TGF-β Signaling Specifies Axons during Brain Development

Yi, Jason; Barnes, Anthony P.; Hand, Randal; Polleux, Franck; Ehlers, Michael

doi:10.1016/j.cell.2010.06.010

Cited by 261 publications

(268 citation statements)

References 57 publications

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“…TGF-b1, TGF-b2, and TGF-b3 have also been shown to increase the number and length of neurites . Together, these findings indicate that TGF-b signaling is required to induce axon formation and neuronal migration (Yi et al 2010).…”

Section: Migration and Axon Guidancementioning

confidence: 74%

TGF-β Family Signaling in Neural and Neuronal Differentiation, Development, and Function

Meyers

Kessler

2017

Cold Spring Harb Perspect Biol

137

107

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Section: Migration and Axon Guidancementioning

confidence: 74%

TGF-β Family Signaling in Neural and Neuronal Differentiation, Development, and Function

Meyers

Kessler

2017

Cold Spring Harb Perspect Biol

137

107

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“…63). In addition, recent findings demonstrate that Tgfbr2 activity is required for axon formation and neuronal migration in the developing mammalian neocortex (64) and that expression of Fgfr1 and Fgfr2 determines brain size (65,66). Richtsmeier et al (67) have pointed out the analogy between human craniosynostosis and the simplification trend of cranial bone elements in synapsid evolution.…”

Section: Discussionmentioning

confidence: 99%

Paleontological and developmental evidence resolve the homology and dual embryonic origin of a mammalian skull bone, the interparietal

Koyabu

Maier

Sánchez‐Villagra

2012

Proc. Natl. Acad. Sci. U.S.A.

119

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The homologies of mammalian skull elements are now fairly well established, except for the controversial interparietal bone. A previous experimental study reported an intriguing mixed origin of the interparietal: the medial portion being derived from the neural crest cells, whereas the lateral portion from the mesoderm. The evolutionary history of such mixed origin remains unresolved, and contradictory reports on the presence or absence and developmental patterns of the interparietal among mammals have complicated the question of its homology. Here we provide an alternative perspective on the evolutionary identity of the interparietal, based on a comprehensive study across more than 300 extinct and extant taxa, integrating embryological and paleontological data. Although the interparietal has been regarded as being lost in various lineages, our investigation on embryos demonstrates its presence in all extant mammalian "orders." The generally accepted paradigm has regarded the interparietal as consisting of two elements that are homologized to the postparietals of basal amniotes. The tabular bones have been postulated as being lost during the rise of modern mammals. However, our results demonstrate that the interparietal consists not of two but of four elements. We propose that the tabulars of basal amniotes are conserved as the lateral interparietal elements, which quickly fuse to the medial elements at the embryonic stage, and that the postparietals are homologous to the medial elements. Hence, the dual developmental origin of the mammalian interparietal can be explained as the evolutionary consequence of the fusion between the crest-derived "postparietals" and the mesoderm-derived "tabulars." embryology | morphological evolution | synapsids | fossil | occipital

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“…6G-K). Co-activation of mitochondrial biogenesis is also a prerequisite for TGFβ-TAK1-induced neuronal growth TAK1, activated by TGFβ signalling, controls axonal growth during brain development (Yi et al, 2010). However, it has also been shown that TAK1 activates AMPK (Xie et al, 2006).…”

Section: Activation Of Mitochondrial Biogenesis Is Required For Ampkimentioning

confidence: 99%

Mitochondrial biogenesis is required for axonal growth

Vaarmann¹,

Mandel²,

Zeb³

et al. 2016

Journal of Cell Science

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During early development, neurons undergo complex morphological rearrangements to assemble into neuronal circuits and propagate signals. Rapid growth requires a large quantity of building materials, efficient intracellular transport and also a considerable amount of energy. To produce this energy, the neuron should first generate new mitochondria because the pre-existing mitochondria are unlikely to provide a sufficient acceleration in ATP production. Here, we demonstrate that mitochondrial biogenesis and ATP production are required for axonal growth and neuronal development in cultured rat cortical neurons. We also demonstrate that growth signals activating the CaMKKβ, LKB1-STRAD or TAK1 pathways also co-activate the AMPK-PGC-1α-NRF1 axis leading to the generation of new mitochondria to ensure energy for upcoming growth. In conclusion, our results suggest that neurons are capable of signalling for upcoming energy requirements. Earlier activation of mitochondrial biogenesis through these pathways will accelerate the generation of new mitochondria, thereby ensuring energy-producing capability for when other factors for axonal growth are synthesized.

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TGF-β Signaling Specifies Axons during Brain Development

Cited by 261 publications

References 57 publications

TGF-β Family Signaling in Neural and Neuronal Differentiation, Development, and Function

TGF-β Family Signaling in Neural and Neuronal Differentiation, Development, and Function

Paleontological and developmental evidence resolve the homology and dual embryonic origin of a mammalian skull bone, the interparietal

Mitochondrial biogenesis is required for axonal growth

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