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Wilson, Sara I
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Publications (10 of 13) Show all publications
Patthey, C., Tong, Y. G., Tait, C. M. & Wilson, S. I. (2017). Evolution of the functionally conserved DCC gene in birds. Scientific Reports, 7, Article ID 42029.
Open this publication in new window or tab >>Evolution of the functionally conserved DCC gene in birds
2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 42029Article in journal (Refereed) Published
Abstract [en]

Understanding the loss of conserved genes is critical for determining how phenotypic diversity is generated. Here we focus on the evolution of DCC, a gene that encodes a highly conserved neural guidance receptor. Disruption of DCC in animal models and humans results in major neurodevelopmental defects including commissural axon defects. Here we examine DCC evolution in birds, which is of particular interest as a major model system in neurodevelopmental research. We found the DCC containing locus was disrupted several times during evolution, resulting in both gene losses and faster evolution rate of salvaged genes. These data suggest that DCC had been lost independently twice during bird evolution, including in chicken and zebra finch, whereas it was preserved in many other closely related bird species, including ducks. Strikingly, we observed that commissural axon trajectory appeared similar regardless of whether DCC could be detected or not. We conclude that the DCC locus is susceptible to genomic instability leading to independent disruptions in different branches of birds and a significant influence on evolution rate. Overall, the phenomenon of loss or molecular evolution of a highly conserved gene without apparent phenotype change is of conceptual importance for understanding molecular evolution of key biological processes.

Place, publisher, year, edition, pages
Macmillan Publishers Ltd., 2017
Keywords
embryology, evolutionary developmental biology, neuronal development
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-131968 (URN)10.1038/srep42029 (DOI)000394782700001 ()
Available from: 2017-02-27 Created: 2017-02-27 Last updated: 2018-06-09Bibliographically approved
Laumonnerie, C., Tong, Y. G., Alstermark, H. & Wilson, S. I. (2015). Commissural axonal corridors instruct neuronal migration in the mouse spinal cord. Nature Communications, 6, Article ID 7028.
Open this publication in new window or tab >>Commissural axonal corridors instruct neuronal migration in the mouse spinal cord
2015 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 6, article id 7028Article in journal (Refereed) Published
Abstract [en]

Unravelling how neurons are guided during vertebrate embryonic development has wide implications for understanding the assembly of the nervous system. During embryogenesis, migration of neuronal cell bodies and axons occurs simultaneously, but to what degree they influence each other's development remains obscure. We show here that within the mouse embryonic spinal cord, commissural axons bisect, delimit or preconfigure ventral interneuron cell body position. Furthermore, genetic disruption of commissural axons results in abnormal ventral interneuron cell body positioning. These data suggest that commissural axonal fascicles instruct cell body position by acting either as border landmarks (axon-restricted migration), which to our knowledge has not been previously addressed, or acting as cellular guides. This study in the developing spinal cord highlights an important function for the interaction of cell bodies and axons, and provides a conceptual proof of principle that is likely to have overarching implications for the development of neuronal architecture.

National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-106511 (URN)10.1038/ncomms8028 (DOI)000355530100002 ()25960414 (PubMedID)
Available from: 2015-07-15 Created: 2015-07-14 Last updated: 2018-06-07Bibliographically approved
Laumonnerie, C., Da Silva, R. V., Kania, A. & Wilson, S. (2014). Netrin 1 and Dcc signalling are required for confinement of central axons within the central nervous system. Development, 141(3), 594-603
Open this publication in new window or tab >>Netrin 1 and Dcc signalling are required for confinement of central axons within the central nervous system
2014 (English)In: Development, ISSN 0950-1991, E-ISSN 1477-9129, Vol. 141, no 3, p. 594-603Article in journal (Refereed) Published
Abstract [en]

The establishment of anatomically stereotyped axonal projections is fundamental to neuronal function. While most neurons project their axons within the central nervous system (CNS), only axons of centrally born motoneurons and peripherally born sensory neurons link the CNS and peripheral nervous system (PNS) together by navigating through specialized CNS/PNS transition zones. Such selective restriction is of importance because inappropriate CNS axonal exit could lead to loss of correct connectivity and also to gain of erroneous functions. However, to date, surprisingly little is known about the molecular-genetic mechanisms that regulate how central axons are confined within the CNS during development. Here, we show that netrin 1/Dcc/Unc5 chemotropism contributes to axonal confinement within the CNS. In both Ntn1 and Dcc mutant mouse embryos, some spinal interneuronal axons exit the CNS by traversing the CNS/PNS transition zones normally reserved for motor and sensory axons. We provide evidence that netrin 1 signalling preserves CNS/PNS axonal integrity in three ways: (1) netrin 1/Dcc ventral attraction diverts axons away from potential exit points; (2) a Dcc/Unc5c-dependent netrin 1 chemoinhibitory barrier in the dorsolateral spinal cord prevents interneurons from being close to the dorsal CNS/PNS transition zone; and (3) a netrin 1/Dcc-dependent, Unc5c-independent mechanism that actively prevents exit from the CNS. Together, these findings provide insights into the molecular mechanisms that maintain CNS/PNS integrity and, to the best of our knowledge, present the first evidence that chemotropic signalling regulates interneuronal CNS axonal confinement in vertebrates.

Keywords
Netrin 1, Dcc, Spinal cord, CNS exit, Unc5, Axonal confinement, Mouse
National Category
General Practice
Identifiers
urn:nbn:se:umu:diva-86827 (URN)10.1242/dev.099606 (DOI)000330573500011 ()
Available from: 2014-03-17 Created: 2014-03-11 Last updated: 2018-06-08Bibliographically approved
Kropp, M. & Wilson, S. I. (2012). The expression profile of the tumor suppressor gene Lzts1 suggests a role in neuronal development. Developmental Dynamics, 241(5), 984-994
Open this publication in new window or tab >>The expression profile of the tumor suppressor gene Lzts1 suggests a role in neuronal development
2012 (English)In: Developmental Dynamics, ISSN 1058-8388, E-ISSN 1097-0177, Vol. 241, no 5, p. 984-994Article in journal (Refereed) Published
Abstract [en]

Background: Neuronal circuit assembly comprises a number of developmental processes that ultimately underlie function. Identifying the molecular events that dictate these processes can give key insights into how neuronal circuit formation is coordinated. To begin to identify such molecular mechanisms, we have analysed the expression of a candidate gene of entirely unknown function within the nervous system. Here we reveal the spatial and temporal distribution of Lzts1 in mouse and chick embryonic spinal cord and propose potential biological functions. Results: Lzts1 mRNA is transiently expressed at the border of the ventricular and mantle zones in subsets of sensory and motor spinal neurons. The protein is localized to the cell body, axon, and trailing process of motor, commissural, and dorsal root neurons during development. Conclusions: Taken together, the spatial and temporal distribution of Lzts1 is consistent with a potential function(s) in cell cycle regulation, axon growth or guidance, and/or migration of neurons. Developmental Dynamics 241:984994, 2012. (c) 2012 Wiley Periodicals, Inc.

Keywords
Lzts1, spinal cord, axon guidance, cell cycle, mouse embryo, chick embryo, tumor suppressor
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-55301 (URN)10.1002/dvdy.23777 (DOI)000302861200014 ()
Available from: 2012-05-19 Created: 2012-05-14 Last updated: 2018-06-08Bibliographically approved
Wilson, S. I. (2010). Target practice: Zic2 hits the bullseye!. EMBO Journal, 29(18), 3037-3038
Open this publication in new window or tab >>Target practice: Zic2 hits the bullseye!
2010 (English)In: EMBO Journal, ISSN 0261-4189, E-ISSN 1460-2075, Vol. 29, no 18, p. 3037-3038Article in journal (Refereed) Published
Place, publisher, year, edition, pages
Nature Publishing Group, 2010
Identifiers
urn:nbn:se:umu:diva-42133 (URN)10.1038/emboj.2010.209 (DOI)000282991900002 ()20842174 (PubMedID)
Available from: 2011-04-06 Created: 2011-04-06 Last updated: 2018-06-08Bibliographically approved
Wilson, S. I., Shafer, B., Lee, K. J. & Dodd, J. (2008). A molecular program for contralateral trajectory: Rig-1 control by LIM homeodomain transcription factors.. Neuron, 59(3), 413-24
Open this publication in new window or tab >>A molecular program for contralateral trajectory: Rig-1 control by LIM homeodomain transcription factors.
2008 (English)In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 59, no 3, p. 413-24Article in journal (Refereed) Published
Abstract [en]

Despite increasing evidence for transcriptional control of neural connectivity, how transcription factors regulate discrete steps in axon guidance remains obscure. Projection neurons in the dorsal spinal cord relay sensory signals to higher brain centers. Some projection neurons send their axons ipsilaterally, whereas others, commissural neurons, send axons contralaterally. We show that two closely related LIM homeodomain proteins, Lhx2 and Lhx9, are expressed by a set of commissural relay neurons (dI1c neurons) and are required for the dI1c axon projection. Midline crossing by dI1c axons is lost in Lhx2/9 double mutants, a defect that results from loss of expression of Rig-1 from dI1c axons. Lhx2 binds to a conserved motif in the Rig-1 gene, suggesting that Lhx2/9 regulate directly the expression of Rig-1. Our findings reveal a link between the transcriptional programs that define neuronal subtype identity and the expression of receptors that guide distinctive aspects of their trajectory.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-109844 (URN)10.1016/j.neuron.2008.07.020 (DOI)18701067 (PubMedID)
Available from: 2015-10-07 Created: 2015-10-07 Last updated: 2018-06-07
Wilson, S. I. & Edlund, T. (2001). Neural induction: toward a unifying mechanism. Nature Neuroscience, 1161-1168
Open this publication in new window or tab >>Neural induction: toward a unifying mechanism
2001 (English)In: Nature Neuroscience, ISSN 1097-6256, E-ISSN 1546-1726, p. 1161-1168Article, review/survey (Refereed) Published
Abstract [en]

Neural induction constitutes the initial step in the generation of the vertebrate nervous system. In attempting to understand the principles that underlie this process, two key issues need to be resolved. When is neural induction initiated, and what is the cellular source and molecular nature of the neural inducing signal(s)? Currently, these aspects of neural induction seem to be very different in amphibian and amniote embryos. Here we highlight the similarities and the differences, and we propose a possible unifying mechanism.

Place, publisher, year, edition, pages
Nature Publishing Group, 2001
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-109842 (URN)10.1038/nn747 (DOI)000172041500007 ()11687825 (PubMedID)
Note

4 Suppl

Available from: 2015-10-07 Created: 2015-10-07 Last updated: 2019-01-23Bibliographically approved
Wilson, S. I., Rydström, A., Trimborn, T., Willert, K., Nusse, R., Jessell, T. M. & Edlund, T. (2001). The status of Wnt signalling regulates neural and epidermal fates in the chick embryo.. Nature, 411(6835), 325-30
Open this publication in new window or tab >>The status of Wnt signalling regulates neural and epidermal fates in the chick embryo.
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2001 (English)In: Nature, ISSN 0028-0836, E-ISSN 1476-4687, Vol. 411, no 6835, p. 325-30Article in journal (Refereed) Published
Abstract [en]

The acquisition of neural fate by embryonic ectodermal cells is a fundamental step in the formation of the vertebrate nervous system. Neural induction seems to involve signalling by fibroblast growth factors (FGFs) and attenuation of the activity of bone morphogenetic protein (BMP). But FGFs, either alone or in combination with BMP antagonists, are not sufficient to induce neural fate in prospective epidermal ectoderm of amniote embryos. These findings suggest that additional signals are involved in the specification of neural fate. Here we show that the state of Wnt signalling is a critical determinant of neural and epidermal fates in the chick embryo. Continual Wnt signalling blocks the response of epiblast cells to FGF signals, permitting the expression and signalling of BMP to direct an epidermal fate. Conversely, a lack of exposure of epiblast cells to Wnt signals permits FGFs to induce a neural fate.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-109843 (URN)10.1038/35077115 (DOI)11357137 (PubMedID)
Available from: 2015-10-07 Created: 2015-10-07 Last updated: 2018-06-07
Wilson, S. I., Graziano, E., Harland, R., Jessell, T. M. & Edlund, T. (2000). An early requirement for FGF signalling in the acquisition of neural cell fate in the chick embryo.. Current Biology, 10(8), 421-9
Open this publication in new window or tab >>An early requirement for FGF signalling in the acquisition of neural cell fate in the chick embryo.
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2000 (English)In: Current Biology, ISSN 0960-9822, E-ISSN 1879-0445, Vol. 10, no 8, p. 421-9Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: In Xenopus embryos, fibroblast growth factors (FGFs) and secreted inhibitors of bone morphogenetic protein (BMP)-mediated signalling have been implicated in neural induction. The precise roles, if any, that these factors play in neural induction in amniotes remains to be established.

RESULTS: To monitor the initial steps of neural induction in the chick embryo, we developed an in vitro assay of neural differentiation in epiblast cells. Using this assay, we found evidence that neural cell fate is specified in utero, before the generation of the primitive streak or Hensen's node. Early epiblast cells expressed both Bmp4 and Bmp7, but the expression of both genes was downregulated as cells acquired neural fate. During prestreak and gastrula stages, exposure of epiblast cells to BMP4 activity in vitro was sufficient to block the acquisition of neural fate and to promote the generation of epidermal cells. Fgf3 was also found to be expressed in the early epiblast, and ongoing FGF signalling in epiblast cells was required for acquisition of neural fate and for the suppression of Bmp4 and Bmp7 expression.

CONCLUSIONS: The onset of neural differentiation in the chick embryo occurs in utero, before the generation of Hensen's node. Fgf3, Bmp4 and Bmp7 are each expressed in prospective neural cells, and FGF signalling appears to be required for the repression of Bmp expression and for the acquisition of neural fate. Subsequent exposure of epiblast cells to BMPs, however, can prevent the generation of neural tissue and induce cells of epidermal character.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-109841 (URN)10801412 (PubMedID)
Available from: 2015-10-07 Created: 2015-10-07 Last updated: 2018-06-07
Muhr, J., Graziano, E., Wilson, S. I., Jessell, T. M. & Edlund, T. (1999). Convergent inductive signals specify midbrain, hindbrain, and spinal cord identity in gastrula stage chick embryos.. Neuron, 23(4), 689-702
Open this publication in new window or tab >>Convergent inductive signals specify midbrain, hindbrain, and spinal cord identity in gastrula stage chick embryos.
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1999 (English)In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 23, no 4, p. 689-702Article in journal (Refereed) Published
Abstract [en]

In the chick embryo, neural cells acquire midbrain, hindbrain, and spinal cord character over a approximately 6 hr period during gastrulation. The convergent actions of four signals appear to specify caudal neural character. Fibroblast growth factors (FGFs) and a paraxial mesoderm-caudalizing (PMC) activity are involved, but neither signal is sufficient to induce any single region. FGFs act indirectly by inducing mesoderm that expresses PMC and retinoid activity and also directly on prospective neural cells, in combination with PMC activity and a rostralizing signal, to induce midbrain character. Hindbrain character emerges from cells that possess the potential to acquire midbrain character upon exposure to higher levels of PMC activity. Induction of spinal cord character appears to involve PMC and retinoid activities.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-109847 (URN)10482236 (PubMedID)
Available from: 2015-10-07 Created: 2015-10-07 Last updated: 2018-06-07

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