Small Shelly Fossil Preservation and the Role of Early Diagenetic Redox in the Early Triassic

Minute fossils from a variety of different metazoan clades, collectively referred to as small shelly fossils, represent a distinctive taphonomic mode that is most commonly reported from the Cambrian Period. Lower Triassic successions of the western United States, deposited in the aftermath of the end-Permian mass extinction, provide an example of small shelly style preservation that significantly post-dates Cambrian occurrences. Glauconitized and phosphatized echinoderms and gastropods are preserved in the insoluble residues of carbonates from the Virgin Limestone Member of the Moenkopi Formation. Echinoderm plates, spines and other skeletal elements are preserved as stereomic molds; gastropods are preserved as steinkerns. All small shelly style fossils are preserved in the small size fractions of the residues (177 to 420 lm), which is consistent with the size selection of small shelly fossils in the Cambrian. Energy-dispersive X-ray spectra of individual fossils coupled with X-ray diffraction of residues confirm that the fossils are dominantly preserved by apatite and glauconite, and sometimes a combination of the two minerals. The nucleation of both of these minerals requires that pore water redox oscillated between oxic and anoxic conditions, which, in turn, implies that Lower Triassic carbonates periodically experienced oxygen depletion after deposition and during early diagenesis. Long-term oxygen depletion persisted through the Early Triassic, creating diagenetic conditions that were instrumental in the preservation of small shelly fossils in Triassic and, likely, Paleozoic examples

The conflict-free Reduction Geometry

AbstractWe investigate mutual dependencies of subexpressions of computable expressions in orthogonal rewrite systems, and identify conditions for their independent concurrent computation. To this end, we introduce concepts familiar from ordinary Euclidean Geometry (such as basis, projection, distance, etc.) for reduction spaces. We show how a basis at an expression can be constructed so that any reduction starting from that expression can be decomposed as the sum of its projections on the axes of the basis. To make the concepts computationally more relevant, we relativize them w.r.t. stable sets of results (such as the set of normal forms, head-normal forms, and weak-head-normal forms, in the λ-calculus), and show that an optimal concurrent computation of an expression w.r.t. S consists of optimal computations of its S-independent subexpressions. All these results are obtained in the framework of Deterministic Family Structures, which are Abstract Reduction Systems with axiomatized residual and family relations on redexes, that model all orthogonal rewrite systems

Recql5 Plays an Important Role in DNA Replication and Cell Survival after Camptothecin Treatment

Disruption of replication can lead to loss of genome integrity and increase of cancer susceptibility in mammals. Thus, a replication impediment constitutes a formidable challenge to these organisms. Recent studies indicate that homologous recombination (HR) plays an important role in suppressing genome instability and promoting cell survival after exposure to various replication inhibitors, including a topoisomerase I inhibitor, camptothecin (CPT). Here, we report that the deletion of RecQ helicase Recql5 in mouse ES cells and embryonic fibroblast (MEF) cells resulted in a significant increase in CPT sensitivity and a profound reduction in DNA replication after the treatment with CPT, but not other DNA-damaging agents. This CPT-induced cell death is replication dependent and occurs primarily after the cells had exited the first cell cycle after CPT treatment. Furthermore, we show that Recql5 functions nonredundantly with Rad51, a key factor for HR to protect mouse ES cells from CPT-induced cytotoxicity. These new findings strongly suggest that Recql5 plays an important role in maintaining active DNA replication to prevent the collapse of replication forks and the accumulation of DSBs in order to preserve genome integrity and to prevent cell death after replication stress as a result of topoisomerase I poisoning