Laserprobe 40Ar/39Ar dating of strain fringes: Mid-Cretaceous synconvergent orogen-parallel extension in the interior of the Sevier orogen:

[1] UV and CO2 laser-probe 40Ar/39Ar in situ analyses of phlogopite and muscovite in fibrous strain fringes from greenschist-facies metamorphic rocks document mica growth ages at temperatures lower than their closure temperatures, and therefore directly date deformation. The new dates resolve the age of the earliest ductile fabric recorded in the Raft River–Albion–Grouse Creek metamorphic core complex of Utah and Idaho. Phlogopite was dated in quartz-calcite-phlogopite strain fringes around pyrite in Pennsylvanian-Permian rocks from the Grouse Creek Mountains (Utah) using both the UV and CO2 laser probe; muscovite was dated in quartz-muscovite strain fringes around pyrite in deformed Jurassic sills from the Black Pine Mountains (Idaho) using the CO2 laser probe. Phlogopite 40Ar/39Ar ages for individual strain fringes (Grouse Creek Mountains) range from 92 Ma to 110 Ma, with the most reliable ages ranging from 101 Ma to 110 Ma (mean age, 105.0 ± 5.8 Ma). Muscovite 40Ar/39Ar ages for individual strain fringes (Black Pine Mountains) range from 97 Ma to 112 Ma (mean age, 104.7 ± 5.8 Ma). Strain fringes are associated with a subhorizontal foliation and a generally N-trending elongation lineation exhibiting components of top-to-the-north simple shear and coaxial strain accommodating N-S extension and subvertical shortening. Midcrustal northward flow at 105 (±6) Ma within the interior of the Sevier orogen, coeval with east-directed shortening in the foreland and with plate convergence, records orogen-parallel synconvergent extension. We favor gravitational relaxation of structural culminations resulting from focused crustal shortening as a driving mechanism for orogen-parallel flow

Sgs1 and Exo1 Redundantly Inhibit Break-Induced Replication and De Novo Telomere Addition at Broken Chromosome Ends

In budding yeast, an HO endonuclease-inducible double-strand break (DSB) is efficiently repaired by several homologous recombination (HR) pathways. In contrast to gene conversion (GC), where both ends of the DSB can recombine with the same template, break-induced replication (BIR) occurs when only the centromere-proximal end of the DSB can locate homologous sequences. Whereas GC results in a small patch of new DNA synthesis, BIR leads to a nonreciprocal translocation. The requirements for completing BIR are significantly different from those of GC, but both processes require 5′ to 3′ resection of DSB ends to create single-stranded DNA that leads to formation of a Rad51 filament required to initiate HR. Resection proceeds by two pathways dependent on Exo1 or the BLM homolog, Sgs1. We report that Exo1 and Sgs1 each inhibit BIR but have little effect on GC, while overexpression of either protein severely inhibits BIR. In contrast, overexpression of Rad51 markedly increases the efficiency of BIR, again with little effect on GC. In sgs1Δ exo1Δ strains, where there is little 5′ to 3′ resection, the level of BIR is not different from either single mutant; surprisingly, there is a two-fold increase in cell viability after HO induction whereby 40% of all cells survive by formation of a new telomere within a few kb of the site of DNA cleavage. De novo telomere addition is rare in wild-type, sgs1Δ, or exo1Δ cells. In sgs1Δ exo1Δ, repair by GC is severely inhibited, but cell viaiblity remains high because of new telomere formation. These data suggest that the extensive 5′ to 3′ resection that occurs before the initiation of new DNA synthesis in BIR may prevent efficient maintenance of a Rad51 filament near the DSB end. The severe constraint on 5′ to 3′ resection, which also abrogates activation of the Mec1-dependent DNA damage checkpoint, permits an unprecedented level of new telomere addition

Nondisjunction of a Single Chromosome Leads to Breakage and Activation of DNA Damage Checkpoint in G2

The resolution of chromosomes during anaphase is a key step in mitosis. Failure to disjoin chromatids compromises the fidelity of chromosome inheritance and generates aneuploidy and chromosome rearrangements, conditions linked to cancer development. Inactivation of topoisomerase II, condensin, or separase leads to gross chromosome nondisjunction. However, the fate of cells when one or a few chromosomes fail to separate has not been determined. Here, we describe a genetic system to induce mitotic progression in the presence of nondisjunction in yeast chromosome XII right arm (cXIIr), which allows the characterisation of the cellular fate of the progeny. Surprisingly, we find that the execution of karyokinesis and cytokinesis is timely and produces severing of cXIIr on or near the repetitive ribosomal gene array. Consequently, one end of the broken chromatid finishes up in each of the new daughter cells, generating a novel type of one-ended double-strand break. Importantly, both daughter cells enter a new cycle and the damage is not detected until the next G2, when cells arrest in a Rad9-dependent manner. Cytologically, we observed the accumulation of damage foci containing RPA/Rad52 proteins but failed to detect Mre11, indicating that cells attempt to repair both chromosome arms through a MRX-independent recombinational pathway. Finally, we analysed several surviving colonies arising after just one cell cycle with cXIIr nondisjunction. We found that aberrant forms of the chromosome were recovered, especially when RAD52 was deleted. Our results demonstrate that, in yeast cells, the Rad9-DNA damage checkpoint plays an important role responding to compromised genome integrity caused by mitotic nondisjunction

Fighting Conflict: Violent Splits or Healthy Divides?

In this study, we develop a theory to understand how groups with strong divisions may, paradoxically, help members to cope with conflict and injustice. We test our theoretical predictions using a survey methodology and the data from 72 work groups across different industries. Consistent with our hypotheses, we found that group faultlines weakened the positive relationships between injustice and psychological health

Structuring reality through the faultlines lens: the effects of structure, fairness, and status conflict on the activated faultlines-performance relationship

We investigate how activated team faultlines represent an informal sensemaking structure through which teammates interpret their social reality. Constructed from inter-subgroup comparisons, activated faultlines likely result in status perceptions that are ambiguous or illegitimate. Thus, activated faultlines threaten the justice climate within the team, which drives status conflict, impairing team performance. We explore the effects of team structure clarity in providing certainty or legitimacy around status and structure, ameliorating the negative effect of activated faultlines on team justice climate. We tested our model using a multi-source (three sources), multi-wave cross-lagged design (four waves) on a sample of 271 employees and 41 leaders in 41 teams. We found that the negative relationship between activated faultlines and team performance was mediated by the team justice climate—status conflict causal chain. We also found that team structure clarity reduced activated faultlines negative effect on team justice climate. The results highlight the value of using team faultlines, the social identity approach, and justice theories to understand how diverse teams interpret their social reality that influences their performance. Furthermore, our research provides practical guidance to managers in building clear team structures that minimize the harmful effects of activated faultlines on justice perceptions and team performance.info:eu-repo/semantics/acceptedVersio

Deletion of Cryptococcus neoformans AIF Ortholog Promotes Chromosome Aneuploidy and Fluconazole-Resistance in a Metacaspase-Independent Manner

Apoptosis is a form of programmed cell death critical for development and homeostasis in multicellular organisms. Apoptosis-like cell death (ALCD) has been described in several fungi, including the opportunistic human pathogen Cryptococcus neoformans. In addition, capsular polysaccharides of C. neoformans are known to induce apoptosis in host immune cells, thereby contributing to its virulence. Our goals were to characterize the apoptotic signaling cascade in C. neoformans as well as its unique features compared to the host machinery to exploit the endogenous fungal apoptotic pathways as a novel antifungal strategy in the future. The dissection of apoptotic pathways revealed that apoptosis-inducing factor (Aif1) and metacaspases (Mca1 and Mca2) are independently required for ALCD in C. neoformans. We show that the apoptotic pathways are required for cell fusion and sporulation during mating, indicating that apoptosis may occur during sexual development. Previous studies showed that antifungal drugs induce ALCD in fungi and that C. neoformans adapts to high concentrations of the antifungal fluconazole (FLC) by acquisition of aneuploidy, especially duplication of chromosome 1 (Chr1). Disruption of aif1, but not the metacaspases, stimulates the emergence of aneuploid subpopulations with Chr1 disomy that are resistant to fluconazole (FLCR) in vitro and in vivo. FLCR isolates in the aif1 background are stable in the absence of the drug, while those in the wild-type background readily revert to FLC sensitivity. We propose that apoptosis orchestrated by Aif1 might eliminate aneuploid cells from the population and defects in this pathway contribute to the selection of aneuploid FLCR subpopulations during treatment. Aneuploid clinical isolates with disomies for chromosomes other than Chr1 exhibit reduced AIF1 expression, suggesting that inactivation of Aif1 might be a novel aneuploidy-tolerating mechanism in fungi that facilitates the selection of antifungal drug resistance

Late Miocene transcurrent tectonics in NW Turkey: evidence from palaeomagnetism and 40Ar–39Ar dating of alkaline volcanic rocks

A number of intra-continental alkaline volcanic sequences in NW Turkey were emplaced along localized extensional gaps within dextral strike-slip fault zones prior to the initiation of the North Anatolian Fault Zone. This study presents new palaeomagnetic and 40Ar–39Ar geochronological results from the lava flows of NW Turkey as a contribution towards understanding the Neogene–Quaternary tectonic evolution of the region and possible roles of block rotations in the kinematic history of the region. 40Ar–39Ar analyses of basalt groundmass indicate that the major volume of alkaline lavas of NW Turkey spans about 4 million years of episodic volcanic activity. Palaeomagnetic results reveal clockwise rotations as high as 73° in Thrace and 33° anticlockwise rotations in the Biga Peninsula. Movement of some of the faults delimiting the areas of lava flows and the timing of volcanic eruptions are both older than the initiation age of the North Anatolian Fault Zone, implying that the region experienced transcurrent tectonics during Late Miocene to Pliocene times and that some of the presently active faults in the region are reactivated pre-existing structures.</jats:p

Magmatism during Gondwana break-up: new geochronological data from Westland, New Zealand

Newly determined Late Cretaceous Ar-40/Ar-39 ages on megacrystic kaersutite from four lamprophyre dikes, and a U-Pb zircon age on a trachyte, from central and north Westland (New Zealand) are presented. These ages suggest that the intrusion of mafic dikes (88-86 and 69 Ma) was not necessarily restricted to the previously established narrow age range of 80-92 Ma. The younger lamprophyre and trachyte dikes (c. 68-70 Ma) imply that tensional stresses in the Western Province were either renewed at this time, or that extension and related magmatism continued during opening of the Tasman Sea. Extension-related magmatism in the region not only preceded Tasman seafloor spreading initiation (starting at c. 83 Ma, lasting to c. 53 Ma), but may have sporadically continued for up to 15 Ma after continental break-up