Fig. 6: Distinct pathways of filament assembly by wild-type and ATPase-deficient MDA5 on dsRNA. | Cell Research

Fig. 6: Distinct pathways of filament assembly by wild-type and ATPase-deficient MDA5 on dsRNA.

From: ATP-dependent one-dimensional movement maintains immune homeostasis by suppressing spontaneous MDA5 filament assembly

Fig. 6

Left: wild-type MDA5 uses ATP hydrolysis to translocate along dsRNA. On self-RNAs, the motors dissociate quickly and fail to assemble into filaments. On viral RNAs, MDA5 forms ATM clusters with spacing between individual molecules. LGP2 binding serves as a roadblock, compressing MDA5 within these clusters and promoting microfilament formation. This translocation-driven assembly proceeds efficiently on long dsRNA duplexes, supporting antiviral signaling. Right: ATPase-deficient MDA5, which lacks 1D translocation activity, assembles into filaments spontaneously on dsRNA, regardless of duplex length. This indiscriminate filament formation causes aberrant activation on self-RNAs.

Back to article page