Robo functions as an attractive cue for glial migration through SYG-1/Neph.

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2020-11-19

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Abstract

As one of the most-studied receptors, Robo plays functions in many biological processes, and its functions highly depend on Slit, the ligand of Robo. Here we uncover a Slit-independent role of Robo in glial migration and show that neurons can release an extracellular fragment of Robo upon cleavage to attract glia during migration in Caenorhabditis elegans. Furthermore, we identified the conserved cell adhesion molecule SYG-1/Neph as a receptor for the cleaved extracellular Robo fragment to mediate glial migration and SYG-1/Neph functions through regulation of the WAVE complex. Our studies reveal a previously unknown Slit-independent function and regulatory mechanism of Robo and show that the cleaved extracellular fragment of Robo can function as a ligand for SYG-1/Neph to guide glial migration. As Robo, the cleaved region of Robo, and SYG-1/Neph are all highly conserved across the animal kingdom, our findings may present a conserved Slit-independent Robo mechanism during brain development.

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10.7554/elife.57921

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Qu, Zhongwei, Albert Zhang and Dong Yan (2020). Robo functions as an attractive cue for glial migration through SYG-1/Neph. eLife, 9. p. e57921. 10.7554/elife.57921 Retrieved from https://hdl.handle.net/10161/25504.

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Scholars@Duke

Qu

Zhongwei Qu

Research Scholar
Yan

Dong Yan

Associate Professor of Molecular Genetics and Microbiology

we are interested in understanding the molecular mechanisms underlying neural circuit formation during development and degeneration in aging. In my lab, We use a free-living tiny roundworm, called Caenorhabditis elegans, as a model. The defined cell lineage, completely mapped connectome and rapid life cycle of this organism greatly facilitate investigating nervous system at the subcellular resolution. Combining classic genetic analysis with in vivo live imaging technique and molecular and cellular manipulations, we are discovering conserved mechanisms playing key roles in neural circuit formation, gap junction dynamics and neurodegeneration


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