Neural recognition molecules of the immunoglobulin superfamily: signaling transducers of axon guidance and neuronal migration

2006 ◽  
Vol 10 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Patricia F Maness ◽  
Melitta Schachner
Keyword(s):  
Axon Guidance ◽  
Neuronal Migration ◽  
Immunoglobulin Superfamily

scholarly journals MACF1 Mutations Encoding Highly Conserved Zinc-Binding Residues of the GAR Domain Cause Defects in Neuronal Migration and Axon Guidance

2018 ◽  
Vol 103 (6) ◽  
pp. 1009-1021 ◽  
Author(s):  
William B. Dobyns ◽  
Kimberly A. Aldinger ◽  
Gisele E. Ishak ◽  
Ghayda M. Mirzaa ◽  
Andrew E. Timms ◽  
...  
Keyword(s):  
Axon Guidance ◽  
Neuronal Migration ◽  
Zinc Binding ◽  
Binding Residues

scholarly journals Molecular basis of synaptic specificity by immunoglobulin superfamily receptors in Drosophila

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Shouqiang Cheng ◽  
James Ashley ◽  
Justyna D Kurleto ◽  
Meike Lobb-Rabe ◽  
Yeonhee Jenny Park ◽  
...  
Keyword(s):  
Axon Guidance ◽  
Molecular Basis ◽  
Surface Proteins ◽  
Synaptic Connectivity ◽  
Immunoglobulin Superfamily ◽  
Neuronal Connectivity ◽  
Cell Surface Proteins ◽  
Synaptic Specificity ◽  
Immunoglobulin Superfamily Proteins ◽  
Synapse Targeting

In stereotyped neuronal networks, synaptic connectivity is dictated by cell surface proteins, which assign unique identities to neurons, and physically mediate axon guidance and synapse targeting. We recently identified two groups of immunoglobulin superfamily proteins in Drosophila, Dprs and DIPs, as strong candidates for synapse targeting functions. Here, we uncover the molecular basis of specificity in Dpr–DIP mediated cellular adhesions and neuronal connectivity. First, we present five crystal structures of Dpr–DIP and DIP–DIP complexes, highlighting the evolutionary and structural origins of diversification in Dpr and DIP proteins and their interactions. We further show that structures can be used to rationally engineer receptors with novel specificities or modified affinities, which can be used to study specific circuits that require Dpr–DIP interactions to help establish connectivity. We investigate one pair, engineered Dpr10 and DIP-α, for function in the neuromuscular circuit in flies, and reveal roles for homophilic and heterophilic binding in wiring.

scholarly journals Tangential Neuronal Migration Controls Axon Guidance: A Role for Neuregulin-1 in Thalamocortical Axon Navigation

Cell ◽  
2006 ◽  
Vol 125 (1) ◽  
pp. 127-142 ◽  
Author(s):  
Guillermina López-Bendito ◽  
Aline Cautinat ◽  
Juan Antonio Sánchez ◽  
Franck Bielle ◽  
Nuria Flames ◽  
...  
Keyword(s):  
Axon Guidance ◽  
Neuronal Migration ◽  
Neuregulin 1

scholarly journals Targeting the SLIT/ROBO pathway in tumor progression: molecular mechanisms and therapeutic perspectives

2019 ◽  
Vol 11 ◽  
pp. 175883591985523 ◽  
Author(s):  
Zhengdong Jiang ◽  
Gang Liang ◽  
Ying Xiao ◽  
Tao Qin ◽  
Xin Chen ◽  
...  
Keyword(s):  
Axon Guidance ◽  
Neuronal Migration ◽  
Molecular Mechanisms ◽  
Vascular System ◽  
Tumor Development ◽  
Tumor Promotion ◽  
Cancer Therapies ◽  
Malignant Cells ◽  
Robo Receptors

The SLITs (SLIT1, SLIT2, and SLIT3) are a family of secreted proteins that mediate positional interactions between cells and their environment during development by signaling through ROBO receptors (ROBO1, ROBO2, ROBO3, and ROBO4). The SLIT/ROBO signaling pathway has been shown to participate in axonal repulsion, axon guidance, and neuronal migration in the nervous system and the formation of the vascular system. However, the role of the SLIT/ROBO pathway has not been thoroughly clarified in tumor development. The SLIT/ROBO pathway can produce both beneficial and detrimental effects in the growth of malignant cells. It has been confirmed that SLIT/ROBO play contradictory roles in tumorigenesis. Here, we discuss the tumor promotion and tumor suppression roles of the SLIT/ROBO pathway in tumor growth, angiogenesis, migration, and the tumor microenvironment. Understanding these roles will help us develop more effective cancer therapies.

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