Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 May 9;9:1842. doi: 10.1038/s41467-018-04239-z

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 8 — Downstream of Sema7A/PlxnC1 signaling. a Signal cascades downstream of Sema7A–PlxnCl interaction. Left, Phosphorylation of PAK and ERK in the Sema7A KO and PlxnCl cKO. OB sections at P3 were immunostained with antibodies against phosphorylated form, and total proteins. Phosphatase-treated samples (de-P) were also analyzed. Relative fluorescent intensities, p-PAK/PAK and p-ERK/ERK, are compared in the rI7 glomeruli. ^**p < 0.01 (Student’s t-test). Error bars indicate SD (n = 7, 3, 4, 5 glomeruli for WT, de-P, Sema7A KO, and PlxnC1 cKO). b Recovery of PAK- phosphorylation in the Sema7A KO by introducing the Tg Sema7A gene. This rescue is blocked by the Sema7A mutation, Y213S, which interferes with PlxnC1 interaction. By mating the transgenic animal, the WT or mutant Sema7A gene was introduced into the Sema7A KO mice, and was expressed constitutively in the rI7-expressing OSNs. OB sections at P3 were immunostained with antibodies against phosphorylated and total PAK. Phosphatase-treated samples (de-P) were also analyzed. Relative fluorescent intensities p-PAK/PAK in the rI7 glomeruli are compared between the WT and mutant Sema7As. ^**p < 0.01 (Student’s t-test). Error bars indicate SD (n = 3 mice for the WT Sema7A, n = 2 mice for the mutant Sema7A). c Inhibition of the trans-synaptic activity in M/T cells. Left, Inhibition of the trans-synaptic activity with an NMDA-R inhibitor, MK801. OB sections at P5 were analyzed by in situ hybridization for the expression of Pcdh21 and cpg15. EYFP-tagged rI7 glomeruli were identified by immunostaining. The expression of cpg15 (synaptic-activity marker) in M/T cells was inhibited after MK801 injection. n = 3 animals. Scale bar=20 μm. Right, Dendrite morphology of the MK801-treated M/T cells at P5. M/T cells were stained in yellow by LY injection into the rI7 glomeruli. The ratios (%) of mature (blue) and immature M/T cells in the rI7 glomeruli are shown: MK801⁻, 19/25 (76.0 %); MK801⁺, 6/25 (24.0 %). n = 19 glomeruli. Scale bar=10 μm. d Schematic diagram of synapse formation regulated by Sema7A signaling. OR-derived-neuronal activity induces Sema7A expression in OSNs. Sema7A interacts with PlxnC1 expressed in M/T-cell dendrites and activates the Rac1/Cdc42-PAK signaling cascade to induce synapse formation. Trans-synaptic activities in M/T cells are responsible for dendrite selection and maturation. MCL, mitral-cell layer