Fig. 6: Daam1-MIC impacts F-actin polymerization and the interplay with RHOA/ROCK signaling cascade. | Nature Communications

Fig. 6: Daam1-MIC impacts F-actin polymerization and the interplay with RHOA/ROCK signaling cascade.

From: A highly conserved neuronal microexon in DAAM1 controls actin dynamics, RHOA/ROCK signaling, and memory formation

Fig. 6

Summary of the observed phenotypes upon Daam1-MIC removal and their relation to the RHOA/ROCK signaling cascade9,14,15. DVL binds to DAAM1, releasing its autoinhibition, which is further facilitated by interaction with RHOA. Active DAAM1 leads to RHOA activation through an unknown mechanism involving DAAM1’s C-terminal part (dashed lined) and is not dependent on direct binding RHOA-DAAM1 interaction. Microexon removal decreases RHOA binding to DAAM1’s N-terminal region. This is proposed to lead to lower hydrolysis of RhoA-GTP, increasing the pool of active RHOA and in turn, hyperactivating the RHOA/ROCK signaling cascade. Arrows indicate the directionality of the event. The dotted arrow indicates a potential, unknown feedback loop from actin polymerization to ROCK pathway activation. GAP - GTPase-activating protein, GEF - guanine nucleotide exchange factor, GTP - Guanosine triphosphate, GDP - Guanosine diphosphate.

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