Coordinated interaction of Down syndrome cell adhesion molecule and deleted in colorectal cancer with dynamic TUBB3 mediates Netrin-1-induced axon branching
Abstract
Modulation of actin and microtubule (MT) dynamics in neurons is implicated in guidance cue-dependent axon outgrowth, branching and pathfinding. Although the role of MTs in axon guidance has been well known, how extracellular guidance signals engage MT behavior in axon branching remains unclear. Previously, we have shown that TUBB3, the most dynamic β-tubulin isoform in neurons, directly binds to deleted in colorectal cancer (DCC) to regulate MT dynamics in Netrin-1-mediated axon guidance. Here, we report that TUBB3 directly interacted with another Netrin-1 receptor Down syndrome cell adhesion molecule (DSCAM) and Netrin-1 increased this interaction in primary neurons. MT dynamics were required for Netrin-1-promoted association of DSCAM with TUBB3. Knockdown of either DSCAM or DCC or addition of a function blocking anti-DCC antibody mutually blocked Netrin-1-induced interactions, suggesting that DSCAM interdependently coordinated with DCC in Netrin-1-induced binding to TUBB3. Both DSCAM and DCC were partially colocalized with TUBB3 in the axon branch and the axon branching point of primary neurons and Netrin-1 increased these colocalizations. Netrin-1 induced the interaction of endogenous DSCAM with polymerized TUBB3 in primary ...Continue Reading
References
Binding of DCC by netrin-1 to mediate axon guidance independent of adenosine A2B receptor activation
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