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  The LRR receptor Islr2 is required for retinal axon routing at the vertebrate optic chiasm

Panza, P., Sitko, A., Maischein, H.-M., Koch, I., Flötenmeyer, M., Wright, G., et al. (2015). The LRR receptor Islr2 is required for retinal axon routing at the vertebrate optic chiasm. Neural Development, 10: 23. doi:10.1186/s13064-015-0050-x.

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Panza, P1, Author           
Sitko, AA, Author
Maischein, H-M1, Author           
Koch, I2, Author           
Flötenmeyer, M2, Author           
Wright, GJ, Author
Mandai , K, Author
Mason, CA, Author
Söllner, C1, Author                 
Affiliations:
1Department Genetics, Max Planck Institute for Developmental Biology, Max Planck Society, ou_3375716              
2Electron Microscopy, Max Planck Institute for Developmental Biology, Max Planck Society, ou_3375794              

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 Abstract: Background: In the visual system of most binocular vertebrates, the axons of retinal ganglion cells (RGCs) diverge at the diencephalic midline and extend to targets on both ipsi- and contralateral sides of the brain. While a molecular mechanism explaining ipsilateral guidance decisions has been characterized, less is known of how RGC axons cross the midline. Results: Here, we took advantage of the zebrafish, in which all RGC axons project contralaterally at the optic chiasm, to characterize Islr2 as an RGC receptor required for complete retinal axon midline crossing. We used a systematic extracellular protein-protein interaction screening assay to identify two Vasorin paralogs, Vasna and Vasnb, as specific Islr2 ligands. Antibodies against Vasna and Vasnb reveal cellular populations surrounding the retinal axon pathway, suggesting the involvement of these proteins in guidance decisions made by axons of the optic nerve. Specifically, Vasnb marks the membranes of a cellular barricade located anteriorly to the optic chiasm, a structure termed the "glial knot" in higher vertebrates. Loss of function mutations in either vasorin paralog, individually or combined, however, do not exhibit an overt retinal axon projection phenotype, suggesting that additional midline factors, acting either independently or redundantly, compensate for their loss. Analysis of Islr2 knockout mice supports a scenario in which Islr2 controls the coherence of RGC axons through the ventral midline and optic tract. Conclusions: Although stereotypic guidance of RGC axons at the vertebrate optic chiasm is controlled by multiple, redundant mechanisms, and despite the differences in ventral diencephalic tissue architecture, we identify a novel role for the LRR receptor Islr2 in ensuring proper axon navigation at the optic chiasm of both zebrafish and mouse.

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 Dates: 2015-10
 Publication Status: Issued
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 Rev. Type: -
 Identifiers: DOI: 10.1186/s13064-015-0050-x
PMID: 26492970
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Title: Neural Development
Source Genre: Journal
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Publ. Info: London : BioMed Central
Pages: 17 Volume / Issue: 10 Sequence Number: 23 Start / End Page: - Identifier: ISSN: 1749-8104
CoNE: https://pure.mpg.de/cone/journals/resource/1000000000240300