دورية أكاديمية
أعرض في EDS

EphA7 isoforms differentially regulate cortical dendrite development.

التفاصيل البيبلوغرافية
العنوان: EphA7 isoforms differentially regulate cortical dendrite development.
المؤلفون: Leonard CE; Department of Biology, Georgetown University, Washington, DC, United States of America.; Interdisciplinary Program in Neuroscience, Georgetown University, Washington, DC, United States of America., Baydyuk M; Department of Biology, Georgetown University, Washington, DC, United States of America., Stepler MA; Department of Biology, Georgetown University, Washington, DC, United States of America., Burton DA; Department of Biology, Georgetown University, Washington, DC, United States of America., Donoghue MJ; Department of Biology, Georgetown University, Washington, DC, United States of America.; Interdisciplinary Program in Neuroscience, Georgetown University, Washington, DC, United States of America.
المصدر: PloS one [PLoS One] 2020 Dec 04; Vol. 15 (12), pp. e0231561. Date of Electronic Publication: 2020 Dec 04 (Print Publication: 2020).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Cerebral Cortex/*embryology , Dendrites/*metabolism , Receptor, EphA7/*metabolism, Animals ; Axons/metabolism ; Cells, Cultured ; Cerebral Cortex/metabolism ; Dendritic Spines/metabolism ; Male ; Mice, Inbred C57BL/embryology ; Neurons/metabolism ; Organogenesis ; Protein Isoforms/physiology ; Rats ; Rats, Sprague-Dawley/embryology ; Receptor, EphA7/physiology ; Signal Transduction
مستخلص: The shape of a neuron facilitates its functionality within neural circuits. Dendrites integrate incoming signals from axons, receiving excitatory input onto small protrusions called dendritic spines. Therefore, understanding dendritic growth and development is fundamental for discerning neural function. We previously demonstrated that EphA7 receptor signaling during cortical development impacts dendrites in two ways: EphA7 restricts dendritic growth early and promotes dendritic spine formation later. Here, the molecular basis for this shift in EphA7 function is defined. Expression analyses reveal that EphA7 full-length (EphA7-FL) and truncated (EphA7-T1; lacking kinase domain) isoforms are dynamically expressed in the developing cortex. Peak expression of EphA7-FL overlaps with dendritic elaboration around birth, while highest expression of EphA7-T1 coincides with dendritic spine formation in early postnatal life. Overexpression studies in cultured neurons demonstrate that EphA7-FL inhibits both dendritic growth and spine formation, while EphA7-T1 increases spine density. Furthermore, signaling downstream of EphA7 shifts during development, such that in vivo inhibition of mTOR by rapamycin in EphA7-mutant neurons ameliorates dendritic branching, but not dendritic spine phenotypes. Finally, direct interaction between EphA7-FL and EphA7-T1 is demonstrated in cultured cells, which results in reduction of EphA7-FL phosphorylation. In cortex, both isoforms are colocalized to synaptic fractions and both transcripts are expressed together within individual neurons, supporting a model where EphA7-T1 modulates EphA7-FL repulsive signaling during development. Thus, the divergent functions of EphA7 during cortical dendrite development are explained by the presence of two variants of the receptor.
Competing Interests: The authors have declared that no competing interests exist.
References: Exp Neurol. 1997 Dec;148(2):616-27. (PMID: 9417837)
Neuron. 2004 Jun 10;42(5):717-30. (PMID: 15182713)
J Neurosci. 1992 Apr;12(4):1382-93. (PMID: 1556599)
Neuron. 2005 Jul 7;47(1):57-69. (PMID: 15996548)
Neuron. 2005 Jan 20;45(2):207-21. (PMID: 15664173)
Nat Neurosci. 2004 May;7(5):501-9. (PMID: 15107857)
Int J Cancer. 2009 Jan 1;124(1):88-94. (PMID: 18821581)
Science. 1998 Dec 4;282(5395):1904-6. (PMID: 9836643)
Mol Cancer Res. 2015 Mar;13(3):548-55. (PMID: 25548102)
Science. 1994 Nov 4;266(5186):816-9. (PMID: 7973638)
Nucleic Acids Res. 2016 Jan 4;44(D1):D710-6. (PMID: 26687719)
Neuron. 1996 Jul;17(1):9-19. (PMID: 8755474)
Cereb Cortex. 2013 Aug;23(8):1765-73. (PMID: 22744705)
Oncogene. 1995 Jan 5;10(1):97-108. (PMID: 7824284)
Neuron. 2005 Nov 23;48(4):563-75. (PMID: 16301174)
Neuron. 2005 May 5;46(3):383-8. (PMID: 15882636)
Annu Rev Neurosci. 2002;25:127-49. (PMID: 12052906)
J Comp Neurol. 2016 Jul 1;524(10):2080-92. (PMID: 26587807)
Cell Rep. 2018 Oct 9;25(2):357-367.e4. (PMID: 30304677)
Nucleic Acids Res. 2016 Jan 4;44(D1):D7-19. (PMID: 26615191)
Neuron. 1995 Oct;15(4):761-8. (PMID: 7576626)
Hum Mol Genet. 2011 Dec 1;20(23):4597-604. (PMID: 21890496)
Brain Res Mol Brain Res. 1995 Dec 1;34(1):154-60. (PMID: 8750872)
Cereb Cortex. 2000 Oct;10(10):981-91. (PMID: 11007549)
Nat Neurosci. 2010 Feb;13(2):163-72. (PMID: 20062052)
Nat Rev Neurosci. 2007 Jun;8(6):427-37. (PMID: 17514196)
Cell Mol Life Sci. 2017 Dec;74(24):4511-4537. (PMID: 28735442)
Mol Cytogenet. 2009 Aug 07;2:17. (PMID: 19664229)
Science. 2000 Oct 27;290(5492):739-44. (PMID: 11052929)
Cytokine Growth Factor Rev. 2012 Feb-Apr;23(1-2):15-24. (PMID: 22341689)
Oncogene. 1995 Apr 20;10(8):1573-80. (PMID: 7731712)
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9779-84. (PMID: 9707552)
J Comp Neurol. 2006 Jun 10;496(5):627-42. (PMID: 16615124)
Brain Res Mol Brain Res. 1999 Dec 10;74(1-2):231-6. (PMID: 10640696)
Nat Rev Cancer. 2010 Mar;10(3):165-80. (PMID: 20179713)
PLoS One. 2011;6(10):e26089. (PMID: 22022520)
Exp Brain Res. 1992;90(2):346-58. (PMID: 1383021)
Acta Neurobiol Exp (Wars). 2008;68(2):289-304. (PMID: 18511962)
Nature. 1961 Nov 25;192:766-8. (PMID: 17533671)
Cell. 1995 Aug 11;82(3):359-70. (PMID: 7634326)
Neuroscience. 2013 Oct 22;251:90-107. (PMID: 22546337)
Science. 1974 Feb 1;183(4123):425-7. (PMID: 4203022)
J Neurosci. 1996 Apr 1;16(7):2283-93. (PMID: 8601808)
Neuron. 1998 May;20(5):847-54. (PMID: 9620690)
Biomolecules. 2019 Sep 09;9(9):. (PMID: 31505877)
Cytometry A. 2004 Apr;58(2):167-76. (PMID: 15057970)
Nat Neurosci. 2004 Feb;7(2):136-44. (PMID: 14703572)
J Neurosci. 2007 May 23;27(21):5546-58. (PMID: 17522300)
Nat Rev Neurosci. 2003 Dec;4(12):941-56. (PMID: 14682358)
Neural Dev. 2011 May 04;6:21. (PMID: 21542907)
Nature. 1996 Oct 24;383(6602):722-5. (PMID: 8878483)
Nature. 2000 Nov 9;408(6809):203-6. (PMID: 11089974)
Neurosci Lett. 2015 Aug 5;601:30-40. (PMID: 25578949)
Brain Res Mol Brain Res. 1999 Dec 10;74(1-2):225-30. (PMID: 10640695)
Nature. 2000 Apr 6;404(6778):567-73. (PMID: 10766232)
Physiology (Bethesda). 2006 Feb;21:38-47. (PMID: 16443821)
Proc Natl Acad Sci U S A. 2014 Apr 1;111(13):4994-9. (PMID: 24707048)
BMC Cancer. 2008 Mar 25;8:79. (PMID: 18366728)
J Neurocytol. 1981 Oct;10(5):859-78. (PMID: 6171624)
Cell Signal. 2004 Jun;16(6):655-66. (PMID: 15093606)
Nat Neurosci. 2012 Dec;15(12):1645-54. (PMID: 23143520)
Cell. 2008 Apr 4;133(1):38-52. (PMID: 18394988)
J Anat. 1953 Oct;87(4):387-406. (PMID: 13117757)
Gene Expr Patterns. 2013 Dec;13(8):454-63. (PMID: 24036135)
J Neurosci. 1996 May 15;16(10):3123-9. (PMID: 8627351)
المشرفين على المادة: 0 (Protein Isoforms)
EC 2.7.10.1 (Receptor, EphA7)
تواريخ الأحداث: Date Created: 20201204 Date Completed: 20210113 Latest Revision: 20240804
رمز التحديث: 20240804
مُعرف محوري في PubMed: PMC7717530
DOI: 10.1371/journal.pone.0231561
PMID: 33275600
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0231561