Rock and fault rheology explain differences between on fault and distributed seismicity.

Analysis of seismicity can illuminate active fault zone structures but also deformation within large volumes of the seismogenic zone. For the Mw 6.5 2016-2017 Central Italy seismic sequence, seismicity not only localizes along the major structures hosting the mainshocks (on-fault seismicity), but also occurs within volumes of Triassic Evaporites, TE, composed of alternated anhydrites and dolostones. These volumes of distributed microseismicity show a different frequency-magnitude distribution than on-fault seismicity. We interpret that, during the sequence, shear strain-rate increase, and fluid overpressure promoted widespread ductile deformation within TE that light-up with distributed microseismicity. This interpretation is supported by field and laboratory observations showing that TE background ductile deformation is complex and dominated by distributed failure and folding of the anhydrites associated with boudinage hydro-fracturing and faulting of dolostones. Our results indicate that ductile crustal deformation can cause distributed microseismicity, which obeys to different scaling laws than on-fault seismicity occurring on structures characterized by elasto-frictional stick-slip behaviour.

Lithological and stress anisotropy control large-scale seismic velocity variations in tight carbonates.

Our knowledge of subsurface structures often derives from seismic velocities that are measured during seismic acquisition surveys. These velocities can greatly change due to lithological, fracture frequencies and/or effective pressure/temperature variations. However, the influence of such intrinsic lithological properties and environmental conditions at the large scale is poorly understood due to the lack of comprehensive datasets. Here, we analyze 43 borehole-derived velocity datasets of 3 end-member tight carbonate sequences from Central Italy, including massive pure limestone (Calcare Massiccio, CM), thick-layered (20-50 cm) pure limestone (Maiolica, MA), and thin-layered (2-20 cm) marly limestone (Calcareous Scaglia, CS). Our results show that the main rock parameters and environmental conditions driving large scale velocity variations are bedding and paleostresses, while mineralogical composition and current tectonic stress also play a role. For each of the 3 end-members, measured VP values vary differently with depth, as the thin-layered CS units show a clear increase in Vp, while velocity slightly increases and remains constant for the thick-layered MA and massive CM units, respectively. Such observations show that velocities are affected by specific characteristics of lithological discontinuities, such as the thickness of bedding. Counterintuitively, larger Vp values were recorded in the deformed mountain range than in the undeformed foreland suggesting that higher paleo-stresses increase velocity values by enhancing diagenesis and healing of discontinuities. Our results thus demonstrate that large scale velocity variations are strictly related to variation of lithological properties and to the geological and tectonic history of an area. We suggest that such lithological and environmental controls should be taken into account when developing velocity and mechanical models for tectonically active regions of the Mediterranean Area, where earthquakes mostly nucleate and propagate through carbonate formations, and for resource exploration in fractured carbonate reservoirs.

Mutations that affect meiosis in male mice influence the dynamics of the mid-preleptotene and bouquet stages.

Meiosis pairs and segregates homologous chromosomes and thereby forms haploid germ cells to compensate the genome doubling at fertilization. Homologue pairing in many eukaryotic species depends on formation of DNA double strand breaks (DSBs) during early prophase I when telomeres begin to cluster at the nuclear periphery (bouquet stage). By fluorescence in situ hybridization criteria, we observe that mid-preleptotene and bouquet stage frequencies are altered in male mice deficient for proteins required for recombination, ubiquitin conjugation and telomere length control. The generally low frequencies of mid-preleptotene spermatocytes were significantly increased in male mice lacking recombination proteins SPO11, MEI1, MLH1, KU80, ubiquitin conjugating enzyme HR6B, and in mice with only one copy of the telomere length regulator Terf1. The bouquet stage was significantly enriched in Atm(-/-), Spo11(-/-), Mei1(m1Jcs/m1Jcs), Mlh1(-/-), Terf1(+/-) and Hr6b(-/-) spermatogenesis, but not in mice lacking recombination proteins DMC1 and HOP2, the non-homologous end-joining DNA repair factor KU80 and the ATM downstream effector GADD45a. Mice defective in spermiogenesis (Tnp1(-/-), Gmcl1(-/-), Asm(-/-)) showed wild-type mid-preleptotene and bouquet frequencies. A low frequency of bouquet spermatocytes in Spo11(-/-)Atm(-/-) spermatogenesis suggests that DSBs contribute to the Atm(-/-)-correlated bouquet stage exit defect. Insignificant changes of bouquet frequencies in mice with defects in early stages of DSB repair (Dmc1(-/-), Hop2(-/-)) suggest that there is an ATM-specific influence on bouquet stage duration. Altogether, it appears that several pathways influence telomere dynamics in mammalian meiosis.

Activation of the mitogen-activated protein kinase ERK1 during meiotic progression of mouse pachytene spermatocytes.

Okadaic acid (OA) causes meiotic progression and chromosome condensation in cultured pachytene spermatocytes and an increase in maturation promoting factor (cyclin B1/cdc2 kinase) activity, as evaluated by H1 phosphorylative activity in anti-cyclin B1 immunoprecipitates. OA also induces a strong increase of phosphorylative activity toward the mitogen-activated protein kinase substrate myelin basic protein (MBP). Immunoprecipitation experiments with anti-extracellular signal-regulated kinase 1 (ERK1) or anti-ERK2 antibodies followed by MBP kinase assays, and direct in-gel kinase assays for MBP, show that p44/ERK1 but not p42/ERK2 is stimulated in OA-treated spermatocytes. OA treatment stimulates phosphorylation of ERK1, but not of ERK2, on a tyrosine residue involved in activation of the enzyme. ERK1 immunoprecipitated from extracts of OA-stimulated spermatocytes induces a stimulation of H1 kinase activity in extracts from control pachytene spermatocytes, whereas immunoprecipitated ERK2 is uneffective. We also show that natural G(2)/M transition in spermatocytes is associated to intracellular redistribution of ERKs, and their association with microtubules of the metaphase spindle. Preincubation of cultured pachytene spermatocytes with PD98059 (a selective inhibitor of ERK-activating kinases MEK1/2) completely blocks the ability of OA to induce chromosome condensation and progression to meiotic metaphases. These results suggest that ERK1 is specifically activated during G(2)/M transition in mouse spermatocytes, that it contributes to the mechanisms of maturation promoting factor activation, and that it is essential for chromosome condensation associated with progression to meiotic metaphases.