T-Box transcription factor Tbx20 regulates a genetic program for cranial motor neuron cell body migration

Song, Mi Ryoung; Shirasaki, Ryuichi; Cai, Chen; Ruiz, Esmeralda C.; Evans, Sylvia M.; Lee, Soo Kyung; Pfaff, Samuel L.

doi:10.1242/dev.02694

Cited by 84 publications

(85 citation statements)

References 62 publications

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“…It has been confirmed that Tbx is required for proper neural crest migration and to stabilize spatial patterns during middle and inner ear development [39]. Furthermore, Tbx gene programs a variety of hindbrain motor neurons for migration, independent of directionality, and in facial neurons is a positive regulator of the non-canonical Wnt signaling pathway [40]. We conclude that Tbx controls neuronal polarity to regulate neural crest migration.…”

Section: Discussionmentioning

confidence: 61%

16p11.2 is required for neuronal polarity

Li¹,

Feng²

2013

WJNS

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Since Autism Spectrum Disorder (ASD) is strongly associated with chromosomal abnormalities of 16p11.2, and Autism has been linked to neuronal polarity defect, our study aimed to explore the role of 16p11.2 genes in regulating neuronal polarity. We performed a neuronal polarity assay in a high throughput manner for candidate genes at 16p11.2. Our most interesting finding was that three 16p11.2 candidate genes, DOC2a, Tbx-6 and KIF 22, affected neuronal polarity. Our research, for the first time, indicates a novel association between 16p11.2 and neuronal polarity. Our results support the hypothesis that 16p11.2 is required for neuronal polarity. Our research provides new important insights into molecular mechanisms underlying the tight association between 16p11.2 and several neural developmental disorders, including autism, epilepsy, mental retardation and schizophrenia.

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Section: Discussionmentioning

confidence: 61%

16p11.2 is required for neuronal polarity

Li¹,

Feng²

2013

WJNS

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“…Moreover, this transcription factor is evolutionarily conserved from flies to humans, suggesting that its transcriptional regulation of Robos and Slits is a conserved mechanism (Takeuchi et al, 2005). Accordingly, both Tbx20 and Slit1/Slit2 knockout mice have defects in the development of hindbrain motoneurons (Hammond et al, 2005;Song et al, 2006). In the mouse, Tbx1 regulates a second transcription factor, Gbx2, which functions in hindbrain and pharyngeal arch artery (PAA) development (Calmont et al, 2009).…”

Section: Transcriptional Regulationmentioning

confidence: 99%

Moving away from the midline: new developments for Slit and Robo

2010

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SummaryIn most tissues, the precise control of cell migration and cellcell interaction is of paramount importance to the development of a functional structure. Several families of secreted molecules have been implicated in regulating these aspects of development, including the Slits and their Robo receptors. These proteins have well described roles in axon guidance but by influencing cell polarity and adhesion, they participate in many developmental processes in diverse cell types. We review recent progress in understanding both the molecular mechanisms that modulate Slit/Robo expression and their functions in neural and non-neural tissue. Key words: Axon guidance, Cell migration, Cell-cell interaction IntroductionIn most organisms, the central nervous system (CNS) develops along a bilateral axis of symmetry located at the midline (Placzek and Briscoe, 2005). During development, the ventral midline or floor plate acts as an organiser through the secretion of diffusible proteins (Placzek and Briscoe, 2005;Gore et al., 2008), which control the growth of axons and dendrites and the migration of neurons across the midline. In the forebrain, glial or neuronal cells delineate the midline (see Glossary, Box 1) and also control axon guidance. For more than two decades, many developmental neurobiologists have tried to understand the mechanisms that control midline crossing in the CNS and to answer some key questions. Firstly, how are commissural axons (see Glossary, Box 1) attracted to the midline and how do their growth cones (see Glossary, Box1) receive and integrate the multiple and contrasting signals released by midline cells? Secondly, what are the molecular and signalling changes that enable commissural axons to leave the midline and often to switch to a longitudinal growth mode? All midline-derived axon guidance factors are expressed at other locations in many developing and mature tissues, where they control a wide range of biological processes.Roundabout receptors (Robo) and their Slit ligands form one of the most crucial ligand-receptor pairings among the axon guidance molecules. Robos were identified in Drosophila in a mutant screen for genes that control the midline crossing of commissural axons (Kidd et al., 1998;Seeger et al., 1993). Similarly, Slit was discovered in Drosophila as a protein secreted by midline glia (Rothberg et al., 1988;Rothberg et al., 1990). Homologues of both proteins have since been discovered in many species (for a review, see . However, the Slit/Robo couple not only functions in axon guidance but also in a variety of developmental Development 137, 1939Development 137, -1952Development 137, (2010 Commissural axons Axons with cell bodies (somata) located on one side of the central nervous system (CNS) that project axons across the midline to contact target cells on the opposite side. Growth cone A specialised bulbous enlargement at the end of growing axons that is characterised by dynamic filamentous extensions, known as filopodia. They sense the environment and respond to adhesi...

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“…7I,J). Previous reports indicated that during neural plate formation in zebrafish, tbx2b expression is regulated by the Wnt receptor frizzled 7a (fzd7a) (Fong et al, 2005), and that in the developing mouse hindbrain, Tbx2 regulates expression of Wnt planar cell polarity (PCP) genes including Fzd7 (Song et al, 2006). However, we find that disrupting the Wnt PCP signaling pathway, by mutation of the proteoglycan knypek (glypican) (Topczewski et al, 2001) or van gogh-like 2 (strabismus; also known as trilobite in zebrafish) (Jessen et al, 2002), has no effect on tbx2b expression, parapineal specification or migration (see Fig.…”

Section: Research Articlementioning

confidence: 99%

Tbx2b is required for the development of the parapineal organ

et al. 2008

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Structural differences between the left and right sides of the brain exist throughout the vertebrate lineage. By studying the zebrafish pineal complex, which exhibits notable asymmetries, both the genes and the cell movements that result in left-right differences can be characterized. The pineal complex consists of the midline pineal organ and the left-sided parapineal organ. The parapineal is responsible for instructing the asymmetric architecture of the bilateral habenulae, the brain nuclei that flank the pineal complex. Using in vivo time-lapse confocal microscopy, we find that the cells that form the parapineal organ migrate as a cluster of cells from the pineal complex anlage to the left side of the brain. In a screen for mutations that disrupted brain laterality, we identified a nonsense mutation in the T-box2b (tbx2b) gene, which encodes a transcription factor expressed in the pineal complex anlage. The tbx2b mutant makes fewer parapineal cells, and they remain as individuals near the midline rather than migrating leftward as a group. The reduced number and incorrect placement of parapineal cells result in symmetric development of the adjacent habenular nuclei. We conclude that tbx2b functions to specify the correct number of parapineal cells and to regulate their asymmetric migration.

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T-Box transcription factor Tbx20 regulates a genetic program for cranial motor neuron cell body migration

Cited by 84 publications

References 62 publications

16p11.2 is required for neuronal polarity

16p11.2 is required for neuronal polarity

Moving away from the midline: new developments for Slit and Robo

Tbx2b is required for the development of the parapineal organ

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