The Agua Blanca fault (ABF) is a west-northwest–trending oblique dextral-­normal fault that defines the southern boundary of the Big Bend domain (BBD) of the Pacific–North American plate margin and the northern limit to the rigid Baja California microplate. Our geologic and geodetic studies demonstrate that finite slip on the ABF reaches a maximum of ~11 km of nearly pure dextral strike slip in central portions of the fault, whereas the magnitude of displacement decreases and the proportion of extension increases in the sections to both the east and west. To the east, the ABF appears to die out before crossing into the San Pedro Mártir fault, with slip transferred onto a series of more northerly-­trending, dip-slip faults. To the west, the ABF bifurcates to form the Santo Tomás fault (STF) in the Valle Santo Tomás section, where we measure ~5 km of dextral offset for the ABF and ~3 km estimated offset on the STF. And we report a measurement of ~7 km of dextral offset on the ABF in the Punta Banda section. Small offset faults proximal to the ABF likely accommodate additional dextral shear in the western sections of the fault. The STF in the Valle Santo Tomás section and the ABF in the Punta Banda section exhibit 0.58 and 0.65 km of extensional heave, or ~7% and 10% of the total displacement in each section, respectively. Block modeling based on geodetic data agrees well with geologic determinations of slip direction and reveals near perfect alignment of the central ABF with the relative block motion vectors and increased proportions of fault-perpendicular extension to both the east (3%–10%) and west (5%–13%). Based on our new estimates of the total offsets combined with existing slip rates, the ABF likely initiated between 3.3 and 1.5 Ma. This age range overlaps with those reported for other faults within the area of the BBD southwest of the San Andreas fault. The ABF has a more westerly orientation than the transpressional restraining-bend segment of the San Andreas, yet it accommodates transtensional shearing. This requires a reevaluation of the processes that control transpression and transtension within the BBD.

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