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  • 1
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    Catastrophic flood of the Mediterranean after the Messinian salinity crisis (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-12-17
    Description: The Mediterranean Sea became disconnected from the world's oceans and mostly desiccated by evaporation about 5.6 million years ago during the Messinian salinity crisis. The Atlantic waters found a way through the present Gibraltar Strait and rapidly refilled the Mediterranean 5.33 million years ago in an event known as the Zanclean flood. The nature, abruptness and evolution of this flood remain poorly constrained. Borehole and seismic data show incisions over 250 m deep on both sides of the Gibraltar Strait that have previously been attributed to fluvial erosion during the desiccation. Here we show the continuity of this 200-km-long channel across the strait and explain its morphology as the result of erosion by the flooding waters, adopting an incision model validated in mountain rivers. This model in turn allows us to estimate the duration of the flood. Although the available data are limited, our findings suggest that the feedback between water flow and incision in the early stages of flooding imply discharges of about 10(8) m(3) s(-1) (three orders of magnitude larger than the present Amazon River) and incision rates above 0.4 m per day. Although the flood started at low water discharges that may have lasted for up to several thousand years, our results suggest that 90 per cent of the water was transferred in a short period ranging from a few months to two years. This extremely abrupt flood may have involved peak rates of sea level rise in the Mediterranean of more than ten metres per day.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia-Castellanos, D -- Estrada, F -- Jimenez-Munt, I -- Gorini, C -- Fernandez, M -- Verges, J -- De Vicente, R -- England -- Nature. 2009 Dec 10;462(7274):778-81. doi: 10.1038/nature08555.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Ciencies de la Terra Jaume Almera, CSIC, Sole i Sabaris s/n, Barcelona, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20010684" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Messinian salinity crisis regulated by competing tectonics and erosion at the Gibraltar arc (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-12-16
    Description: The Messinian salinity crisis (5.96 to 5.33 million years ago) was caused by reduced water inflow from the Atlantic Ocean to the Mediterranean Sea resulting in widespread salt precipitation and a decrease in Mediterranean sea level of about 1.5 kilometres due to evaporation. The reduced connectivity between the Atlantic and the Mediterranean at the time of the salinity crisis is thought to have resulted from tectonic uplift of the Gibraltar arc seaway and global sea-level changes, both of which control the inflow of water required to compensate for the hydrological deficit of the Mediterranean. However, the different timescales on which tectonic uplift and changes in sea level occur are difficult to reconcile with the long duration of the shallow connection between the Mediterranean and the Atlantic needed to explain the large amount of salt precipitated. Here we use numerical modelling to show that seaway erosion caused by the Atlantic inflow could sustain such a shallow connection between the Atlantic and the Mediterranean by counteracting tectonic uplift. The erosion and uplift rates required are consistent with previous mountain erosion studies, with the present altitude of marine sediments in the Gibraltar arc and with geodynamic models suggesting a lithospheric slab tear underneath the region. The moderate Mediterranean sea-level drawdown during the early stages of the Messinian salinity crisis can be explained by an uplift of a few millimetres per year counteracted by similar rates of erosion due to Atlantic inflow. Our findings suggest that the competition between uplift and erosion can result in harmonic coupling between erosion and the Mediterranean sea level, providing an alternative mechanism for the cyclicity observed in early salt precipitation deposits and calling into question previous ideas regarding the timing of the events that occurred during the Messinian salinity crisis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garcia-Castellanos, D -- Villasenor, A -- England -- Nature. 2011 Dec 14;480(7377):359-63. doi: 10.1038/nature10651.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Ciencias de la Tierra Jaume Almera, CSIC, Sole i Sabaris s/n, 08028 Barcelona, Spain. danielgc@ictja.csic.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22170684" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Endophilin-A2 functions in membrane scission in clathrin-independent endocytosis (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-18
    Description: During endocytosis, energy is invested to narrow the necks of cargo-containing plasma membrane invaginations to radii at which the opposing segments spontaneously coalesce, thereby leading to the detachment by scission of endocytic uptake carriers. In the clathrin pathway, dynamin uses mechanical energy from GTP hydrolysis to this effect, assisted by the BIN/amphiphysin/Rvs (BAR) domain-containing protein endophilin. Clathrin-independent endocytic events are often less reliant on dynamin, and whether in these cases BAR domain proteins such as endophilin contribute to scission has remained unexplored. Here we show, in human and other mammalian cell lines, that endophilin-A2 (endoA2) specifically and functionally associates with very early uptake structures that are induced by the bacterial Shiga and cholera toxins, which are both clathrin-independent endocytic cargoes. In controlled in vitro systems, endoA2 reshapes membranes before scission. Furthermore, we demonstrate that endoA2, dynamin and actin contribute in parallel to the scission of Shiga-toxin-induced tubules. Our results establish a novel function of endoA2 in clathrin-independent endocytosis. They document that distinct scission factors operate in an additive manner, and predict that specificity within a given uptake process arises from defined combinations of universal modules. Our findings highlight a previously unnoticed link between membrane scaffolding by endoA2 and pulling-force-driven dynamic scission.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342003/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342003/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Renard, Henri-Francois -- Simunovic, Mijo -- Lemiere, Joel -- Boucrot, Emmanuel -- Garcia-Castillo, Maria Daniela -- Arumugam, Senthil -- Chambon, Valerie -- Lamaze, Christophe -- Wunder, Christian -- Kenworthy, Anne K -- Schmidt, Anne A -- McMahon, Harvey T -- Sykes, Cecile -- Bassereau, Patricia -- Johannes, Ludger -- R01 GM106720/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Jan 22;517(7535):493-6. doi: 10.1038/nature14064. Epub 2014 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institut Curie - Centre de Recherche, Endocytic Trafficking and Therapeutic Delivery group, 26 rue d'Ulm, 75248 Paris Cedex 05, France [2] CNRS UMR3666, 75005 Paris, France [3] U1143 INSERM, 75005 Paris, France. ; 1] Institut Curie - Centre de Recherche, Membrane and Cell Functions group, CNRS UMR 168, Physico-Chimie Curie, Universite Pierre et Marie Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France [2] The University of Chicago, Department of Chemistry, 5735 S Ellis Ave, Chicago, Ilinois 60637, USA. ; 1] Institut Curie - Centre de Recherche, Biomimetism of Cell Movement group, CNRS UMR 168, Physico-Chimie Curie, Universite Pierre et Marie Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France [2] Universite Paris Diderot, Sorbonne Paris Cite, 75205 Paris, France. ; Institute of Structural and Molecular Biology, University College London &Birkbeck College, London WC1E 6BT, UK. ; 1] CNRS UMR3666, 75005 Paris, France [2] U1143 INSERM, 75005 Paris, France [3] Institut Curie - Centre de Recherche, Membrane Dynamics and Mechanics of Intracellular Signaling group, 26 rue d'Ulm, 75248 Paris Cedex 05, France. ; Vanderbilt School of Medicine, Department of Molecular Physiology and Biophysics, 718 Light Hall, Nashville, Tennessee 37232, USA. ; CNRS, UMR7592, Institut Jacques Monod, Universite Paris Diderot, Sorbonne Paris Cite, 15 rue Helene Brion, 75205 Paris Cedex 13, France. ; Medical Research Council, Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge CB2 0QH, UK. ; Institut Curie - Centre de Recherche, Biomimetism of Cell Movement group, CNRS UMR 168, Physico-Chimie Curie, Universite Pierre et Marie Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France. ; Institut Curie - Centre de Recherche, Membrane and Cell Functions group, CNRS UMR 168, Physico-Chimie Curie, Universite Pierre et Marie Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25517096" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Acyltransferases/*metabolism ; Animals ; Cell Line ; Cell Membrane/*metabolism ; Cholera Toxin/metabolism ; Clathrin ; Dynamins/metabolism ; *Endocytosis ; Humans ; Rats ; Shiga Toxin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-08
    Description: Left ventricular mass (LVM) is a highly heritable trait and an independent risk factor for all-cause mortality. So far, genome-wide association studies have not identified the genetic factors that underlie LVM variation, and the regulatory mechanisms for blood-pressure-independent cardiac hypertrophy remain poorly understood. Unbiased systems genetics approaches in the rat now provide a powerful complementary tool to genome-wide association studies, and we applied integrative genomics to dissect a highly replicated, blood-pressure-independent LVM locus on rat chromosome 3p. Here we identified endonuclease G (Endog), which previously was implicated in apoptosis but not hypertrophy, as the gene at the locus, and we found a loss-of-function mutation in Endog that is associated with increased LVM and impaired cardiac function. Inhibition of Endog in cultured cardiomyocytes resulted in an increase in cell size and hypertrophic biomarkers in the absence of pro-hypertrophic stimulation. Genome-wide network analysis unexpectedly implicated ENDOG in fundamental mitochondrial processes that are unrelated to apoptosis. We showed direct regulation of ENDOG by ERR-alpha and PGC1alpha (which are master regulators of mitochondrial and cardiac function), interaction of ENDOG with the mitochondrial genome and ENDOG-mediated regulation of mitochondrial mass. At baseline, the Endog-deleted mouse heart had depleted mitochondria, mitochondrial dysfunction and elevated levels of reactive oxygen species, which were associated with enlarged and steatotic cardiomyocytes. Our study has further established the link between mitochondrial dysfunction, reactive oxygen species and heart disease and has uncovered a role for Endog in maladaptive cardiac hypertrophy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189541/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189541/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDermott-Roe, Chris -- Ye, Junmei -- Ahmed, Rizwan -- Sun, Xi-Ming -- Serafin, Anna -- Ware, James -- Bottolo, Leonardo -- Muckett, Phil -- Canas, Xavier -- Zhang, Jisheng -- Rowe, Glenn C -- Buchan, Rachel -- Lu, Han -- Braithwaite, Adam -- Mancini, Massimiliano -- Hauton, David -- Marti, Ramon -- Garcia-Arumi, Elena -- Hubner, Norbert -- Jacob, Howard -- Serikawa, Tadao -- Zidek, Vaclav -- Papousek, Frantisek -- Kolar, Frantisek -- Cardona, Maria -- Ruiz-Meana, Marisol -- Garcia-Dorado, David -- Comella, Joan X -- Felkin, Leanne E -- Barton, Paul J R -- Arany, Zoltan -- Pravenec, Michal -- Petretto, Enrico -- Sanchis, Daniel -- Cook, Stuart A -- 087183/Wellcome Trust/United Kingdom -- MC_U120085815/Medical Research Council/United Kingdom -- MC_U120097112/Medical Research Council/United Kingdom -- British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Oct 5;478(7367):114-8. doi: 10.1038/nature10490.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21979051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Body Weight/genetics ; Cardiomegaly/*enzymology/genetics/*pathology/physiopathology ; Cell Respiration ; Chromosomes, Mammalian/genetics ; Crosses, Genetic ; Endodeoxyribonucleases/deficiency/genetics/*metabolism ; Female ; Gene Expression Regulation ; Genes, Mitochondrial/genetics ; Hypertrophy, Left Ventricular/enzymology/genetics/pathology/physiopathology ; Lipid Metabolism ; Male ; Mitochondria/genetics/*metabolism/pathology ; Organ Size/genetics ; Quantitative Trait Loci/genetics ; RNA-Binding Proteins/metabolism ; Rats ; Rats, Inbred Strains ; Reactive Oxygen Species/metabolism ; Receptors, Estrogen/metabolism ; Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Pif1 family helicases suppress genome instability at G-quadruplex motifs (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-05-10
    Description: The Saccharomyces cerevisiae Pif1 helicase is the prototypical member of the Pif1 DNA helicase family, which is conserved from bacteria to humans. Here we show that exceptionally potent G-quadruplex unwinding is conserved among Pif1 helicases. Moreover, Pif1 helicases from organisms separated by more than 3 billion years of evolution suppressed DNA damage at G-quadruplex motifs in yeast. The G-quadruplex-induced damage generated in the absence of Pif1 helicases led to new genetic and epigenetic changes. Furthermore, when expressed in yeast, human PIF1 suppressed both G-quadruplex-associated DNA damage and telomere lengthening.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680789/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680789/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paeschke, Katrin -- Bochman, Matthew L -- Garcia, P Daniela -- Cejka, Petr -- Friedman, Katherine L -- Kowalczykowski, Stephen C -- Zakian, Virginia A -- R01 GM026938/GM/NIGMS NIH HHS/ -- R01 GM041347/GM/NIGMS NIH HHS/ -- R01 GM043265/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 May 23;497(7450):458-62. doi: 10.1038/nature12149. Epub 2013 May 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23657261" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Conserved Sequence ; DNA Damage/genetics ; DNA Helicases/deficiency/genetics/*metabolism ; Epigenesis, Genetic ; Evolution, Molecular ; *G-Quadruplexes ; Gene Silencing ; Genetic Complementation Test ; *Genomic Instability ; Humans ; Molecular Sequence Data ; Mutation Rate ; Saccharomyces cerevisiae/*genetics/*metabolism ; Saccharomyces cerevisiae Proteins/genetics ; Telomere Homeostasis/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Selective activation of p53-mediated tumour suppression in high-grade tumours (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-26
    Description: Non-small cell lung carcinoma (NSCLC) is the leading cause of cancer-related death worldwide, with an overall 5-year survival rate of only 10-15%. Deregulation of the Ras pathway is a frequent hallmark of NSCLC, often through mutations that directly activate Kras. p53 is also frequently inactivated in NSCLC and, because oncogenic Ras can be a potent trigger of p53 (ref. 3), it seems likely that oncogenic Ras signalling has a major and persistent role in driving the selection against p53. Hence, pharmacological restoration of p53 is an appealing therapeutic strategy for treating this disease. Here we model the probable therapeutic impact of p53 restoration in a spontaneously evolving mouse model of NSCLC initiated by sporadic oncogenic activation of endogenous Kras. Surprisingly, p53 restoration failed to induce significant regression of established tumours, although it did result in a significant decrease in the relative proportion of high-grade tumours. This is due to selective activation of p53 only in the more aggressive tumour cells within each tumour. Such selective activation of p53 correlates with marked upregulation in Ras signal intensity and induction of the oncogenic signalling sensor p19(ARF)( )(ref. 6). Our data indicate that p53-mediated tumour suppression is triggered only when oncogenic Ras signal flux exceeds a critical threshold. Importantly, the failure of low-level oncogenic Kras to engage p53 reveals inherent limits in the capacity of p53 to restrain early tumour evolution and in the efficacy of therapeutic p53 restoration to eradicate cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3011233/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3011233/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Junttila, Melissa R -- Karnezis, Anthony N -- Garcia, Daniel -- Madriles, Francesc -- Kortlever, Roderik M -- Rostker, Fanya -- Brown Swigart, Lamorna -- Pham, David M -- Seo, Youngho -- Evan, Gerard I -- Martins, Carla P -- CA100193/CA/NCI NIH HHS/ -- CA98018/CA/NCI NIH HHS/ -- R01 CA100193/CA/NCI NIH HHS/ -- R01 CA100193-09/CA/NCI NIH HHS/ -- England -- Nature. 2010 Nov 25;468(7323):567-71. doi: 10.1038/nature09526.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California San Francisco, Department of Pathology and Helen Diller Family Comprehensive Cancer Center, San Francisco, California 94143-0502, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107427" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Non-Small-Cell Lung/metabolism/*physiopathology ; Cell Proliferation ; Disease Models, Animal ; *Gene Expression Regulation, Neoplastic ; Lung Neoplasms/metabolism/*physiopathology ; Mice ; Proto-Oncogene Proteins p21(ras)/metabolism ; Tumor Suppressor Protein p53/genetics/*metabolism ; ras Proteins/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Burial Diagenesis of the Eocene Sobrarbe Delta (Ainsa Basin, Spain) Inferred From Dolomitic Concretions (2015)
    Society for Sedimentary Geology (SEPM)
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    Publication Date: 2015-09-26
    Description: :  Little attention has been focused on the burial diagenesis of deltas deposited on active foreland-basin margins, where tectonics is likely to strongly impact fluid–rock interactions. A petrographic, geochemical, and microthermometric study of several fractured dolomite concretions and enclosing prodelta marls provides insights into the evolution of burial diagenesis in the Eocene Sobrarbe deltaic complex (Ainsa Basin, Spain), and more generally, on the paleohydrology of the South Pyrenean foreland basin. Shallow burial diagenesis was controlled by microbial activity in marine-derived porewaters. Microbial sulfate reduction was first responsible for the formation of pyrite and early calcite, followed by the growth of dolomite concretions during methanogenesis. Subsequent diagenesis was limited to temperatures and depth of less than approximately 75°C and 2 km, respectively. Diagenesis was recorded in porous bioturbation traces and septarian fractures found inside dolomite concretions, as well as in tectonic shear fractures. Neomorphic tabular barite, found only in the bioturbation traces, is interpreted to have formed early in marine-derived porewaters. Septarian fractures were then filled by Fe-rich calcite and centimeter-size celestine. Stable isotopes indicate that calcite probably formed in meteoric-derived waters coming from the overlying fluvial delta plain. The sulfur isotope composition of celestine is compatible with precipitation in waters of mixed parentage, but the exact origin of dissolved sulfate remains poorly constrained. In tectonic fractures, celestine precipitated coevally with calcite displaying evidence of strong fluid–rock interaction. Dissolved sulfate may have migrated to the fractures during active tectonics from the late Eocene to the Oligocene. The paragenesis and the proposed paleohydrologic model are similar to those previously described for other deltaic systems deposited in active foreland basins, including the South Pyrenean foreland basin. These features point to common diagenetic processes in syntectonic foreland-basin deltas, involving both meteoric and marine fluid sources. Similar to passive margin settings, early diagenesis appears to be controlled mainly by relative variations of sea level, whereas during further burial, the development of permeable tectonic fractures is likely to facilitate the influx of basinal or continental waters into fine slope deposits, impacting the diagenetic record. These results emphasize the importance of fracture development in the fluid-flow regime of syntectonic foreland-basin deltas. They demonstrate the necessity to take this parameter into account in fluid-flow modeling of foreland-basin margins.
    Print ISSN: 1527-1404
    Topics: Geosciences
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