SALM5 trans-synaptically interacts with LAR-RPTPs in a splicing-dependent manner to regulate synapse development.

SALM5 trans-synaptically interacts with LAR-RPTPs in a splicing-dependent manner to regulate synapse development.
复制标题

DOI:
10.1038/srep26676
复制
发表时间:
2016-05-26
期刊:
影响因子:
4.6
通讯作者:
Kim E
Kim E
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Choi Y;Nam J;Whitcomb DJ;Song YS;Kim D;Jeon S;Um JW;Lee SG;Woo J;Kwon SK;Li Y;Mah W;Kim HM;Ko J;Cho K;Kim E

文献摘要

参考文献

被引文献

相似文献

突触发生粘附分子在突触形成中起关键作用。SALM 5/Lrfn 5是一种与自闭症谱系障碍(ASD)和精神分裂症有关的SALM/Lrfn家族粘附分子,诱导接触轴突的突触前分化,但其突触前配体仍然未知。我们发现SALM 5与LAR家族受体蛋白酪氨酸磷酸酶(LAR-RPTP; LAR、PTPδ和PTPσ)的IG结构域相互作用。这些相互作用被LAR-RPTP的IG结构域区域中的剪接插入片段B强烈抑制,并介导接触轴突中的SALM 5依赖性突触前分化。此外,SALM 5通过涉及突触后SALM 5与突触前LAR-RPTP相互作用的机制调节AMPA受体介导的突触传递。这些结果表明,突触后SALM 5通过与突触前LAR-RPTPs的跨突触相互作用促进突触发育,并且对于兴奋性突触强度的调节是重要的。
Synaptogenic adhesion molecules play critical roles in synapse formation. SALM5/Lrfn5, a SALM/Lrfn family adhesion molecule implicated in autism spectrum disorders (ASDs) and schizophrenia, induces presynaptic differentiation in contacting axons, but its presynaptic ligand remains unknown. We found that SALM5 interacts with the Ig domains of LAR family receptor protein tyrosine phosphatases (LAR-RPTPs; LAR, PTPδ, and PTPσ). These interactions are strongly inhibited by the splice insert B in the Ig domain region of LAR-RPTPs, and mediate SALM5-dependent presynaptic differentiation in contacting axons. In addition, SALM5 regulates AMPA receptor-mediated synaptic transmission through mechanisms involving the interaction of postsynaptic SALM5 with presynaptic LAR-RPTPs. These results suggest that postsynaptic SALM5 promotes synapse development by trans-synaptically interacting with presynaptic LAR-RPTPs and is important for the regulation of excitatory synaptic strength.
DOI: 10.1038/mp.2010.75
发表时间: 2010-09-14
影响因子: 11
作者:
Elia, J.;Gai, X.;Xie, H. M.;Perin, J. C.;Geiger, E.;Glessner, J. T.;D'arcy, M.;deBerardinis, R.;Frackelton, E.;Kim, C.;Lantieri, F.;Muganga, B. M.;Wang, L.;Takeda, T.;Rappaport, E. F.;Grant, S. F. A.;Berrettini, W.;Devoto, M.;Shaikh, T. H.;Hakonarson, H.;White, P. S.
通讯作者: White, P. S.