Interactions of <i>Wnt</i>‐1 and <i>Wnt</i>‐3a are essential for neural tube patterning

Augustine, Karen A.; Liu, Edison T.; Sadler, T. W.

doi:10.1002/tera.1420510209

Cited by 30 publications

(15 citation statements)

References 27 publications

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“…Thus, the antisense method used in this study was useful to investigate the roles of ß-catenin in development of the inner ear. Antisense methods to suppress expression of specific genes have been reported in rodent and avian embryos (Augustine et al 1993(Augustine et al , 1995Nieto et al 1994;Chen and Hales 1995;Srivastava et al 1995;Borycki et al 1998).…”

Section: Discussionmentioning

confidence: 99%

“…Antisense methods to suppress expression of specific genes have been reported in rodent and avian embryos (Augustine et al 1993(Augustine et al , 1995Nieto et al 1994;Chen et al 1995;Srivastava et al 1995;Borycki et al 1998). Augustine et al (1993Augustine et al ( , 1995 and Chen et al (1995) combined antisense technology with rat whole-embryo culture to develop a method for investigating gene function during organogenesis.…”

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confidence: 99%

“…Augustine et al (1993Augustine et al ( , 1995 and Chen et al (1995) combined antisense technology with rat whole-embryo culture to develop a method for investigating gene function during organogenesis. Whole-embryo culture supports the normal growth and development of rat embryos in vitro from the egg cylinder (day 9.5 of gestation, E9.5) to the early limb bud stage (E11.5; New, 1978).…”

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Roles of ß-catenin in inner ear development in rat embryos

Matsuda¹,

Keino²

2000

Anat Embryol

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We studied the roles of beta-catenin in inner ear development in rat embryos using immunostaining and antisense experiments. High levels of beta-catenin appeared transiently in the otic cup during inner ear development. While beta-catenin accumulation was not yet observed in the thickened surface ectoderm at the otic placode, it became to be detected at the apical surface of the otic cup. Then it disappeared from the otocyst. When embryos were treated with the beta-catenin antisense oligodeoxynucleotide (ODN), accumulation of beta-catenin in the otic cup was suppressed and the beta-catenin protein level was significantly less in treated embryos than in controls. The number of cells in the otic cup in treated embryos was smaller than in control embryos. Cells that incorporated bromodeoxyuridine (BrdU) in the otic placode were fewer in number in treated embryos than in controls. In control embryos, acoustic neurons were detected by 2H3 (anti-neurofilament 165 kDa antibody) staining within the acoustic neural crest complex, while only a little staining of 2H3 was observed in the complex of the treated embryos. These results suggested that beta-catenin plays a role in cell proliferation in the otic placodes and in differentiation of acoustic neurons within the acoustic neural crest complex.

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Section: Discussionmentioning

confidence: 99%

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Roles of ß-catenin in inner ear development in rat embryos

Matsuda¹,

Keino²

2000

Anat Embryol

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“…One of these genes is Wnt3a, which is highly expressed in the developing nervous system (60, 61) and whose gene product has been shown to be essential for neural tube patterning (62), for the promotion of proliferation of dopaminergic neuronal precursor cells (59), and for induction of neuronal differentiation of ES cells in vitro (63). The differential expression of Wnt3a in wild-type versus Hoxa1 knockout cells was demonstrated by RT-PCR (Fig.…”

Section: Expression Of Polycomb Group Genes In the Emc-eshoxa1-15mentioning

confidence: 99%

Differences in Gene Expression between Wild Type and Hoxa1 Knockout Embryonic Stem Cells after Retinoic Acid Treatment or Leukemia Inhibitory Factor (LIF) Removal

Martinez‐Ceballos

Chambon

Gudas

2005

Journal of Biological Chemistry

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Homeobox (Hox) genes encode a family of transcription factors that regulate embryonic patterning and organogenesis. In embryos, alterations of the normal pattern of Hox gene expression result in homeotic transformations and malformations. Disruption of the Hoxa1 gene, the most 3 member of the Hoxa cluster and a retinoic acid (RA) direct target gene, results in abnormal ossification of the skull, hindbrain, and inner ear deficiencies, and neonatal death. We have generated Hoxa1 genes positioned at the 3Ј-end are expressed earlier and more anterior, whereas 5Ј-end genes are expressed at later times and more posterior (reviewed in Refs. 1 and 5). Colinear gene expression from these Hox gene clusters may involve an initial change in chromatin structure (histone modification and chromatin decondensation) of the entire loci, which would then facilitate the programmed expression of genes along the clusters by a progressive 3Ј to 5Ј change in higher order chromatin structure (6). Treatment of teratocarcinoma cells or embryonic stem cells with retinoic acid (RA), which acts via the retinoic acid receptors (RAR␣, -␤, and -␥ and their isoforms (reviewed in Refs. 7 and 8), results in the sequential activation of several Hox genes in a manner that resembles their positions in the clusters, e.g. 3Ј genes are activated before 5Ј genes (7-9). Moreover, our laboratory discovered the presence of a retinoic acid response element (RARE) in the 3Ј enhancer of the Hoxa1 gene (10 -13). This RARE is also functional in transgenic mice (14 -16). We also demonstrated that unlike F9 Wt cells, F9 RAR␥ Ϫ/Ϫ cells fail to express the Hoxa1 gene in response to RA (17). Alterations in the normal pattern of Hox gene expression in embryos result in homeotic transformations and malformations, and frequently, in perinatal lethality (3,18). For instance, the targeted inactivation in mice of both alleles of the most 3Ј member of the Hoxa cluster, the Hoxa1 gene, leads to numerous developmental defects, including hindbrain deficiencies and abnormal skull ossification, and ultimately, to neonatal death (19 -22). Numerous studies have demonstrated that the hindbrain defects in Hoxa1 Ϫ/Ϫ mice result in part from the failure of Hoxb1 to reach its anterior limit of expression at the presumptive rhombomere 3/rhombomere 4 (r3/4) boundary, which initiates a cascade of gene misexpression that results in the misspecification of the hindbrain compartments from r2 to r5 (23-26). Furthermore, the ectopic expression of Hoxa1 in transgenic mice leads to the ectopic activation of Hoxb1 in r2, produces anterior abnormalities, including the reorganization of the developing hindbrain, and ultimately results in embryonic death (27). These observations highlight the importance of the Hoxa1 gene and suggest that the regulatory effects of retinoids on cell growth and on embryonic patterning may be * This work was supported by National Institutes of Health Grants R01CA43796 (to L. J. G.) and UR 2U19HDO35466. The costs of publication of this article were defrayed in part by th...

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“…In addition, Ascl1 represses genes that function in early dorsal-ventral patterning of the spinal cord, such as Wnt1 (Augustine et al, 1995;Lee and Jessell, 1999) and the sonic hedgehog pathway gene Gli3 (supplementary material Table S5) (Persson et al, 2002). Ascl1 also represses several genes involved broadly in differentiation of non-neuronal lineages.…”

Section: Ascl1 Directly Regulates Genes Involved In Multiple Processementioning

confidence: 99%

A transcription factor network specifying inhibitory versus excitatory neurons in the dorsal spinal cord

Borromeo¹,

Meredith²,

Castro³

et al. 2014

Development

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The proper balance of excitatory and inhibitory neurons is crucial for normal processing of somatosensory information in the dorsal spinal cord. Two neural basic helix-loop-helix transcription factors (TFs), Ascl1 and Ptf1a, have contrasting functions in specifying these neurons. To understand how Ascl1 and Ptf1a function in this process, we identified their direct transcriptional targets genome-wide in the embryonic mouse neural tube using ChIP-Seq and RNA-Seq. We show that Ascl1 and Ptf1a directly regulate distinct homeodomain TFs that specify excitatory or inhibitory neuronal fates. In addition, Ascl1 directly regulates genes with roles in several steps of the neurogenic program, including Notch signaling, neuronal differentiation, axon guidance and synapse formation. By contrast, Ptf1a directly regulates genes encoding components of the neurotransmitter machinery in inhibitory neurons, and other later aspects of neural development distinct from those regulated by Ascl1. Moreover, Ptf1a represses the excitatory neuronal fate by directly repressing several targets of Ascl1. Ascl1 and Ptf1a bind sequences primarily enriched for a specific E-Box motif (CAGCTG) and for secondary motifs used by Sox, Rfx, Pou and homeodomain factors. Ptf1a also binds sequences uniquely enriched in the CAGATG E-box and in the binding motif for its co-factor Rbpj, providing two factors that influence the specificity of Ptf1a binding. The direct transcriptional targets identified for Ascl1 and Ptf1a provide a molecular understanding of how these DNAbinding proteins function in neuronal development, particularly as key regulators of homeodomain TFs required for neuronal subtype specification.

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Interactions of Wnt‐1 and Wnt‐3a are essential for neural tube patterning

Cited by 30 publications

References 27 publications

Roles of ß-catenin in inner ear development in rat embryos

Roles of ß-catenin in inner ear development in rat embryos

Differences in Gene Expression between Wild Type and Hoxa1 Knockout Embryonic Stem Cells after Retinoic Acid Treatment or Leukemia Inhibitory Factor (LIF) Removal

A transcription factor network specifying inhibitory versus excitatory neurons in the dorsal spinal cord

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