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Rupturing of the primary fault may trigger secondary fault activity in a complex multi-fault system. The mainshock focal mechanism and well-constrained aftershock locations reveal vital information about aftershock migration patterns, the regional tectonic stress field, and the seismogenic process. Aftershock relocations of the events in the Utah Mw5.7 earthquake sequence that occurred on March 18, 2020, indicate that the mainshock ruptured a listric normal fault; this fault is characterized by a shallow concave upward fault surface and a dip that decreases with depth. The aftershocks were largely organized into two clusters. The first small cluster, which is located ~ 8 km east of the mainshock, resides on part of a fault that is steeply dipping to the east; the second larger cluster is spread across multiple conjugate faults. Using local and regional waveforms to estimate the seismic moment tensor solutions, we determined that the Utah MW5.7 mainshock was a shallow crustal normal faulting event. Furthermore, 11 selected aftershocks (MW ≥ 3.3) are also characterized by normal faulting. The nearly EW-oriented extensional stress pattern in the focal area has an orientation that is similar to that of the regional maximum horizontal extensional stress field. Our analysis of the Coulomb stress variations showed that the Utah Mw5.7 earthquake triggered the aftershocks that formed along conjugate normal faults near the West Valley fault zone. These results provide evidence for the triggering hypothesis, wherein subsequent seismic events are caused by static stress changes triggered by large mainshock earthquakes. [ABSTRACT FROM AUTHOR]

S‐adenosyl‐L‐methionine (SAM)‐dependent methyltransferases (MTases) are widely distributed among almost all organisms and often characterized with conserved Rossmann fold, TIM barrel, and D×G×G×G motif. However, some MTases show no methyltransferase activity. In the present study, the crystal structure of LepI, one MTase‐like enzyme isolated from A. flavus that catalyzes pericyclic reactions, was investigated to determine its structure‐function relationship. The overall structure of LepI in complex with the SAM mimic S‐adenosyl‐L‐homocysteine (SAH) (PDB ID: 6IV7) indicated that LepI is a tetramer in solution. The residues His133, Arg197, Arg295, and Asp296 located near the active site can form hydrogen bonds with the substrate, thus participating in catalytic reactions. The binding of SAH in LepI is almost identical to that in other resolved MTases; however, the location of catalytic residues differs significantly. Phylogenetic trials suggest that LepI proteins share a common ancestor in plants and algae, which may explain the conserved SAM‐binding site. However, the accelerated evolution of A. flavus has introduced both functional and structural changes in LepI. More importantly, the residue Arg295, which is unique to LepI, might be a key determinant for the altered enzymatic behavior. Collectively, the differences in the composition of catalytic residues, as well as the unique tetrameric form of LepI, define its unique enzymatic behavior. The present work provides an additional understanding of the structure‐function relationship of MTases and MTase‐like enzymes. [ABSTRACT FROM AUTHOR]

Summary: Despite of important functions of strigolactones (SLs) and karrikins (KARs) in plant development, plant–parasite and plant–fungi interactions, their roles in soybean–rhizobia interaction remain elusive. SL/KAR signaling genes GmMAX2a, GmD14s, and GmKAIs are activated by rhizobia infection. GmMAX2a restored atmax2 root hair defects and soybean root hairs were changed in GmMAX2a overexpression (GmMAX2a‐OE) or knockdown (GmMAX2a‐KD) mutants. GmMAX2a‐KD gave fewer, whereas GmMAX2a‐OE produced more nodules than GUS hairy roots. Mutation of GmMAX2a in its KD or OE transgenic hairy roots affected the rhizobia infection‐induced increases in early nodulation gene expression. Both mutant hairy roots also displayed the altered auxin, jasmonate and abscisic acid levels, as further verified by transcriptomic analyses of their synthetic genes. Overexpression of an auxin synthetic gene GmYUC2a also affected SL and KAR signaling genes. GmMAX2a physically interacted with SL/KAR receptors GmD14s, GmKAIs, and GmD14Ls with different binding affinities, depending on variations in the critical amino acids, forming active D14/KAI‐SCFMAX2 complexes. The knockdown mutant roots of the nodule‐specifically expressing GmKAIs and GmD14Ls gave fewer nodules, with altered expression of several early nodulation genes. The expression levels of GmKAIs, and GmD14Ls were markedly changed in GmMAX2a mutant roots, so did their target repressor genes GmD53s and GmSMAX1s. Thus, SL and KAR signaling were involved in soybean–rhizobia interaction and nodulation partly through interactions with hormones, and this may explain the different effects of MXA2 orthologs on legume determinate and indeterminate nodulation. The study provides fresh insights into the roles of GmMAX2‐mediated SL/KAR signaling in soybean root hair and nodule formation. Significance Statement: Soybean strigolactone and karrikin signaling genes are specifically expressed in root and nodules and respond to rhizobia infection. GmMAX2a mutant roots display altered root hairs, nodule numbers, and hormone levels, and GmMAX2a interacts with GmD14s, GmKAIs, and GmD14Ls, the last two of which gave fewer nodules in their knockdown mutants. The study expands the functions of GmMAX2‐mediated SL/KAR signaling in modulating root hair and nodule formation, and interactions with auxins and other hormone signaling. [ABSTRACT FROM AUTHOR]