TY - JOUR
T1 - The SAX-3 Receptor Stimulates Axon Outgrowth and the Signal Sequence and Transmembrane Domain Are Critical for SAX-3 Membrane Localization in the PDE Neuron of C. elegans
AU - Li, Jia
AU - Pu, Pu
AU - Le, Weidong
N1 - Funding Information:
We are grateful to Dr. Meng Wang (Baylor College of Medicine) for her critical review and constructive comments. We thank Drs. Ken-ichi Ogura (Yokohama City University Graduate School of Medicine) and Gian Garriga (University of California, Berkeley) for vectors and some strains. We also thank Dr. Zhang Hong (NIBS, Beijing) for the help of microinjection, Dr. Cai Shiqing (ION, Shanghai) for the help of UV integration, and Dr. Yu Tang and Ting Li for editing the manuscript. Most strains used in this paper are provided by Caenorhabditis Genetics Center, which is funded by the NIH National Center for Research Resources.
PY - 2013/6/12
Y1 - 2013/6/12
N2 - SAX-3, a receptor for Slit in C. elegans, is well characterized for its function in axonal development. However, the mechanism that regulates the membrane localization of SAX-3 and the role of SAX-3 in axon outgrowth are still elusive. Here we show that SAX-3::GFP caused ectopic axon outgrowth, which could be suppressed by the loss-of-function mutation in unc-73 (a guanine nucleotide exchange factor for small GTPases) and unc-115 (an actin binding protein), suggesting that they might act downstream of SAX-3 in axon outgrowth. We also examined genes related to axon development for their possible involvement in the subcellular localization of SAX-3. We found the unc-51 mutants appeared to accumulate SAX-3::GFP in the neuronal cell body of the posterior deirid (PDE) neuron, indicating that UNC-51 might play a role in SAX-3 membrane localization. Furthermore, we demonstrate that the N-terminal signal sequence and the transmembrane domain are essential for the subcellular localization of SAX-3 in the PDE neurons.
AB - SAX-3, a receptor for Slit in C. elegans, is well characterized for its function in axonal development. However, the mechanism that regulates the membrane localization of SAX-3 and the role of SAX-3 in axon outgrowth are still elusive. Here we show that SAX-3::GFP caused ectopic axon outgrowth, which could be suppressed by the loss-of-function mutation in unc-73 (a guanine nucleotide exchange factor for small GTPases) and unc-115 (an actin binding protein), suggesting that they might act downstream of SAX-3 in axon outgrowth. We also examined genes related to axon development for their possible involvement in the subcellular localization of SAX-3. We found the unc-51 mutants appeared to accumulate SAX-3::GFP in the neuronal cell body of the posterior deirid (PDE) neuron, indicating that UNC-51 might play a role in SAX-3 membrane localization. Furthermore, we demonstrate that the N-terminal signal sequence and the transmembrane domain are essential for the subcellular localization of SAX-3 in the PDE neurons.
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U2 - 10.1371/journal.pone.0065658
DO - 10.1371/journal.pone.0065658
M3 - Article
C2 - 23776520
AN - SCOPUS:84878932050
SN - 1932-6203
VL - 8
JO - PLoS ONE
JF - PLoS ONE
IS - 6
M1 - e65658
ER -