@article{9290af5cde4f43bca54245cce0d54ce4,
title = "Class 5 transmembrane semaphorins control selective mammalian retinal lamination and function",
abstract = "In the vertebrate retina, neurites from distinct neuronal cell types are constrained within the plexiform layers, allowing for establishment of retinal lamination. However, the mechanisms by which retinal neurites are segregated within the inner or outer plexiform layers are not known. We find that the transmembrane semaphorins Sema5A and Sema5B constrain neurites from multiple retinal neuron subtypes within the inner plexiform layer (IPL). In Sema5A-/-; Sema5B-/- mice, retinal ganglion cells (RGCs) and amacrine and bipolar cells exhibit severe defects leading to neurite mistargeting into the outer portions of the retina. These targeting abnormalities are more prominent in the outer (OFF) layers of the IPL and result in functional defects in select RGC response properties. Sema5A and Sema5B inhibit retinal neurite outgrowth through PlexinA1 and PlexinA3 receptors both in vitro and in vivo. These findings define a set of ligands and receptors required for the establishment of inner retinal lamination and function.",
author = "Matsuoka, {Ryota L.} and Onanong Chivatakarn and Badea, {Tudor C.} and Samuels, {Ivy S.} and Hugh Cahill and Katayama, {Kei ichi} and Kumar, {Sumit R.} and Fumikazu Suto and Alain Ch{\'e}dotal and Peachey, {Neal S.} and Jeremy Nathans and Yutaka Yoshida and Giger, {Roman J.} and Kolodkin, {Alex L.}",
note = "Funding Information: We thank K.-W. Yau and T. Xue for the Opn4 Tau-LacZ/Tau-LacZ mice, M. Tessier-Lavigne for the PlexA3 −/− mice, B. Howell for the Dab-1 antibody, and F. Haeseleer for the CaBP5 antibody. We also thank D. Kantor, S. Kozlov, C. Hawkins, and K. Takamiya for their assistance with the generation of the Sema5A −/− and Sema5B −/− mice. We thank M. Riccomagno, K. Mandai, S.-H. Wang, Y. Duan, and T. Tran for helpful suggestions and discussions throughout this project, D. Johnson for assistance with mouse experiments, and members of the Kolodkin laboratory for assistance. This work was supported by R01 NS35165 (to A.L.K.), a predoctoral fellowship from the Nakajima Foundation (to R.L.M.), NRSA F31NS056558-01A1 (to O.C.), the Veterans Administration (to I.S.S. and N.S.P.), the Foundation Fighting Blindness (to N.S.P.), R01 NS065048 (to Y.Y.), the Foundation pour la Rechereche M{\'e}dicale (Programme {\'e}quipe FRM) (to A.C.), and R01 NS047333 (to R.J.G.). A.L.K. and J.N. are investigators of the Howard Hughes Medical Institute. ",
year = "2011",
month = aug,
day = "11",
doi = "10.1016/j.neuron.2011.06.009",
language = "English (US)",
volume = "71",
pages = "460--473",
journal = "Neuron",
issn = "0896-6273",
publisher = "Cell Press",
number = "3",
}