500), as previously described (Ungos et al., 2003) and imaged by confocal microscopy. Genetic screenWe treated *AB males with 3 mM ethylnitrosourea (Solnica-Krezel et al., 1994). F 3 progeny were screened by immunostaining for Elavl1. Sdp w15 was identified in the *AB background during screening. Three additional alleles were identified: sdp w13 by complementation screening against sdp w15 carriers and sdp w12 and sdp w14 isolated as novel mutations and later established as sdp alleles by complementation. Mutation identificationsdp w12 heterozygotes were outcrossed to the Wik strain and F 2 progeny were subjected to bulked segregant analysis using SSLP markers followed b...

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Genes dependent on zebrafishcyclops function identified by AFLP differential gene expression screen

Cited by 108 publications

References 75 publications

The mother superior mutation ablates foxd3 activity in neural crest progenitor cells and depletes neural crest derivatives in zebrafish

The mother superior mutation ablates foxd3 activity in neural crest progenitor cells and depletes neural crest derivatives in zebrafish

The basic helix–loop–helix olig3 establishes the neural plate boundary of the trunk and is necessary for development of the dorsal spinal cord

The metalloproteinase inhibitor Reck is essential for zebrafish DRG development

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