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Journal articles on the topic 'Axon guidance'

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Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Kim, Sung Wook, and Kyong-Tai Kim. "Expression of Genes Involved in Axon Guidance: How Much Have We Learned?" International Journal of Molecular Sciences 21, no. 10 (May 18, 2020): 3566. http://dx.doi.org/10.3390/ijms21103566.

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Neuronal axons are guided to their target during the development of the brain. Axon guidance allows the formation of intricate neural circuits that control the function of the brain, and thus the behavior. As the axons travel in the brain to find their target, they encounter various axon guidance cues, which interact with the receptors on the tip of the growth cone to permit growth along different signaling pathways. Although many scientists have performed numerous studies on axon guidance signaling pathways, we still have an incomplete understanding of the axon guidance system. Lately, studies on axon guidance have shifted from studying the signal transduction pathways to studying other molecular features of axon guidance, such as the gene expression. These new studies present evidence for different molecular features that broaden our understanding of axon guidance. Hence, in this review we will introduce recent studies that illustrate different molecular features of axon guidance. In particular, we will review literature that demonstrates how axon guidance cues and receptors regulate local translation of axonal genes and how the expression of guidance cues and receptors are regulated both transcriptionally and post-transcriptionally. Moreover, we will highlight the pathological relevance of axon guidance molecules to specific diseases.

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2

Vactor, David Van. "Axon guidance." Current Biology 9, no. 21 (November 1999): R797—R799. http://dx.doi.org/10.1016/s0960-9822(99)80492-8.

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3

Zallen, J. A., S. A. Kirch, and C. I. Bargmann. "Genes required for axon pathfinding and extension in the C. elegans nerve ring." Development 126, no. 16 (August 15, 1999): 3679–92. http://dx.doi.org/10.1242/dev.126.16.3679.

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Over half of the neurons in Caenorhabditis elegans send axons to the nerve ring, a large neuropil in the head of the animal. Genetic screens in animals that express the green fluorescent protein in a subset of sensory neurons identified eight new sax genes that affect the morphology of nerve ring axons. sax-3/robo mutations disrupt axon guidance in the nerve ring, while sax-5, sax-9 and unc-44 disrupt both axon guidance and axon extension. Axon extension and guidance proceed normally in sax-1, sax-2, sax-6, sax-7 and sax-8 mutants, but these animals exhibit later defects in the maintenance of nerve ring structure. The functions of existing guidance genes in nerve ring development were also examined, revealing that SAX-3/Robo acts in parallel to the VAB-1/Eph receptor and the UNC-6/netrin, UNC-40/DCC guidance systems for ventral guidance of axons in the amphid commissure, a major route of axon entry into the nerve ring. In addition, SAX-3/Robo and the VAB-1/Eph receptor both function to prevent aberrant axon crossing at the ventral midline. Together, these genes define pathways required for axon growth, guidance and maintenance during nervous system development.

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4

Nishikimi, Mitsuaki, Koji Oishi, and Kazunori Nakajima. "Axon Guidance Mechanisms for Establishment of Callosal Connections." Neural Plasticity 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/149060.

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Numerous studies have investigated the formation of interhemispheric connections which are involved in high-ordered functions of the cerebral cortex in eutherian animals, including humans. The development of callosal axons, which transfer and integrate information between the right/left hemispheres and represent the most prominent commissural system, must be strictly regulated. From the beginning of their growth, until reaching their targets in the contralateral cortex, the callosal axons are guided mainly by two environmental cues: (1) the midline structures and (2) neighboring? axons. Recent studies have shown the importance of axona guidance by such cues and the underlying molecular mechanisms. In this paper, we review these guidance mechanisms during the development of the callosal neurons. Midline populations express and secrete guidance molecules, and “pioneer” axons as well as interactions between the medial and lateral axons are also involved in the axon pathfinding of the callosal neurons. Finally, we describe callosal dysgenesis in humans and mice, that results from a disruption of these navigational mechanisms.

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5

Stoeckli, Esther. "Where does axon guidance lead us?" F1000Research 6 (January 25, 2017): 78. http://dx.doi.org/10.12688/f1000research.10126.1.

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During neural circuit formation, axons need to navigate to their target cells in a complex, constantly changing environment. Although we most likely have identified most axon guidance cues and their receptors, we still cannot explain the molecular background of pathfinding for any subpopulation of axons. We lack mechanistic insight into the regulation of interactions between guidance receptors and their ligands. Recent developments in the field of axon guidance suggest that the regulation of surface expression of guidance receptors comprises transcriptional, translational, and post-translational mechanisms, such as trafficking of vesicles with specific cargos, protein-protein interactions, and specific proteolysis of guidance receptors. Not only axon guidance molecules but also the regulatory mechanisms that control their spatial and temporal expression are involved in synaptogenesis and synaptic plasticity. Therefore, it is not surprising that genes associated with axon guidance are frequently found in genetic and genomic studies of neurodevelopmental disorders.

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6

Liu, Zhi-Zhi, Jian Zhu, Chang-Ling Wang, Xin Wang, Ying-Ying Han, Ling-Yan Liu, and Hong A. Xu. "CRMP2 and CRMP4 Are Differentially Required for Axon Guidance and Growth in Zebrafish Retinal Neurons." Neural Plasticity 2018 (June 21, 2018): 1–9. http://dx.doi.org/10.1155/2018/8791304.

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Axons are directed to their correct targets by guidance cues during neurodevelopment. Many axon guidance cues have been discovered; however, much less known is about how the growth cones transduce the extracellular guidance cues to intracellular responses. Collapsin response mediator proteins (CRMPs) are a family of intracellular proteins that have been found to mediate growth cone behavior in vitro; however, their roles in vivo in axon development are much less explored. In zebrafish embryos, we find that CRMP2 and CRMP4 are expressed in the retinal ganglion cell layer when retinal axons are crossing the midline. Knocking down CRMP2 causes reduced elongation and premature termination of the retinal axons, while knocking down CRMP4 results in ipsilateral misprojections of retinal axons that would normally project to the contralateral brain. Furthermore, CRMP4 synchronizes with neuropilin 1 in retinal axon guidance, suggesting that CRMP4 might mediate the semaphorin/neuropilin signaling pathway. These results demonstrate that CRMP2 and CRMP4 function differentially in axon development in vivo.

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7

Shigeoka, Toshiaki, Bo Lu, and Christine E. Holt. "RNA-based mechanisms underlying axon guidance." Journal of Cell Biology 202, no. 7 (September 30, 2013): 991–99. http://dx.doi.org/10.1083/jcb.201305139.

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Axon guidance plays a key role in establishing neuronal circuitry. The motile tips of growing axons, the growth cones, navigate by responding directionally to guidance cues that pattern the embryonic neural pathways via receptor-mediated signaling. Evidence in vitro in the last decade supports the notion that RNA-based mechanisms contribute to cue-directed steering during axon guidance. Different cues trigger translation of distinct subsets of mRNAs and localized translation provides precise spatiotemporal control over the growth cone proteome in response to localized receptor activation. Recent evidence has now demonstrated a role for localized translational control in axon guidance decisions in vivo.

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8

Kellermeyer, Riley, Leah Heydman, Grant Mastick, and Thomas Kidd. "The Role of Apoptotic Signaling in Axon Guidance." Journal of Developmental Biology 6, no. 4 (October 18, 2018): 24. http://dx.doi.org/10.3390/jdb6040024.

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Navigating growth cones are exposed to multiple signals simultaneously and have to integrate competing cues into a coherent navigational response. Integration of guidance cues is traditionally thought to occur at the level of cytoskeletal dynamics. Drosophila studies indicate that cells exhibit a low level of continuous caspase protease activation, and that axon guidance cues can activate or suppress caspase activity. We base a model for axon guidance on these observations. By analogy with other systems in which caspase signaling has non-apoptotic functions, we propose that caspase signaling can either reinforce repulsion or negate attraction in response to external guidance cues by cleaving cytoskeletal proteins. Over the course of an entire trajectory, incorrectly navigating axons may pass the threshold for apoptosis and be eliminated, whereas axons making correct decisions will survive. These observations would also explain why neurotrophic factors can act as axon guidance cues and why axon guidance systems such as Slit/Robo signaling may act as tumor suppressors in cancer.

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9

Tuttle, R., J. E. Braisted, L. J. Richards, and D. D. O'Leary. "Retinal axon guidance by region-specific cues in diencephalon." Development 125, no. 5 (March 1, 1998): 791–801. http://dx.doi.org/10.1242/dev.125.5.791.

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Retinal axons show region-specific patterning along the dorsal-ventral axis of diencephalon: retinal axons grow in a compact bundle over hypothalamus, dramatically splay out over thalamus, and circumvent epithalamus as they continue toward the dorsal midbrain. In vitro, retinal axons are repulsed by substrate-bound and soluble activities in hypothalamus and epithalamus, but invade thalamus. The repulsion is mimicked by a soluble floor plate activity. Tenascin and neurocan, extracellular matrix molecules that inhibit retinal axon growth in vitro, are enriched in hypothalamus and epithalamus. Within thalamus, a stimulatory activity is specifically upregulated in target nuclei at the time that retinal axons invade them. These findings suggest that region-specific, axon repulsive and stimulatory activities control retinal axon patterning in the embryonic diencephalon.

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10

Bashaw, Greg J., Thomas Kidd, Dave Murray, Tony Pawson, and Corey S. Goodman. "Repulsive Axon Guidance." Cell 101, no. 7 (June 2000): 703–15. http://dx.doi.org/10.1016/s0092-8674(00)80883-1.

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11

Keynes, Roger, and Geoffrey M. W. Cook. "Axon guidance molecules." Cell 83, no. 2 (October 1995): 161–69. http://dx.doi.org/10.1016/0092-8674(95)90157-4.

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12

Stoeckli, Esther T. "Longitudinal axon guidance." Current Opinion in Neurobiology 16, no. 1 (February 2006): 35–39. http://dx.doi.org/10.1016/j.conb.2006.01.008.

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13

Pasterkamp, R. Jeroen, and Alex L. Kolodkin. "SnapShot: Axon Guidance." Cell 153, no. 2 (April 2013): 494–494. http://dx.doi.org/10.1016/j.cell.2013.03.031.

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14

Birgbauer, Eric, Stephen F. Oster, Christophe G. Severin, and David W. Sretavan. "Retinal axon growth cones respond to EphB extracellular domains as inhibitory axon guidance cues." Development 128, no. 15 (August 1, 2001): 3041–48. http://dx.doi.org/10.1242/dev.128.15.3041.

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Axon pathfinding relies on cellular signaling mediated by growth cone receptor proteins responding to ligands, or guidance cues, in the environment. Eph proteins are a family of receptor tyrosine kinases that govern axon pathway development, including retinal axon projections to CNS targets. Recent examination of EphB mutant mice, however, has shown that axon pathfinding within the retina to the optic disc is dependent on EphB receptors, but independent of their kinase activity. Here we show a function for EphB1, B2 and B3 receptor extracellular domains (ECDs) in inhibiting mouse retinal axons when presented either as substratum-bound proteins or as soluble proteins directly applied to growth cones via micropipettes. In substratum choice assays, retinal axons tended to avoid EphB-ECDs, while time-lapse microscopy showed that exposure to soluble EphB-ECD led to growth cone collapse or other inhibitory responses. These results demonstrate that, in addition to the conventional role of Eph proteins signaling as receptors, EphB receptor ECDs can also function in the opposite role as guidance cues to alter axon behavior. Furthermore, the data support a model in which dorsal retinal ganglion cell axons heading to the optic disc encounter a gradient of inhibitory EphB proteins which helps maintain tight axon fasciculation and prevents aberrant axon growth into ventral retina. In conclusion, development of neuronal connectivity may involve the combined activity of Eph proteins serving as guidance receptors and as axon guidance cues.

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15

Sherry, Tessa, Ava Handley, Hannah R. Nicholas, and Roger Pocock. "Harmonization of L1CAM expression facilitates axon outgrowth and guidance of a motor neuron." Development 147, no. 20 (September 29, 2020): dev193805. http://dx.doi.org/10.1242/dev.193805.

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ABSTRACTBrain development requires precise regulation of axon outgrowth, guidance and termination by multiple signaling and adhesion molecules. How the expression of these neurodevelopmental regulators is transcriptionally controlled is poorly understood. The Caenorhabditis elegans SMD motor neurons terminate axon outgrowth upon sexual maturity and partially retract their axons during early adulthood. Here we show that C-terminal binding protein 1 (CTBP-1), a transcriptional corepressor, is required for correct SMD axonal development. Loss of CTBP-1 causes multiple defects in SMD axon development: premature outgrowth, defective guidance, delayed termination and absence of retraction. CTBP-1 controls SMD axon guidance by repressing the expression of SAX-7, an L1 cell adhesion molecule (L1CAM). CTBP-1-regulated repression is crucial because deregulated SAX-7/L1CAM causes severely aberrant SMD axons. We found that axonal defects caused by deregulated SAX-7/L1CAM are dependent on a distinct L1CAM, called LAD-2, which itself plays a parallel role in SMD axon guidance. Our results reveal that harmonization of L1CAM expression controls the development and maturation of a single neuron.

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16

Yu, Hung-Hsiang, Alex S. Huang, and Alex L. Kolodkin. "Semaphorin-1a Acts in Concert With the Cell Adhesion Molecules Fasciclin II and Connectin to Regulate Axon Fasciculation in Drosophila." Genetics 156, no. 2 (October 1, 2000): 723–31. http://dx.doi.org/10.1093/genetics/156.2.723.

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Abstract Semaphorins comprise a large family of phylogenetically conserved secreted and transmembrane glycoproteins, many of which have been implicated in repulsive axon guidance events. The transmembrane semaphorin Sema-1a in Drosophila is expressed on motor axons and is required for the generation of neuromuscular connectivity. Sema-1a can function as an axonal repellent and mediates motor axon defasciculation. Here, by manipulating the levels of Sema-1a and the cell adhesion molecules fasciclin II (Fas II) and connectin (Conn) on motor axons, we provide further evidence that Sema-1a mediates axonal defasciculation events by acting as an axonally localized repellent and that correct motor axon guidance results from a balance between attractive and repulsive guidance cues expressed on motor neurons.

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17

Rangarajan, R., Q. Gong, and U. Gaul. "Migration and function of glia in the developing Drosophila eye." Development 126, no. 15 (August 1, 1999): 3285–92. http://dx.doi.org/10.1242/dev.126.15.3285.

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Although glial cells have been implicated widely in the formation of axon tracts in both insects and vertebrates, their specific function appears to be context-dependent, ranging from providing essential guidance cues to playing a merely facilitory role. Here we examine the role of the retinal basal glia (RBG) in photoreceptor axon guidance in Drosophila. The RBG originate in the optic stalk and have been thought to migrate into the eye disc along photoreceptor axons, thus precluding any role in axon guidance. Here we show the following. (1) The RBG can, in fact, migrate into the eye disc even in the absence of photoreceptor axons in the optic stalk; they also migrate to ectopic patches of differentiating photoreceptors without axons providing a continuous physical substratum. This suggests that glial cells are attracted into the eye disc not through haptotaxis along established axons, but through another mechanism, possibly chemotaxis. (2) If no glial cells are present in the eye disc, photoreceptor axons are able to grow and direct their growth posteriorly as in wild type, but are unable to enter the optic stalk. This indicates that the RBG have a crucial role in axon guidance, but not in axonal outgrowth per se. (3) A few glia close to the entry of the optic stalk suffice to guide the axons into the stalk, suggesting that glia instruct axons by local interaction.

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18

Newsome, T. P., B. Asling, and B. J. Dickson. "Analysis of Drosophila photoreceptor axon guidance in eye-specific mosaics." Development 127, no. 4 (February 15, 2000): 851–60. http://dx.doi.org/10.1242/dev.127.4.851.

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During development of the adult Drosophila visual system, axons of the eight photoreceptors in each ommatidium fasciculate together and project as a single bundle towards the optic lobes of the brain. Within the brain, individual photoreceptor axons from each bundle then seek specific targets in distinct layers of the optic lobes. The axons of photoreceptors R1-R6 terminate in the lamina, while R7 and R8 axons pass through the lamina to terminate in separate layers of the medulla. To identify genes required for photoreceptor axon guidance, including those with essential functions during early development, we have devised a strategy for the simple and efficient generation of genetic mosaics in which mutant photoreceptor axons innervate a predominantly wild-type brain. In a large-scale saturation mutagenesis performed using this system, we recovered new alleles of the gene encoding the receptor tyrosine phosphatase PTP69D. PTP69D has previously been shown to function in the correct targeting of motor axons in the embryo and R1-R6 axons in the visual system. Here, we show that PTP69D is also required for correct targeting of R7 axons. Whereas mutant R1-R6 axons occasionally extend beyond their normal targets in the lamina, mutant R7 axons often fail to reach their targets in the medulla, stopping instead at the same level as the R8 axon. These targeting errors are difficult to reconcile with models in which PTP69D plays an instructive role in photoreceptor axon targeting, as previously proposed. Rather, we suggest that PTP69D plays a permissive role, perhaps reducing the adhesion of R1-R6 and R7 growth cones to the pioneer R8 axon so that they can respond independently to their specific targeting cues.

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19

Han, Peng, Yuanchu She, Zhuoxuan Yang, Mengru Zhuang, Qingjun Wang, Xiaopeng Luo, Chaoqun Yin, Junda Zhu, Samie R. Jaffrey, and Sheng-Jian Ji. "Cbln1 regulates axon growth and guidance in multiple neural regions." PLOS Biology 20, no. 11 (November 17, 2022): e3001853. http://dx.doi.org/10.1371/journal.pbio.3001853.

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The accurate construction of neural circuits requires the precise control of axon growth and guidance, which is regulated by multiple growth and guidance cues during early nervous system development. It is generally thought that the growth and guidance cues that control the major steps of axon development have been defined. Here, we describe cerebellin-1 (Cbln1) as a novel cue that controls diverse aspects of axon growth and guidance throughout the central nervous system (CNS) by experiments using mouse and chick embryos. Cbln1 has previously been shown to function in late neural development to influence synapse organization. Here, we find that Cbln1 has an essential role in early neural development. Cbln1 is expressed on the axons and growth cones of developing commissural neurons and functions in an autocrine manner to promote axon growth. Cbln1 is also expressed in intermediate target tissues and functions as an attractive guidance cue. We find that these functions of Cbln1 are mediated by neurexin-2 (Nrxn2), which functions as the Cbln1 receptor for axon growth and guidance. In addition to the developing spinal cord, we further show that Cbln1 functions in diverse parts of the CNS with major roles in cerebellar parallel fiber growth and retinal ganglion cell axon guidance. Despite the prevailing role of Cbln1 as a synaptic organizer, our study discovers a new and unexpected function for Cbln1 as a general axon growth and guidance cue throughout the nervous system.

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20

Crowner, Daniel, Knut Madden, Scott Goeke, and Edward Giniger. "Lola regulates midline crossing of CNS axons inDrosophila." Development 129, no. 6 (March 15, 2002): 1317–25. http://dx.doi.org/10.1242/dev.129.6.1317.

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The pattern and level of expression of axon guidance proteins must be choreographed with exquisite precision for the nervous system to develop its proper connectivity. Previous work has shown that the transcription factor Lola is required for central nervous system (CNS) axons of Drosophila to extend longitudinally. We show here that Lola is simultaneously required to repel these same longitudinal axons away from the midline, and that it acts, in part, by augmenting the expression both of the midline repellant, Slit, and of its axonal receptor, Robo. Lola is thus the examplar of a class of axon guidance molecules that control axon patterning by coordinating the regulation of multiple, independent guidance genes, ensuring that they are co-expressed at the correct time, place and relative level.

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21

Gallo, Gianluca, and Paul C. Letourneau. "Axon guidance: GTPases help axons reach their targets." Current Biology 8, no. 3 (January 1998): R80—R82. http://dx.doi.org/10.1016/s0960-9822(98)70051-x.

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22

Vaidya, Ashish, Anna Pniak, Greg Lemke, and Arthur Brown. "EphA3 Null Mutants Do Not Demonstrate Motor Axon Guidance Defects." Molecular and Cellular Biology 23, no. 22 (November 15, 2003): 8092–98. http://dx.doi.org/10.1128/mcb.23.22.8092-8098.2003.

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ABSTRACT Motor axon projections are topographically ordered. Medial motor column axons project to axial muscles, whereas lateral motor column axons project to limb muscles and, along the rostrocaudal axis of the animal, the more rostral motor neuron pools project to more rostral muscle targets. We have shown that EphA3 is specifically expressed in the developing medial motor column and have postulated that EphA3 might be responsible for directing their axons to axial muscle targets. This hypothesis was supported by our demonstration that EphA3 can direct retinal ganglion cell axon targeting and by studies of ephrin-A5−/− mutants that show that EphA receptor signaling controls the topographic innervation of the acromiotrapezius. To test the role of EphA3 in motor axon guidance, we generated an EphA3 null mutant. Retrograde labeling studies in EphA3−/− embryos and adults indicate that, contrary to our predictions, EphA3 is not necessary to direct motor axons to axial muscle targets. Our results also demonstrate that ephrin A5's ability to direct topographic innervation of the acromiotrapezius must be mediated through EphA receptors other than, or in addition to, EphA3.

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23

Hidalgo, A. "Neuron–glia interactions during axon guidance in Drosophila." Biochemical Society Transactions 31, no. 1 (February 1, 2003): 50–55. http://dx.doi.org/10.1042/bst0310050.

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Axons navigate to trace stereotypic trajectories over an environment often rich in glial cells. Once axonal trajectories are defined, their structuring proceeds through multiple fasciculation and defasciculation events, to finally establish the mature bundles. Fasciculation and ensheathment also proceed in close association between axons and glial cells, and ultimately require glia. The cross-talk between axons and glia during axon guidance is manifested in: (i) axonal fasciculation and bundling, promoted by glia; (ii) growth cone guidance, as glia function as guidepost cells at choice points; (iii) glial migration patterns, which are influenced by neurons; (iv) cell survival control, which constrains position and number of both cell types; and (iv) connectivity, where an axon contacts its final target aided by glial cells. Understanding the reciprocal interactions between neurons and glia during guidance and fasciculation is absolutely necessary to implement repair of axonal trajectories upon damage. Drosophila can be used as a model system for these purposes.

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24

Chen, Shih-Yu, Chun-Ta Ho, Wei-Wen Liu, Mark Lucanic, Hsiu-Ming Shih, Pei-Hsin Huang, and Hwai-Jong Cheng. "Regulation of axon repulsion by MAX-1 SUMOylation and AP-3." Proceedings of the National Academy of Sciences 115, no. 35 (August 13, 2018): E8236—E8245. http://dx.doi.org/10.1073/pnas.1804373115.

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During neural development, growing axons express specific surface receptors in response to various environmental guidance cues. These axon guidance receptors are regulated through intracellular trafficking and degradation to enable navigating axons to reach their targets. In Caenorhabditis elegans, the UNC-5 receptor is necessary for dorsal migration of developing motor axons. We previously found that MAX-1 is required for UNC-5–mediated axon repulsion, but its mechanism of action remained unclear. Here, we demonstrate that UNC-5–mediated axon repulsion in C. elegans motor axons requires both max-1 SUMOylation and the AP-3 complex β subunit gene, apb-3. Genetic interaction studies show that max-1 is SUMOylated by gei-17/PIAS1 and acts upstream of apb-3. Biochemical analysis suggests that constitutive interaction of MAX-1 and UNC-5 receptor is weakened by MAX-1 SUMOylation and by the presence of APB-3, a competitive interactor with UNC-5. Overexpression of APB-3 reroutes the trafficking of UNC-5 receptor into the lysosome for protein degradation. In vivo fluorescence recovery after photobleaching experiments shows that MAX-1 SUMOylation and APB-3 are required for proper trafficking of UNC-5 receptor in the axon. Our results demonstrate that SUMOylation of MAX-1 plays an important role in regulating AP-3–mediated trafficking and degradation of UNC-5 receptors during axon guidance.

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Onishi, Keisuke, Runyi Tian, Bo Feng, Yiqiong Liu, Junkai Wang, Yinan Li, and Yimin Zou. "LRRK2 mediates axon development by regulating Frizzled3 phosphorylation and growth cone–growth cone communication." Proceedings of the National Academy of Sciences 117, no. 30 (July 8, 2020): 18037–48. http://dx.doi.org/10.1073/pnas.1921878117.

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Axon–axon interactions are essential for axon guidance during nervous system wiring. However, it is unknown whether and how the growth cones communicate with each other while sensing and responding to guidance cues. We found that the Parkinson’s disease gene, leucine-rich repeat kinase 2 (LRRK2), has an unexpected role in growth cone–growth cone communication. The LRRK2 protein acts as a scaffold and induces Frizzled3 hyperphosphorylation indirectly by recruiting other kinases and also directly phosphorylates Frizzled3 on threonine 598 (T598). InLRRK1orLRRK2single knockout,LRRK1/2double knockout, andLRRK2 G2019Sknockin, the postcrossing spinal cord commissural axons are disorganized and showed anterior–posterior guidance errors after midline crossing. Growth cones from eitherLRRK2knockout orG2019Sknockin mice showed altered interactions, suggesting impaired communication. Intercellular interaction between Frizzled3 and Vangl2 is essential for planar cell polarity signaling. We show here that this interaction is regulated by phosphorylation of Frizzled3 at T598 and can be regulated by LRRK2 in a kinase activity-dependent way. In theLRRK1/2double knockout orLRRK2 G2019Sknockin, the dopaminergic axon bundle in the midbrain was significantly widened and appeared disorganized, showing aberrant posterior-directed growth. Our findings demonstrate that LRRK2 regulates growth cone–growth cone communication in axon guidance and that both loss-of-function mutation and a gain-of-function mutation (G2019S)cause axon guidance defects in development.

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26

Wells, William. "Diversity in axon guidance." Genome Biology 1 (2000): spotlight—20000616–01. http://dx.doi.org/10.1186/gb-spotlight-20000616-01.

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27

Goodhill, Geoffrey J. "Diffusion in Axon Guidance." European Journal of Neuroscience 9, no. 7 (July 1997): 1414–21. http://dx.doi.org/10.1111/j.1460-9568.1997.tb01496.x.

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28

Ray, L. B. "Serotonin's Axon Guidance Switch." Science's STKE 2007, no. 384 (April 25, 2007): tw150. http://dx.doi.org/10.1126/stke.3842007tw150.

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29

Hines, P. J. "Draxin and Axon Guidance." Science Signaling 2, no. 54 (January 13, 2009): ec23-ec23. http://dx.doi.org/10.1126/scisignal.254ec23.

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30

Baier, H., and F. Bonhoeffer. "Attractive axon guidance molecules." Science 265, no. 5178 (September 9, 1994): 1541–42. http://dx.doi.org/10.1126/science.8079167.

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31

Bashaw, Greg J., and Corey S. Goodman. "Chimeric Axon Guidance Receptors." Cell 97, no. 7 (June 1999): 917–26. http://dx.doi.org/10.1016/s0092-8674(00)80803-x.

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32

Steward, Oswald. "Translating Axon Guidance Cues." Cell 110, no. 5 (September 2002): 537–40. http://dx.doi.org/10.1016/s0092-8674(02)00934-0.

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33

Tannahill, David, Geoff M. W. Cook, and Roger J. Keynes. "Axon guidance and somites." Cell and Tissue Research 290, no. 2 (October 2, 1997): 275–83. http://dx.doi.org/10.1007/s004410050932.

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34

Kolodkin, Alex L., and R. Jeroen Pasterkamp. "SnapShot: Axon Guidance II." Cell 153, no. 3 (April 2013): 722–722. http://dx.doi.org/10.1016/j.cell.2013.04.004.

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35

Palka, J. "Epithelial axon guidance inDrosophila." Journal of Neurobiology 17, no. 6 (November 1986): 581–84. http://dx.doi.org/10.1002/neu.480170602.

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36

Tannahill, David, Geoff M. W. Cook, and Roger J. Keynes. "Axon guidance and somites." Cell and Tissue Research 291, no. 2 (January 12, 1998): 363. http://dx.doi.org/10.1007/s004410051005.

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Williams, Darren W., and David Shepherd. "Persistent larval sensory neurones are required for the normal development of the adult sensory afferent projections inDrosophila." Development 129, no. 3 (February 1, 2002): 617–24. http://dx.doi.org/10.1242/dev.129.3.617.

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We have tested the hypothesis that larval neurones guide growth of adult sensory axons in Drosophila. We show that ablation of larval sensory neurones causes defects in the central projections of adult sensory neurones. Spiralling axons and ectopic projections indicate failure in axon growth guidance. We show that larval sensory neurones are required for peripheral pathfinding, entry into the CNS and growth guidance within the CNS. Ablation of subsets of neurones shows that larval sensory neurones serve specific guidance roles. Dorsal neurones are required for axon guidance across the midline, whereas lateral neurones are required for posterior growth. We conclude that larval sensory neurones pioneer the assembly of sensory arrays in adults.

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Gallo, Gianluca, Hal F. Yee, and Paul C. Letourneau. "Actin turnover is required to prevent axon retraction driven by endogenous actomyosin contractility." Journal of Cell Biology 158, no. 7 (September 30, 2002): 1219–28. http://dx.doi.org/10.1083/jcb.200204140.

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Growth cone motility and guidance depend on the dynamic reorganization of filamentous actin (F-actin). In the growth cone, F-actin undergoes turnover, which is the exchange of actin subunits from existing filaments. However, the function of F-actin turnover is not clear. We used jasplakinolide (jasp), a cell-permeable macrocyclic peptide that inhibits F-actin turnover, to study the role of F-actin turnover in axon extension. Treatment with jasp caused axon retraction, demonstrating that axon extension requires F-actin turnover. The retraction of axons in response to the inhibition of F-actin turnover was dependent on myosin activity and regulated by RhoA and myosin light chain kinase. Significantly, the endogenous myosin-based contractility was sufficient to cause axon retraction, because jasp did not alter myosin activity. Based on these observations, we asked whether guidance cues that cause axon retraction (ephrin-A2) inhibit F-actin turnover. Axon retraction in response to ephrin-A2 correlated with decreased F-actin turnover and required RhoA activity. These observations demonstrate that axon extension depends on an interaction between endogenous myosin-driven contractility and F-actin turnover, and that guidance cues that cause axon retraction inhibit F-actin turnover.

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Goodhill, Geoffrey J., and Herwig Baier. "Axon Guidance: Stretching Gradients to the Limit." Neural Computation 10, no. 3 (April 1, 1998): 521–27. http://dx.doi.org/10.1162/089976698300017638.

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Neuronal growth cones, the sensory-motile structures at the tips of developing axons, navigate to their targets over distances that can be many times greater than their diameter. They may accomplish this impressive task by following spatial gradients of axon guidance molecules in their environment (Bonhoeffer & Gierer, 1984; Tessier-Lavigne & Placzek, 1991; Baier & Bonhoeffer, 1994). We calculate the optimal shape of a gradient and the distance over which it can be detected by a growth cone for two competing mechanistic models of axon guidance. The results are surprisingly simple: Regardless of the mechanism, the maximum distance is about 1 cm. Since gradients and growth cones have coevolved, we suggest that the shape of the gradient in situ will predict the mechanism of gradient detection. In addition, we show that the experimentally determined dissociation constants for receptor-ligand complexes implicated in axon guidance are about optimal with respect to maximizing guidance distance. The relevance of these results to the retinotectal system is discussed.

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Imai, Takeshi, Takahiro Yamazaki, Reiko Kobayakawa, Ko Kobayakawa, Takaya Abe, Misao Suzuki, and Hitoshi Sakano. "Pre-Target Axon Sorting Establishes the Neural Map Topography." Science 325, no. 5940 (July 9, 2009): 585–90. http://dx.doi.org/10.1126/science.1173596.

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Sensory information detected by the peripheral nervous system is represented as a topographic map in the brain. It has long been thought that the topography of the map is determined by graded positional cues that are expressed by the target. Here, we analyzed the pre-target axon sorting for olfactory map formation in mice. In olfactory sensory neurons, an axon guidance receptor, Neuropilin-1, and its repulsive ligand, Semaphorin-3A, are expressed in a complementary manner. We found that expression levels of Neuropilin-1 determined both pre-target sorting and projection sites of axons. Olfactory sensory neuron–specific knockout of Semaphorin-3A perturbed axon sorting and altered the olfactory map topography. Thus, pre-target axon sorting plays an important role in establishing the topographic order based on the relative levels of guidance molecules expressed by axons.

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Kaufmann, N., Z. P. Wills, and D. Van Vactor. "Drosophila Rac1 controls motor axon guidance." Development 125, no. 3 (February 1, 1998): 453–61. http://dx.doi.org/10.1242/dev.125.3.453.

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Previous genetic studies of intersegmental nerve b development have identified several cell-surface proteins required for correct axon guidance to appropriate target muscles. Here we provide evidence that the small GTPase Drac1 also plays a key role in this guidance process. Neuronal expression of the dominant negative mutation Drac1(N17) causes axons to bypass and extend beyond normal synaptic partners. This phenotype is consistently reproduced by pharmacological blockade of actin assembly. Genetic interactions between Drac1(N17) and the receptor-tyrosine phosphatase Dlar suggest that intersegmental nerve b guidance requires the integration of multiple, convergent signals.

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Whitlock, K. E. "Development of Drosophila wing sensory neurons in mutants with missing or modified cell surface molecules." Development 117, no. 4 (April 1, 1993): 1251–60. http://dx.doi.org/10.1242/dev.117.4.1251.

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The neurons of the sensory receptors on the wing of Drosophila melanogaster have highly characteristic axon projections in the central nervous system (CNS). The morphology of these projections was studied in flies bearing mutations that affect cell surface molecules thought to be important in axon guidance. The animals used were mutant for the fasciclinI (fasI), fasciclinII (fasII), fasciclinIII (fasIII) and neurally altered carbohydrate (nac) genes. Axon populations were visualized by staining with DiI and light-reacting the dye with diaminobenzidine to yield permanent preparations. The fasI, fasII and fasIII mutants as well as the nac mutant display altered axonal trajectories in the CNS. One phenotype seen in fasII mutants and in animals mutant for both fasI and fasIII was extra branching within the axon projection pattern. A second phenotype observed was a reduction or complete loss of one of the tracts, apparently due to the axons shifting to a neighboring tract. This was seen in the most extreme form in nac mutants and to a lesser degree in fasIII mutants. To determine if the mutations discussed here affected axon guidance, wing discs were analyzed using the antibody 22C10 to label sensory neurons in the wing during metamorphosis. Both misrouting of axons and the appearance of ectopic neurons in the wing were observed. In the fasI:fasIII, the fasII and the nac mutants, there was misrouting of sensory axons in the developing wing. In addition, the fasII and nac mutants displayed ectopic sensory neurons in the wing. This implies that the cell surface molecules missing (fasciclins) or modified (by the nac gene product), in these mutants may play a role in both neurogenesis and axon guidance.

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Fitzli, Dora, Esther T. Stoeckli, Stefan Kunz, Kingsley Siribour, Christoph Rader, Beat Kunz, Serguei V. Kozlov, et al. "A Direct Interaction of Axonin-1 with Ngcam-Related Cell Adhesion Molecule (Nrcam) Results in Guidance, but Not Growth of Commissural Axons." Journal of Cell Biology 149, no. 4 (May 15, 2000): 951–68. http://dx.doi.org/10.1083/jcb.149.4.951.

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An interaction of growth cone axonin-1 with the floor-plate NgCAM-related cell adhesion molecule (NrCAM) was shown to play a crucial role in commissural axon guidance across the midline of the spinal cord. We now provide evidence that axonin-1 mediates a guidance signal without promoting axon elongation. In an in vitro assay, commissural axons grew preferentially on stripes coated with a mixture of NrCAM and NgCAM. This preference was abolished in the presence of anti–axonin-1 antibodies without a decrease in neurite length. Consistent with these findings, commissural axons in vivo only fail to extend along the longitudinal axis when both NrCAM and NgCAM interactions, but not when axonin-1 and NrCAM or axonin-1 and NgCAM interactions, are perturbed. Thus, we conclude that axonin-1 is involved in guidance of commissural axons without promoting their growth.

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Damo, Elisa, and Manuela Simonetti. "Axon Guidance Molecules and Pain." Cells 11, no. 19 (October 6, 2022): 3143. http://dx.doi.org/10.3390/cells11193143.

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Chronic pain is a debilitating condition that influences the social, economic, and psychological aspects of patients’ lives. Hence, the need for better treatment is drawing extensive interest from the research community. Developmental molecules such as Wnt, ephrins, and semaphorins are acknowledged as central players in the proper growth of a biological system. Their receptors and ligands are expressed in a wide variety in both neurons and glial cells, which are implicated in pain development, maintenance, and resolution. Thereby, it is not surprising that the impairment of those pathways affects the activities and functions of the entire cell. Evidence indicates aberrant activation of their pathways in the nervous system in rodent models of chronic pain. In those conditions, Wnt, ephrin, and semaphorin signaling participate in enhancing neuronal excitability, peripheral sensitization, synaptic plasticity, and the production and release of inflammatory cytokines. This review summarizes the current knowledge on three main developmental pathways and their mechanisms linked with the pathogenesis and progression of pain, considering their impacts on neuronal and glial cells in experimental animal models. Elucidations of the downstream pathways may provide a new mechanism for the involvement of Wnt, ephrin, and semaphorin pathways in pain chronicity.

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Lee, Won Suk, Won-Ha Lee, Yong Chul Bae, and Kyoungho Suk. "Axon Guidance Molecules Guiding Neuroinflammation." Experimental Neurobiology 28, no. 3 (June 30, 2019): 311–19. http://dx.doi.org/10.5607/en.2019.28.3.311.

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Giger, R. J., E. R. Hollis, and M. H. Tuszynski. "Guidance Molecules in Axon Regeneration." Cold Spring Harbor Perspectives in Biology 2, no. 7 (June 2, 2010): a001867. http://dx.doi.org/10.1101/cshperspect.a001867.

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Bashaw, G. J., and R. Klein. "Signaling from Axon Guidance Receptors." Cold Spring Harbor Perspectives in Biology 2, no. 5 (March 24, 2010): a001941. http://dx.doi.org/10.1101/cshperspect.a001941.

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Seiradake, Elena, E. Yvonne Jones, and Rüdiger Klein. "Structural Perspectives on Axon Guidance." Annual Review of Cell and Developmental Biology 32, no. 1 (October 6, 2016): 577–608. http://dx.doi.org/10.1146/annurev-cellbio-111315-125008.

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49

Yu, Timothy W., and Cornelia I. Bargmann. "Dynamic regulation of axon guidance." Nature Neuroscience 4, S11 (October 29, 2001): 1169–76. http://dx.doi.org/10.1038/nn748.

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50

Dickson, B. J. "Molecular Mechanisms of Axon Guidance." Science 298, no. 5600 (December 6, 2002): 1959–64. http://dx.doi.org/10.1126/science.1072165.

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