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DCLK1 Inhibits Vesicular Trafficking in Non-Neuronal Cells


Normal brain development, involving neuronal migration, polarity and differentiation, requires synaptic trafficking of essential cargo. These cargo are primarily transported on microtubules (MTs), which play a key role in neuronal morphology. Mutations in MT-related proteins were previously found to be associated with epilepsy. Specifically, Dcx and Dclk1 (doublecortin family proteins) were found to regulate Kif1a (a kinesin motor protein) mediated transport and localization in neurons (Liu et. al 2012). However, it is unknown whether Dclk1 alone is sufficient for transport.Vamp2, a vesicle membrane protein carried by Kif1a, has been found to be transported by other kinesins, including Kif53 and Kif23.6 In particular, these kinesins are expressed significantly more in conventional non-neuronal HEK and HeLa cells as opposed to Kif1a7. It is possible that Dclk1 plays a different role in trafficking when Kif1a is not the primary transporter of Vamp2-containing vesicles. Our experiments show that Dclk1 inhibits mobile vesicle movement in two cell culture models expressing low levels of Kif1a, indicating a potential role for Dclk1 in mediating other modes of vesicle trafficking.

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Lee, Jenny, McCarthy-Sinclair, Brendan, Papendorf, Carin, et al., "DCLK1 Inhibits Vesicular Trafficking in Non-Neuronal Cells" (2019). Summer Research Symposium. Brown Digital Repository. Brown University Library.



  • Summer Research Symposium

    Each year, Brown University showcases the research of its undergraduates at the Summer Research Symposium. More than half of the student-researchers are UTRA recipients, while others receive funding from a variety of Brown-administered and national programs and fellowships and go …