GPS time series in northeast Japan exhibit nonlinear trends from 1996 to 2011 before the Mw 9.0, 2011 Tohoku‐oki earthquake. After removing reference frame noise, we model time series as linear trends plus constant acceleration, correcting for coseismic and postseismic effects from the numerous Mw ∼ 6.5+ earthquakes during this period. We find spatially coherent and statistically significant accelerations throughout northern Honshu. Large areas of Japan outside the Tohoku region show insignificant accelerations, demonstrating that the observation is not due to network‐wide artifacts. While the accelerations in northern Tohoku (Sanriku area) can be explained by decaying postseismic deformation from pre‐1996 earthquakes, the accelerations in south‐central Tohoku appear unrelated to postseismic effects. The latter accelerations are associated with a decrease in average trench‐normal strain rate and can be explained by increasing slip rate on the Japan trench plate interface and/or updip migration of deep aseismic slip in the decades before the 2011 Tohoku‐oki earthquake.

A decadal‐scale deformation transient preceding the 2011 Mw 9 Tohoku‐oki, Japan, earthquake was reported from continuous GPS data and interpreted as accelerating aseismic slip on the Japan Trench megathrust. Given the unprecedented nature of this transient, independent confirmation of accelerating slip is required. Here we show that changes in the recurrence intervals of repeating earthquakes on the Japan Trench megathrust in the period 1996 to 2011 are consistent with accelerating slip preceding the Tohoku‐oki earthquake. All sequences of repeating earthquakes with statistically significant trends in recurrence interval (at 95% confidence) offshore south central Tohoku occurred at an accelerating rate. Furthermore, estimates of the magnitude of slip acceleration from repeating earthquakes are consistent with the completely independent geodetic estimates. From a joint inversion of the GPS and seismicity data, we infer that a substantial portion of the megathrust experienced accelerating slip, partly surrounding the eventual rupture zone of the Mw 9 earthquake.

The canonical model of fault coupling assumes that slip is partitioned into fixed asperities that display stick‐slip behavior and regions that creep stably. We show that this simple asperity model is inconsistent with GPS‐derived deformation in northern Japan associated with interseismic coupling on the subduction interface and the transient response to Mw 6.3–7.2 earthquakes during 2003–2011. Comparisons of GPS data with simulations of earthquakes on asperities and associated velocity‐strengthening afterslip require that afterslip overlaps areas of the fault that ruptured in previous earthquakes, including the 2011 Mw 9 Tohoku‐oki earthquake. Whereas about 55% of the plate interface ruptured in earthquakes during 2003–2011, we infer that only 9% of the plate interface was fully locked between earthquakes. Inferred locked asperities are roughly 25% the size of rupture areas determined by seismic source inversions. These smaller asperities are consistent with interseismic strain accumulation in 2009, although more extensive locking is required a decade earlier in 1998.

The conventional “asperity model” posits that faults are partitioned into fixed velocity‐weakening (VW) patches (asperities) that are locked interseismically and velocity‐strengthening (VS) regions that creep stably without accumulating stress. However, studies of GPS‐derived deformation in northern Japan have shown that interseismic strain in the Tohoku region did not accumulate at a constant rate (as expected) but gradually decreased from 1996 to 2011. This change in strain rate is consistent with locked asperities shrinking by ∼75% in area during this period. Here we consider a modification to the conventional asperity model, such that thermal pressurization (TP) is active over an area that encompasses a VW region and part of the surrounding VS region. In our quasi‐dynamic simulations, TP causes shear stress during rapid slip to decrease to very low levels. During the interseismic period, stress gradually recovers to steady state friction at the plate rate, at which point stable creep initiates. The creep front propagates inward, effectively eroding the locked asperity. For uniform properties, the locked area shrinks roughly linearly in time through the VS region. Locked asperities shrink more slowly with higher nominal friction coefficient or background effective normal stress in the VS region, lower hydraulic diffusivity, and larger TP zones. Lateral heterogeneity in properties can give rise to nonlinear erosion. Predictions from this model can be compared against GPS data to test whether the model can explain the observed changes in interseismic strain rate in Tohoku.

Cell migration is a fundamental cell biological process essential both for normal development and for tissue regeneration after damage. Cells can migrate individually or as a collective. To better understand the genetic requirements for collective migration, we expressed RNA interference (RNAi) against 30 genes in the Drosophila embryonic salivary gland cells that are known to migrate collectively. The genes were selected based on their effect on cell and membrane morphology, cytoskeleton and cell adhesion in cell culture-based screens or in Drosophila tissues other than salivary glands. Of these, eight disrupted salivary gland migration, targeting: Rac2, Rab35 and Rab40 GTPases, MAP kinase-activated kinase-2 (MAPk-AK2), RdgA diacylglycerol kinase, Cdk9, the PDSW subunit of NADH dehydrogenase (ND-PDSW) and actin regulator Enabled (Ena). The same RNAi lines were used to determine their effect during regeneration of X-ray-damaged larval wing discs. Cells translocate during this process, but it remained unknown whether they do so by directed cell divisions, by cell migration or both. We found that RNAi targeting Rac2, MAPk-AK2 and RdgA disrupted cell translocation during wing disc regeneration, but RNAi against Ena and ND-PDSW had little effect. We conclude that, in Drosophila, cell movements in development and regeneration have common as well as distinct genetic requirements.