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Abstract The devastating 6 February 2023 Kahramanmaraş earthquake sequence in southeastern Türkiye started with a moment magnitude (Mw) 7.8 earthquake, for which the initial rupture broke the Sakçagöz segment near Nurdağı and then jumped into a bilateral rupture along multiple segments of the Eastern Anatolian fault zone (EAFZ). This complicated rupture was followed nine hours later by an Mw 7.6 event near Ekinözü. To better understand the spatiotemporal evolution of aftershocks, site amplification, and the structural and tectonic framework of the EAFZ in this diffuse triple junction, we deployed a dense seismometer array covering both aftershock zones for nearly four months. The main Eastern Anatolian Seismic Temporary (EAST) array includes 125 nodal, 10 broadband, and 6 strong-motion seismic stations distributed around the rupture zone. An additional linear array of 73 nodal stations was also installed across the Pazarcık segment of the EAFZ and the Sakçagöz segment near the Mw 7.8 epicenter to record fault-zone waves for ∼30 days. This article shows example recordings and the EAST array geometry, preliminary research results, and the metadata related to all of the stations in this array. A deep-learning-based phase picking for one month of continuous recording yielded millions of seismic phase readings and tens of thousands of aftershock locations after phase associations. We also give examples of both local and teleseismic waveforms recorded by the nodal arrays, which can be used for subsequent high-resolution earthquake relocation, imaging of crustal structures, and fault-zone imaging. 

Cell spreading and migration play central roles in many physiological and pathophysiological processes. We have previously shown that MFN2 regulates the migration of human neutrophil-like cells via suppressing Rac activation. Here, we show that in mouse embryonic fibroblasts, MFN2 suppresses RhoA activation and supports cell polarization. After initial spreading, the wild-type cells polarize and migrate, whereas theMfn2^-/-cells maintain a circular shape. Increased cytosolic Ca²⁺resulting from the loss of Mfn2 is directly responsible for this phenotype, which can be rescued by expressing an artificial tether to bring mitochondria and endoplasmic reticulum to close vicinity. Elevated cytosolic Ca²⁺activates Ca²⁺/calmodulin-dependent protein kinase II, RhoA, and myosin light-chain kinase, causing an overactivation of nonmuscle myosin II, leading to a formation of a prominent F-actin ring at the cell periphery and increased cell contractility. The peripheral actin band alters cell physics and is dependent on substrate rigidity. Our results provide a novel molecular basis to understand how MFN2 regulates distinct signaling pathways in different cells and tissue environments, which is instrumental in understanding and treating MFN2-related diseases.