Fig. 8 | Nature Communications

Fig. 8

From: Arf6-driven cell invasion is intrinsically linked to TRAK1-mediated mitochondrial anterograde trafficking to avoid oxidative catastrophe

Fig. 8

A schematic model of mitochondrial distribution regulated by the Arf6–AMAP1–ILK pathway. Integrin recycling mediated by the Arf6–AMAP1 pathway, which is activated in invasive cancer cells, is essential for the formation of mature FAs (1). The ILK–RhoT1 complex formed at or recruited to FAs (2) might interact with some component(s) of the adhesion complex, which causes alteration of the molecular properties of RhoT1. RhoT1 modified as such would be released and inserted into the mitochondrial outer membrane (3), and negatively regulates the interaction between RhoT1 and TRAK2, leading to relatively increased anterograde trafficking of mitochondria (4). Another possibility is that RhoT1 anchored to the mitochondrial outer membrane may interact with ILK, which is diffusely localized in the cytoplasm, and the above modification(s) may occur when mitochondria reach in close proximity to the mitochondria (2′). Disruption of these mechanisms reduces invasiveness and enhances the molecular interaction between RhoT1 and TRAK2, which preferentially mediates mitochondrial retrograde trafficking (i). The mitochondrial aggregation that is thus caused tends to result in ROS amplification via a RIRR-like mechanism (ii)