Zebrafish foxc1a is required for appendage specific neural circuit development
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ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE64125 | GEO | 2015/03/05
SECONDARY ACCESSION(S): PRJNA270226
REPOSITORIES: GEO
Similar Datasets
Project description:RNA-seq analysis of zebrafish foxc1a mutant For RNA-seq, mRNA was extracted from 38-40 hpf old embryos. We isolated wild type and foxc1a mutant samples by dissecting the entire first 6 anterior somitic segments (AS) through which the fin nerves migrate, and the adjacent posterior segments (PS; segments 7 through ~12) devoid of fin innervating nerves. Heads and yolks were excluded from all samples. Tissues were stored in RNAlater solution (Life Technologies) for up to 2 days at 4 degree before RNA was extracted using the RNAeasy kit (Qiagen) according to the manufactureM-bM-^@M-^Ys protocol. RNA was tested for integrity using a Bioanalyzer (Agilent technologies). RNA samples showing RIN value of 8 or higher were used for generating cDNA libraries as described in the TruSeqM-BM-. Stranded mRNA sample preparation guide. At the final stage, 15 cycles of PCR amplifications was performed. Barcoded libraries representing duplicates of AS and PS samples of wild type and mutants were validated using Bionalyzer (Agilent Technology) and finally sequenced in Illumina HiSeq 2500 yielding paired end reads of 100bp. The RNA-seq Unified Mapper (RUM) (Grant et al., 2011) was used to align the reads to the Zv9/danRer7 reference genome and to assign each read uniquely to a transcript. We investigated transcripts that showed the highest fold changes of expression between the different groups. For Gene Ontology annotations, genes tagged by the GO term M-bM-^@M-^\axon guidanceM-bM-^@M-^] were obtained from the gene ontology database (http://www.geneontology.org/). Next we filtered this list for the M-bM-^@M-^\Danio rerioM-bM-^@M-^] taxon (resulting in 116 unique genes) and used them to annotate our RNA-seq results.
2015-03-05 | E-GEOD-64125 | biostudies-arrayexpress
Project description:Neural connectivity between the spinal cord and paired appendages is key to the superior locomotion of tetrapods and aquatic vertebrates. In contrast to nerves that innervate axial muscles, those innervating appendages converge at a specialized structure, the plexus, where they topographically reorganize before navigating towards their muscle targets. Despite its importance for providing appendage mobility, the genetic program that drives nerve convergence at the plexus, as well as the functional role of this convergence, are not well understood. Here, we show that in zebrafish the transcription factor foxc1a is dispensable for trunk motor nerve guidance but is required to guide spinal nerves innervating the pectoral fins, equivalent to the tetrapod forelimbs. In foxc1a null mutants, instead of converging with other nerves at the plexus, pectoral fin nerves frequently bypass the plexus. We demonstrate that foxc1a expression in muscle cells delineating the nerve path between the spinal cord and the plexus region restores convergence at the plexus. By labeling individual fin nerves, we show that mutant nerves bypassing the plexus enter the fin at ectopic positions, yet innervate their designated target areas, suggesting that motor axons can select their appropriate fin target area independently of their migration through the plexus. Although foxc1a mutants display topographically correct fin innervation, mutant fin muscles exhibit a reduction in the levels of pre- and postsynaptic structures, concomitant with reduced pectoral fin function. Combined, our results reveal foxc1a as a key player in the development of connectivity between the spinal cord and paired appendages, which is crucial for appendage mobility.
| S-EPMC4325381 | biostudies-literature
Project description:To understand the underlying cause of the swimming defect in Cavin4/Murcb deficient larvae, we isolated mRNA from mutant and sibling zebrafish at 72 hpf and subjected it to microarray analysis. RNA and gDNA were extracted from individual larvae at 72 hpf using Trizol (Life Technologies). Following genotyping, the aqueous phases from at least 10 Trizol extractions were combined by genotype and purified over microspin columns (ZymoResearch). RNA expression from heterozygous and mutant larvae was analyzed by single-color microarray (8x60K Zebrafish Array XS, Oaklabs, Germany).
2015-07-14 | E-GEOD-70858 | biostudies-arrayexpress
Project description:To understand the underlying cause of the swimming defect in Cavin4/Murcb deficient larvae, we isolated mRNA from mutant and sibling zebrafish at 72 hpf and subjected it to microarray analysis.
2015-07-14 | GSE70858 | GEO
Project description:BackgroundAlthough the embryonic expression pattern of ADP ribosylation factor-like 6 interacting protein 1 (Arl6ip1) has been reported, its function in neural crest development is unclear.Methods/principal findingsWe found that knockdown of Arl6ip1 caused defective embryonic neural crest derivatives that were particularly severe in craniofacial cartilages. Expressions of the ectodermal patterning factors msxb, dlx3b, and pax3 were normal, but the expressions of the neural crest specifier genes foxd3, snai1b, and sox10 were greatly reduced. These findings suggest that arl6ip1 is essential for specification of neural crest derivatives, but not neural crest induction. Furthermore, we revealed that the streams of crestin- and sox10-expressing neural crest cells, which migrate ventrally from neural tube into trunk, were disrupted in arl6ip1 morphants. This migration defect was not only in the trunk neural crest, but also in the enteric tract where the vagal-derived neural crest cells failed to populate the enteric nervous system. We found that this migration defect was induced by dampened Shh signaling, which may have resulted from defective cilia. These data further suggested that arl6ip1 is required for neural crest migration. Finally, by double-staining of TUNEL and crestin, we confirmed that the loss of neural crest cells could not be attributed to apoptosis.Conclusions/significanceTherefore, we concluded that arl6ip1 is required for neural crest migration and sublineage specification.
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Project description:identification of differentially expressed genes in hoxb1b homozygous mutant hindbrain when compared to wildtype in zebrafish
2018-07-15 | GSE113398 | GEO
Project description:mbnl mutant zebrafish RNA-Seq experiments
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Project description:Invertebrate and vertebrate vestigial (vg) and vestigial-like (VGLL) genes are involved in embryonic patterning and cell fate determination. These genes encode cofactors that interact with members of the Scalloped/TEAD family of transcription factors and modulate their activity. We have previously shown that, in mice, Vgll2 is differentially expressed in the developing facial prominences. In this study, we show that the zebrafish ortholog vgll2a is expressed in the pharyngeal endoderm and ectoderm surrounding the neural crest derived mesenchyme of the pharyngeal arches. Moreover, both the FGF and retinoic acid (RA) signaling pathways, which are critical components of the hierarchy controlling craniofacial patterning, regulate this domain of vgll2a expression. Consistent with these observations, vgll2a is required within the pharyngeal endoderm for NCC survival and pharyngeal cartilage development. Specifically, knockdown of Vgll2a in zebrafish embryos using Morpholino injection results in increased cell death within the pharyngeal arches, aberrant endodermal pouch morphogenesis, and hypoplastic cranial cartilages. Overall, our data reveal a novel non-cell autonomous role for Vgll2a in development of the NCC-derived vertebrate craniofacial skeleton.
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Project description:Among Myc family genes, c-Myc is known to have a role in neural crest specification in Xenopus and in craniofacial development in the mouse. There is no information on the function of other Myc genes in neural crest development, or about any developmental role of zebrafish Myc genes.We isolated the zebrafish mych (myc homologue) gene. Knockdown of mych leads to severe defects in craniofacial development and in certain other tissues including the eye. These phenotypes appear to be caused by cell death in the neural crest and in the eye field in the anterior brain.Mych is a novel factor required for neural crest cell survival in zebrafish.
| S-EPMC2323570 | biostudies-literature
Project description:Zebrafish tissue around the inner ear was dissected from wild-type, heterozygote and mutant ~16-22 hpf embryos and subjected to single cell RNAseq
2023-02-22 | GSE197270 | GEO