Six3 Represses Nodal Activity to Establish Early Brain Asymmetry in Zebrafish.
From: Department of Biological Sciences, Vanderbilt University, VU Station B 351634, Nashville, TN 37235-1634, USA.
Neuron
- Publish Date: Aug 2007
- ISSN: 0896-6273
- Volume: 55
- Issue: 3
- Pages: 407-15
- Medium: Print
- Language: English
- Citation (JAMA): Inbal Adi, Kim Seok-Hyung, Shin Jimann, et al. Six3 Represses Nodal Activity to Establish Early Brain Asymmetry in Zebrafish.. Neuron Aug 2007;55:407-15
Abstract
The vertebrate brain is anatomically and functionally asymmetric; however, the molecular mechanisms that establish left-right brain patterning are largely unknown. In zebrafish, asymmetric left-sided Nodal signaling within the developing dorsal diencephalon is required for determining the direction of epithalamic asymmetries. Here, we show that Six3, a transcription factor essential for forebrain formation and associated with holoprosencephaly in humans, regulates diencephalic Nodal activity during initial establishment of brain asymmetry. Reduction of Six3 function causes brain-specific deregulation of Nodal pathway activity, resulting in epithalamic laterality defects. Based on misexpression and genetic epistasis experiments, we propose that Six3 acts in the neuroectoderm to establish a prepattern of bilateral repression of Nodal activity. Subsequently, Nodal signaling from the left lateral plate mesoderm alleviates this repression ipsilaterally. Our data reveal a Six3-dependent mechanism for establishment of correct brain laterality and provide an entry point to understanding the genetic regulation of Nodal signaling in the brain.
Mesh Headings (Keywords): Animals, Brain, Dominance, Cerebral, Embryonic Development, Epistasis, Genetic, Epithalamus, Eye Proteins, Homeodomain Proteins, Nerve Tissue Proteins, Transforming Growth Factor beta, Zebrafish
Check for Full Text / PubMed Unique Identifier (PMID): 17678854
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