Thermal regime of the Southeast Indian Ridge between 88°E and 140°E: Remarks on the subsidence of the ridge flanks

International audienceThe flanks of the Southeast Indian Ridge are characterized by anomalously low subsidence rates for the 0–25 Ma period: less than 300 m Ma−1/2 between 101°E and 120°E and less than 260 m Ma−1/2 within the Australian-Antarctic Discordance (AAD), between 120°E and 128°E. The expected along-axis variation in mantle temperature (∼50°C) is too small to explain this observation, even when the temperature dependence of the mantle physical properties is accounted for. We successively analyze the effect on subsidence of different factors, such as variations in crustal thickness; the dynamic contribution of an old, detached slab supposedly present within the mantle below the AAD; and depletion in ϕ m, a parameter here defined as the “ubiquitously distributed melt fraction” within the asthenosphere. These effects may all contribute to the observed, anomalously low subsidence rate of the ridge flanks, with the most significant contribution being probably related to the depletion in ϕ m. However, these effects have a deep-seated origin that cannot explain the abruptness of the transition across the fracture zones that delineate the boundaries of the AAD, near 120°E and near 128°E, respectively

Chromatin assembly factor-1 preserves genome stability in ctf4∆ cells by promoting sister chromatid cohesion

Chromatin assembly and the establishment of sister chromatid cohesion are intimately connected to the progression of DNA replication forks. Here we examined the genetic interaction between the heterotrimeric chromatin assembly factor-1 (CAF-1), a central component of chromatin assembly during replication, and the core replisome component Ctf4. We find that CAF-1 deficient cells as well as cells affected in newly-synthesized H3-H4 histones deposition during DNA rep-lication exhibit a severe negative growth with ctf4∆ mutant. We dissected the role of CAF-1 in the maintenance of genome stability in ctf4∆ yeast cells. In the absence of CTF4, CAF-1 is essential for viability in cells experiencing replication problems, in cells lacking functional S-phase checkpoint or functional spindle checkpoint, and in cells lacking DNA repair pathways involving homologous recombination. We present evidence that CAF-1 affects cohesin association to chromatin in a DNA-damage-dependent manner and is essential to maintain cohesion in the absence of CTF4. We also show that Eco1-catalyzed Smc3 acetylation is reduced in absence of CAF-1. Furthermore, we describe genetic interactions between CAF-1 and essential genes involved in cohesin loading, cohesin stabilization, and cohesin component indicating that CAF-1 is crucial for viability when sister chromatid cohesion is affected. Finally, our data indicate that the CAF-1-dependent pathway required for cohesion is functionally distinct from the Rtt101-Mms1-Mms22 pathway which functions in replicated chromatin assembly. Collectively, our results suggest that the deposition by CAF-1 of newly-synthesized H3-H4 histones during DNA replication creates a chromatin environment that favors sister chromatid cohesion and maintains genome integrity

Evidence for sinistral strike-slip deformation in the Solomon Island arc

6 pages, 4 figuresDuring the SOPACMAPS 2 crusie carried out by IFREMER (Institut Français de Recherche pour l'Exploitation de la Mer) and ORSTOM (Institut Français de Recherche Scientifique pour le dévelopement en Coopération) on theR/V L'Atalante, in the Central Solomon Arc area, multibeam bathymetric and imagery data and single-channel seismic reflection profiles were collected from an area of about 3500 km2, to evaluate regional tectonics. Structural data geophysical profiles interpretation provide evidence for left-lateral transtensional tectonics on the southern edge of the Central Solomon Trough. This transtensional deformation is represented by faulting, block tilting, and rhombohedral deformation. The regional geology and the analysis of the sedimentary cover allow us to demonstrate that this tectonic occurred in two different phases during Oligocene to Miocene and Pliocene to Pleistocene timesPeer reviewe

Protein interactions within the Set1 complex and their roles in the regulation of histone 3 lysine 4 methylation

Set1 is the catalytic subunit and the central component of the evolutionarily conserved Set1 complex (Set1C) that methylates histone 3 lysine 4 (H3K4). Here we have determined protein/protein interactions within the complex and related the substructure to function. The loss of individual Set1C subunits differentially affects Set1 stability, complex integrity, global H3K4 methylation, and distribution of H3K4 methylation along active genes. The complex requires Set1, Swd1, and Swd3 for integrity, and Set1 amount is greatly reduced in the absence of the Swd1-Swd3 heterodimer. Bre2 and Sdc1 also form a heteromeric subunit, which requires the SET domain for interaction with the complex, and Sdc1 strongly interacts with itself. Inactivation of either Bre2 or Sdc1 has very similar effects. Neither is required for complex integrity, and their removal results in an increase of H3K4 mono- and dimethylation and a severe decrease of trimethylation at the 5′ end of active coding regions but a decrease of H3K4 dimethylation at the 3′ end of coding regions. Cells lacking Spp1 have a reduced amount of Set1 and retain a fraction of trimethylated H3K4, whereas cells lacking Shg1 show slightly elevated levels of both di- and trimethylation. Set1C associates with both serine 5- and serine 2-phosphorylated forms of polymerase II, indicating that the association persists to the 3′ end of transcribed genes. Taken together, our results suggest that Set1C subunits stimulate Set1 catalytic activity all along active genes.Acciones Integradas Hispano-Francesas HF2003-0170Ministerio de Educación y Ciencia BFU2005-02603Ministerio de Ciencia y Tecnología BMC2003- 07072-C03-0

Two distinct repressive mechanisms for histone 3 lysine 4 methylation through promoting 3'-end antisense transcription

International audienceHistone H3 di- and trimethylation on lysine 4 are major chromatin marks that correlate with active transcription. The influence of these modifications on transcription itself is, however, poorly understood. We have investigated the roles of H3K4 methylation in Saccharomyces cerevisiae by determining genome-wide expression-profiles of mutants in the Set1 complex, COMPASS, that lays down these marks. Loss of H3K4 trimethylation has virtually no effect on steady-state or dynamically-changing mRNA levels. Combined loss of H3K4 tri- and dimethylation results in steady-state mRNA upregulation and delays in the repression kinetics of specific groups of genes. COMPASS-repressed genes have distinct H3K4 methylation patterns, with enrichment of H3K4me3 at the 3'-end, indicating that repression is coupled to 3'-end antisense transcription. Further analyses reveal that repression is mediated by H3K4me3-dependent 3'-end antisense transcription in two ways. For a small group of genes including PHO84, repression is mediated by a previously reported trans-effect that requires the antisense transcript itself. For the majority of COMPASS-repressed genes, however, it is the process of 3'-end antisense transcription itself that is the important factor for repression. Strand-specific qPCR analyses of various mutants indicate that this more prevalent mechanism of COMPASS-mediated repression requires H3K4me3-dependent 3'-end antisense transcription to lay down H3K4me2, which seems to serve as the actual repressive mark. Removal of the 3'-end antisense promoter also results in derepression of sense transcription and renders sense transcription insensitive to the additional loss of SET1. The derepression observed in COMPASS mutants is mimicked by reduction of global histone H3 and H4 levels, suggesting that the H3K4me2 repressive effect is linked to establishment of a repressive chromatin structure. These results indicate that in S. cerevisiae, the non-redundant role of H3K4 methylation by Set1 is repression, achieved through promotion of 3'-end antisense transcription to achieve specific rather than global effects through two distinct mechanisms

Gas emissions and active tectonics within the submerged section of the North Anatolian Fault zone in the Sea of Marmara

The submerged section of the North Anatolian fault within the Marmara Sea was investigated using acoustic techniques and submersible dives. Most gas emissions in the water column were found near the surface expression of known active faults. Gas emissions are unevenly distributed. The linear fault segment crossing the Central High and forming a seismic gap – as it has not ruptured since 1766, based on historical seismicity, exhibits relatively less gas emissions than the adjacent segments. In the eastern Sea of Marmara, active gas emissions are also found above a buried transtensional fault zone, which displayed micro-seismic activity after the 1999 events. Remarkably, this zone of gas emission extends westward all along the southern edge of Cinarcik basin, well beyond the zone where 1999 aftershocks were observed. The long term monitoring of gas seeps could hence be highly valuable for the understanding of the evolution of the fluid-fault coupling processes during the earthquake cycle within the Marmara Sea

Seismic precursors linked to super-critical fluids at oceanic transform faults

Large earthquakes on mid-ocean ridge transform faults are commonly preceded by foreshocks[superscript 1–3] and changes in the seismic properties of the fault zone³. These seismic precursors could be linked to fluid-related processes[superscript 2,3]. Hydrothermal fluids within young, hot crust near the intersection of oceanic transform faults are probably in a supercritical condition⁴. At constant temperature, supercritical fluids become significantly more compressible with decreasing pressure, with potential impacts on fault behaviour. Here we use a theoretical model to show that oceanic transform faults can switch from dilatant and progressive deformation to rupture in response to fluid-related processes. We assume that the fault core material behaves according to a Cam-clay-type⁵ constitutive law, which is commonly used to account for the behaviour of clays. According to our model, we find that the fault is initially stable, with stresses gradually increasing over a timescale of years in response to tectonic loading. The fault evolves into a metastable phase, lasting a few days, during which the fault rocks dilate and pore pressures decrease, causing the compressibility of the supercritical fluids to increase. This in turn triggers fault-slip instability that creates foreshock swarms. In the final phase, the fault fails in the mainshock rupture. Our results imply that seismic precursors are caused by changes in fluid pressure which result in variations in fluid compressibility, in response to rock deformation just before rupture