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The criteria for zoning the surface fault rupture hazard (SFRH) along thrust faults are defined by analysing the characteristics of the areas of coseismic surface faulting in thrust earthquakes. Normal and strike–slip faults have been deeply studied by other authors concerning the SFRH, while thrust faults have not been studied with comparable attention. Surface faulting data were compiled for 11 well-studied historic thrust earthquakes occurred globally (5.4 ≤ M ≤ 7.9). Several different types of coseismic fault scarps characterize the analysed earthquakes, depending on the topography, fault geometry and near-surface materials (simple and hanging wall collapse scarps, pressure ridges, fold scarps and thrust or pressure ridges with bending-moment or flexural-slip fault ruptures due to large-scale folding). For all the earthquakes, the distance of distributed ruptures from the principal fault rupture (r) and the width of the rupture zone (WRZ) were compiled directly from the literature or measured systematically in GIS-georeferenced published maps. Overall, surface ruptures can occur up to large distances from the main fault ( ∼ 2150 m on the footwall and  ∼  3100 m on the hanging wall). Most of the ruptures occur on the hanging wall, preferentially in the vicinity of the principal fault trace ( >   ∼  50 % at distances  <   ∼  250 m). The widest WRZ are recorded where sympathetic slip (Sy) on distant faults occurs, and/or where bending-moment (B-M) or flexural-slip (F-S) fault ruptures, associated with large-scale folds (hundreds of metres to kilometres in wavelength), are present. A positive relation between the earthquake magnitude and the total WRZ is evident, while a clear correlation between the vertical displacement on the principal fault and the total WRZ is not found. The distribution of surface ruptures is fitted with probability density functions, in order to define a criterion to remove outliers (e.g. 90 % probability of the cumulative distribution function) and define the zone where the likelihood of having surface ruptures is the highest. This might help in sizing the zones of SFRH during seismic microzonation (SM) mapping. In order to shape zones of SFRH, a very detailed earthquake geologic study of the fault is necessary (the highest level of SM, i.e. Level 3 SM according to Italian guidelines). In the absence of such a very detailed study (basic SM, i.e. Level 1 SM of Italian guidelines) a width of  ∼  840 m (90 % probability from \"simple thrust\" database of distributed ruptures, excluding B-M, F-S and Sy fault ruptures) is suggested to be sufficiently precautionary. For more detailed SM, where the fault is carefully mapped, one must consider that the highest SFRH is concentrated in a narrow zone,  ∼ 60 m in width, that should be considered as a fault avoidance zone (more than one-third of the distributed ruptures are expected to occur within this zone). The fault rupture hazard zones should be asymmetric compared to the trace of the principal fault. The average footwall to hanging wall ratio (FW  :  HW) is close to 1  :  2 in all analysed cases. These criteria are applicable to \"simple thrust\" faults, without considering possible B-M or F-S fault ruptures due to large-scale folding, and without considering sympathetic slip on distant faults. Areas potentially susceptible to B-M or F-S fault ruptures should have their own zones of fault rupture hazard that can be defined by detailed knowledge of the structural setting of the area (shape, wavelength, tightness and lithology of the thrust-related large-scale folds) and by geomorphic evidence of past secondary faulting. Distant active faults, potentially susceptible to sympathetic triggering, should be zoned as separate principal faults. The entire database of distributed ruptures (including B-M, F-S and Sy fault ruptures) can be useful in poorly known areas, in order to assess the extent of the area within which potential sources of fault displacement hazard can be present. The results from this study and the database made available in the Supplement can be used for improving the attenuation relationships for distributed faulting, with possible applications in probabilistic studies of fault displacement hazard.

We present a 1:25,000 scale map of the coseismic surface ruptures following the 30 October 2016 M w 6.5 Norcia normal-faulting earthquake, central Italy. Detailed rupture mapping is based on almost 11,000 oblique photographs taken from helicopter flights, that has been verified and integrated with field data (>7000 measurements). Thanks to the common efforts of the Open EMERGEO Working Group (130 people, 25 research institutions and universities from Europe), we were able to document a complex surface faulting pattern with a dominant strike of N135°-160° (SW-dipping) and a subordinate strike of N320°-345° (NE-dipping) along about 28 km of the active Mt. Vettore-Mt. Bove fault system. Geometric and kinematic characteristics of the rupture were observed and recorded along closely spaced, parallel or subparallel, overlapping or step-like synthetic and antithetic fault splays of the activated fault systems, comprising a total surface rupture length of approximately 46 km when all ruptures were considered.

The replication checkpoint controls the integrity of replicating chromosomes by stabilizing stalled forks, thus preventing the accumulation of abnormal replication and recombination intermediates that contribute to genome instability. Checkpoint-defective cells are susceptible to rearrangements at chromosome fragile sites when replication pauses, and certain human cancer prone diseases suffer checkpoint abnormalities. It is unclear as to how the checkpoint stabilizes stalled forks and how cells sense replication blocks. We have analysed the checkpoint contribution in controlling replisome–fork association when replication pauses. We show that in yeast wild-type cells, stalled forks exhibit stable replisome complexes and the checkpoint sensors Ddc1 and Ddc2, thus activating Rad53 checkpoint kinase. Ddc1/Ddc2 recruitment on stalled forks and Rad53 activation are influenced by the single-strand-binding protein replication factor A (RFA). rad53 forks exhibit a defective association with DNA polymerases α , ɛ and δ . Further, in rad53 mutants, stalled forks progressively generate abnormal structures that turn into checkpoint signals by accumulating RFA, Ddc1 and Ddc2. We suggest that, following replication blocks, checkpoint activation mediated by RFA-ssDNA filaments stabilizes stalled forks by controlling replisome–fork association, thus preventing unscheduled recruitment of recombination enzymes that could otherwise cause the pathological processing of the forks.

Eukaryotic chromosomes are duplicated during S phase and transmitted to progeny during mitosis with high fidelity. Chromosome duplication is controlled at the level of replication initiation, which occurs at cis-acting replicator sequences that are spaced at intervals of ∼40 kb along the chromosomes of the budding yeast Saccharomyces cerevisiae. Surprisingly, we found that derivatives of yeast chromosome III that lack known replicators were replicated and segregated properly in at least 96% of cell divisions. To gain insight into the mechanisms that maintain these “originless” chromosome fragments, we screened for mutants defective in the maintenance of an “originless” chromosome fragment, but proficient in the maintenance of the same fragment that carries its normal complement of replicators (originless fragment maintenance mutants, or ofm). We show that three of these Ofm mutations appear to disrupt different processes involved in chromosome transmission. The OFM1-1 mutant seems to disrupt an alternative initiation mechanism, and the ofm6 mutant appears to be defective in replication fork progression. ofm14 is an allele of RAD9, which is required for the activation of the DNA damage checkpoint, suggesting that this checkpoint plays a key role in the maintenance of the “originless” fragment.

The Rad17-Mec3-Ddc1 complex is essential for the cellular response to genotoxic agents and is thought to be important for sensing DNA lesions. Deletion of any of the RAD17, MEC3 or DDC1 genes abolishes the G1and G2and impairs the intra-S DNA-damage checkpoints. We characterize a dominant-negative mec3-dn mutation that has an unexpected phenotype. It inactives the G1checkpoint while it leaves the G2response functional, thus revealing a difference in the requirements of the DNA-damage response in different phases of the cell cycle. In an attempt to identify the molecular defect imparted by the mutation, we dissected step-by-step the signaling cascade, which is triggered by DNA lesions and requires the activity of Mec1 and Rad53 kinases. The analysis of the phosphorylation state of checkpoint factors and critical protein interactions showed that, in mec3-dn cells, the signal transduction cascade is triggered normally, and the central kinase Mec1 can be activated. In G1cells expressing the mutation, the signaling cannot proceed any further along the pathway, indicating that the Rad17 complex acts after the activation of Mec1, possibly recruiting targets for the kinase. We also show that the function of the G2checkpoint in mutant cells is maintained by an uncharacterized activity of Tel1, the yeast homologue of ATM. This work thus reports a previously undiscovered role for Tel1 in checkpoint control.