Skip to main content
. 2019 Apr 2;27(4):651–659.e3. doi: 10.1016/j.str.2019.01.010

Figure 4.

Figure 4

Transport Models for Type I Importer ModBC-A and TYPE II IMPorter BtuCD-F

(A) Transport model for ModBC-A. The formation of the complex in the absence of molybdate is unfavorable (state I). Binding of molybdate triggers the docking of ModA onto ModBC (state II). Following a rearrangement of the TMDs, molybdate moves toward the SBS (state III). ATP binding and hydrolysis triggers a further conformational change that translocate the substrate into the cytoplasm (state IV). The release of ADP resets the transporter to the resting state (state I).

(B) Transport model for BtuCD-F. BtuCD and BtuF form a stable complex even in the absence of vitamin B12 (state I). ATP binds cooperatively, leading to a partial displacement of BtuF from BtuCD (state II). When vitamin B12 is available, a transient BtuCD-F⋅2ADP⋅B12 complex is formed (state III). This unstable conformation is relaxed through ADP and Pi dissociation, followed by vitamin B12 release (state IV) leading to the resetting of the transporter.