prdm1a Regulates sox10 and islet1 in the development of neural crest and Rohon‐Beard sensory neurons

Olesnicky, Eugenia C.; Hernandez-Lagunas, Laura; Artinger, Kristin

doi:10.1002/dvg.20673

Cited by 34 publications

(46 citation statements)

References 60 publications

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“…Our previously published microarray (Olesnicky et al, 2010) as well as mRNA-seq data from embryos at this early stage (unpublished data) demonstrate both upregulation and downregulation of various genes in prdm1a knockdown embryos as compared with WT embryos, suggesting that, if these targets are direct, Prdm1a might have both transcriptional activator and repressor functions during embryogenesis. To demonstrate the mode of Prdm1a transcriptional regulation during NCC development, we expressed the prdm1aDBD-VP16 dominant activator and EnR dominant repressor constructs in prdm1a mutants.…”

Section: Prdm1a Functions As Both a Transcriptional Activator And Repmentioning

confidence: 78%

“…Single-embryo genotyping of prdm1a −/− following ISH was performed as described (Rossi et al, 2009). DIG-conjugated antisense probes were synthesized from full-length transcript sequences in the pCS2+ plasmid to the following genes: snai1b (primers 5Ј-GCTAGGGATCCGCCGCCA -CCATGCCACGCTCATTTC TTGTCA-3Ј and 5Ј-GAATTCTAGATG -TGTGTCCACTAGAGCGCC-3Ј); foxd3 (see above); sox10 (Olesnicky et al, 2010); crestin (Rubinstein et al, 2000); and tfap2a (from T. Williams). Fluorescent ISH was performed as described (Pineda et al, 2006) and used the TSA Biotin System (Perkin Elmer, NEL700A001KT) followed by streptavidin Alexa Fluor 488 antibody (Invitrogen, S11223) to develop FITC-labeled antisense probes and the Fast Red Kit (Sigma, F4648) to develop DIG-labeled probes.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

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Prdm1a directly activates foxd3 and tfap2a during zebrafish neural crest specification

et al. 2013

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SUMMARYThe neural crest comprises multipotent precursor cells that are induced at the neural plate border by a series of complex signaling and genetic interactions. Several transcription factors, termed neural crest specifiers, are necessary for early neural crest development; however, the nature of their interactions and regulation is not well understood. Here, we have established that the PR/SET domaincontaining transcription factor Prdm1a is co-expressed with two essential neural crest specifiers, foxd3 and tfap2a, at the neural plate border. Through rescue experiments, chromatin immunoprecipitation and reporter assays, we have determined that Prdm1a directly binds to and transcriptionally activates enhancers for foxd3 and tfap2a and that they are functional, direct targets of Prdm1a at the neural plate border. Additionally, analysis of dominant activator and dominant repressor Prdm1a constructs suggests that Prdm1a is required both as a transcriptional activator and transcriptional repressor for neural crest development in zebrafish embryos.

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Section: Prdm1a Functions As Both a Transcriptional Activator And Repmentioning

confidence: 78%

Section: In Situ Hybridizationmentioning

confidence: 99%

Prdm1a directly activates foxd3 and tfap2a during zebrafish neural crest specification

et al. 2013

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“…In Drosophila, Hamlet, the homolog of Prdm16, controls odorant gene choice and axon targeting specificity through modifying cellular responses to Notch signals in a context-dependent manner (Endo et al, 2011). In zebrafish, Prdm1a is expressed at the edge of the neural plate and is required for the specification of neural crest and RohonBeard (RB) sensory neurons (Hernandez-Lagunas et al, 2005;Olesnicky et al, 2010;Rossi et al, 2009). Prdm6, 8, 12, 13 and 16 were shown to be expressed in the developing mouse CNS (Kinameri et al, 2008), but their exact functions remain to be defined.…”

Section: Introductionmentioning

confidence: 99%

Prdm14 acts upstream of islet2 transcription to regulate axon growth of primary motoneurons in zebrafish

Liu

et al. 2012

Development

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SUMMARYThe precise formation of three-dimensional motor circuits is essential for movement control. Within these circuits, motoneurons (MNs) are specified from spinal progenitors by dorsoventral signals and distinct transcriptional programs. Different MN subpopulations have stereotypic cell body positions and show specific spatial axon trajectories. Our knowledge of MN axon outgrowth remains incomplete. Here, we report a zebrafish gene-trap mutant, short lightning (slg), in which prdm14 expression is disrupted. slg mutant embryos show shortened axons in caudal primary (CaP) MNs resulting in defective embryonic movement. Both the CaP neuronal defects and behavior abnormality of the mutants can be phenocopied by injection of a prdm14 morpholino into wild-type embryos. By removing a copy of the inserted transposon from homozygous mutants, prdm14 expression and normal embryonic movement were restored, confirming that loss of prdm14 expression accounts for the observed defects. Mechanistically, Prdm14 protein binds to the promoter region of islet2, a known transcription factor required for CaP development. Notably, disruption of islet2 function caused similar CaP axon outgrowth defects as observed in slg mutant embryos. Furthermore, overexpression of islet2 in slg mutant embryos rescued the shortened CaP axon phenotypes. Together, these data reveal that prdm14 regulates CaP axon outgrowth through activation of islet2 expression.

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“…5J). Islet-1/2 is expressed in the dorsal Rohon-Beard cells and ventral motor neurons (MNs) (Diez del Corral and Storey, 2001;Olesnicky et al, 2010;Yajima et al, 2014) ( Fig. 5J; Fig.…”

Section: Tbx3 Is Required For Normal Eye Formationmentioning

confidence: 99%

Tbx3 represses bmp4 expression and, with Pax6, is required and sufficient for retina formation

et al. 2016

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Vertebrate eye formation begins in the anterior neural plate in the eye field. Seven eye field transcription factors (EFTFs) are expressed in eye field cells and when expressed together are sufficient to generate retina from pluripotent cells. The EFTF Tbx3 can regulate the expression of some EFTFs; however, its role in retina formation is unknown. Here, we show that Tbx3 represses bmp4 transcription and is required in the eye field for both neural induction and normal eye formation in Xenopus laevis. Although sufficient for neural induction, Tbx3-expressing pluripotent cells only form retina in the context of the eye field. Unlike Tbx3, the neural inducer Noggin can generate retina both within and outside the eye field. We found that the neural and retina-inducing activity of Noggin requires Tbx3. Noggin, but not Tbx3, induces Pax6 and coexpression of Tbx3 and Pax6 is sufficient to determine pluripotent cells to a retinal lineage. Our results suggest that Tbx3 represses bmp4 expression and maintains eye field neural progenitors in a multipotent state; then, in combination with Pax6, Tbx3 causes eye field cells to form retina.

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prdm1a Regulates sox10 and islet1 in the development of neural crest and Rohon‐Beard sensory neurons

Cited by 34 publications

References 60 publications

Prdm1a directly activates foxd3 and tfap2a during zebrafish neural crest specification

Prdm1a directly activates foxd3 and tfap2a during zebrafish neural crest specification

Prdm14 acts upstream of islet2 transcription to regulate axon growth of primary motoneurons in zebrafish

Tbx3 represses bmp4 expression and, with Pax6, is required and sufficient for retina formation

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