TY - JOUR
T1 - High content screening of cortical neurons identifies novel regulators of axon growth
AU - Blackmore, Murray G.
AU - Moore, Darcie L.
AU - Smith, Robin P.
AU - Goldberg, Jeffrey L.
AU - Bixby, John L.
AU - Lemmon, Vance P.
N1 - Funding Information:
This work was supported by the C.H. Neilsen Foundation , the R. Wilson Foundation , and The Buoniconti Fund to Cure Paralysis (VPL/JLB) ; and by NINDS ( R01-NS061348 , JLG), the Seigal Foundation (JLG), NEI ( P30-EY014801 ), and an unrestricted grant from Research to Prevent Blindness to the University of Miami . V. Lemmon holds the Walter G. Ross Distinguished Chair in Developmental Neuroscience at the University of Miami. D.L.M. is a Lois Pope LIFE Fellow, with support from NINDS training grants T32 S07492 and T32 NS007459 . We are indebted to Roger Tsien (UCSD) for the generous gift of mCherry plasmid. We are grateful to Guerline Lambert for her technical assistance, as well as to lab members Yan Shi, Eli Weaver, Eleut Hernandez, and Raul Corredor.
PY - 2010/5
Y1 - 2010/5
N2 - Neurons in the central nervous system lose their intrinsic capacity for axon regeneration as they mature, and it is widely hypothesized that changes in gene expression are responsible. Testing this hypothesis and identifying the relevant genes has been challenging because hundreds to thousands of genes are developmentally regulated in CNS neurons, but only a small subset are likely relevant to axon growth. Here we used automated high content analysis (HCA) methods to functionally test 743 plasmids encoding developmentally regulated genes in neurite outgrowth assays using postnatal cortical neurons. We identified both growth inhibitors (Ephexin, Aldolase A, Solute Carrier 2A3, and Chimerin), and growth enhancers (Doublecortin, Doublecortin-like, Kruppel-like Factor 6, and CaM-Kinase II gamma), some of which regulate established growth mechanisms like microtubule dynamics and small GTPase signaling. Interestingly, with only one exception the growth-suppressing genes were developmentally upregulated, and the growth-enhancing genes downregulated. These data provide important support for the hypothesis that developmental changes in gene expression control neurite outgrowth, and identify potential new gene targets to promote neurite outgrowth.
AB - Neurons in the central nervous system lose their intrinsic capacity for axon regeneration as they mature, and it is widely hypothesized that changes in gene expression are responsible. Testing this hypothesis and identifying the relevant genes has been challenging because hundreds to thousands of genes are developmentally regulated in CNS neurons, but only a small subset are likely relevant to axon growth. Here we used automated high content analysis (HCA) methods to functionally test 743 plasmids encoding developmentally regulated genes in neurite outgrowth assays using postnatal cortical neurons. We identified both growth inhibitors (Ephexin, Aldolase A, Solute Carrier 2A3, and Chimerin), and growth enhancers (Doublecortin, Doublecortin-like, Kruppel-like Factor 6, and CaM-Kinase II gamma), some of which regulate established growth mechanisms like microtubule dynamics and small GTPase signaling. Interestingly, with only one exception the growth-suppressing genes were developmentally upregulated, and the growth-enhancing genes downregulated. These data provide important support for the hypothesis that developmental changes in gene expression control neurite outgrowth, and identify potential new gene targets to promote neurite outgrowth.
KW - Axon regeneration
KW - Corticospinal tract
KW - Development
KW - Doublecortin
KW - High content analysis
KW - Kruppel-like transcription factor
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U2 - 10.1016/j.mcn.2010.02.002
DO - 10.1016/j.mcn.2010.02.002
M3 - Article
C2 - 20159039
AN - SCOPUS:77950339970
VL - 44
SP - 43
EP - 54
JO - Molecular and Cellular Neuroscience
JF - Molecular and Cellular Neuroscience
SN - 1044-7431
IS - 1
ER -