Home > Publications Database > RhoA Controls Axon Extension Independent of Specification in the Developing Brain. > print

001     141611
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024 7 _ |a 10.1016/j.cub.2019.09.040
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024 7 _ |a pmid:31679934
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024 7 _ |a 0960-9822
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024 7 _ |a 1879-0445
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037 _ _ |a DZNE-2020-07935
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Dupraz, Sebastian
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245 _ _ |a RhoA Controls Axon Extension Independent of Specification in the Developing Brain.
260 _ _ |a London
|c 2019
|b Current Biology Ltd.
264 _ 1 |3 print
|2 Crossref
|b Elsevier BV
|c 2019-11-01
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520 _ _ |a The specification of an axon and its subsequent outgrowth are key steps during neuronal polarization, a prerequisite to wire the brain. The Rho-guanosine triphosphatase (GTPase) RhoA is believed to be a central player in these processes. However, its physiological role has remained undefined. Here, genetic loss- and gain-of-function experiments combined with time-lapse microscopy, cell culture, and in vivo analysis show that RhoA is not involved in axon specification but confines the initiation of neuronal polarization and axon outgrowth during development. Biochemical analysis and super-resolution microscopy together with molecular and pharmacological manipulations reveal that RhoA restrains axon growth by activating myosin-II-mediated actin arc formation in the growth cone to prevent microtubules from protruding toward the leading edge. Through this mechanism, RhoA regulates the duration of axon growth and pause phases, thus controlling the tightly timed extension of developing axons. Thereby, this work unravels physiologically relevant players coordinating actin-microtubule interactions during axon growth.
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542 _ _ |i 2019-11-01
|2 Crossref
|u https://www.elsevier.com/tdm/userlicense/1.0/
542 _ _ |i 2019-09-19
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|u http://creativecommons.org/licenses/by-nc-nd/4.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 2 |a Actin Cytoskeleton: metabolism
|2 MeSH
650 _ 2 |a Actins: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Axons: metabolism
|2 MeSH
650 _ 2 |a Axons: physiology
|2 MeSH
650 _ 2 |a Brain: embryology
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Cell Polarity: physiology
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Gain of Function Mutation: genetics
|2 MeSH
650 _ 2 |a Growth Cones: metabolism
|2 MeSH
650 _ 2 |a Loss of Function Mutation: genetics
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a Microtubules: metabolism
|2 MeSH
650 _ 2 |a Myosin Type II: metabolism
|2 MeSH
650 _ 2 |a Neurogenesis: physiology
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a rhoA GTP-Binding Protein: genetics
|2 MeSH
650 _ 2 |a rhoA GTP-Binding Protein: metabolism
|2 MeSH
650 _ 2 |a rhoA GTP-Binding Protein: physiology
|2 MeSH
700 1 _ |a Hilton, Brett J
|0 P:(DE-2719)2812271
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700 1 _ |a Husch, Andreas
|0 P:(DE-2719)2811971
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700 1 _ |a Da Silva Santos, Telma
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700 1 _ |a Coles, Charlotte H
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700 1 _ |a Stern, Sina
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700 1 _ |a Brakebusch, Cord
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700 1 _ |a Bradke, Frank
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773 1 8 |a 10.1016/j.cub.2019.09.040
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|v 29
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773 _ _ |a 10.1016/j.cub.2019.09.040
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