Figure 2. Model for the Role of CLIP-170 in MTOC Repositioning during T Cell Activation (IMAGE)

Tokyo Institute of Technology

Figure 2. Model for the Role of CLIP-170 in MTOC Repositioning during T Cell Activation

Caption

In resting T cells, the majority of dynein is immobile on the contacted cell surface and is located at the periphery region. T cell stimulation increases the fraction of dynein undergoing minus-end-directed motility ("mobilize"), which is a "weakly processive" state. Then, the dynein is anchored to the surface ("anchor"). Alongside this, stimulation induces some fraction of dynein to colocalize with CLIP-170 and dynactin and follow plus-end tracking ("recruit"). After tracking of one or two micrometers, the dynein is released from the complex and anchored ("release"). As a result, dynein relocation increases to the center region of the contact surface, the immunological synapse, where "anchored" dynein molecules are immobile and or weakly processive at a velocity in good agreement with the velocity of MTOC repositioning. "Anchored" and weakly processive dynein pulls the microtubules and the MTOC ("pull"), which causes MTOC repositioning near the immunological synapse and full activation of T cells. Phosphorylation of CLIP-170 is essential for dynein recruitment to the plus-end and for dynein relocation.

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<i>Scientific Reports</i>

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