The Effect of Structural Complexity, Prey Density, and “Predator-Free Space” on Prey Survivorship at Created Oyster Reef Mesocosms

Interactions between predators and their prey are influenced by the habitat they occupy. Using created oyster (Crassostrea virginica) reef mesocosms, we conducted a series of laboratory experiments that created structure and manipulated complexity as well as prey density and “predator-free space” to examine the relationship between structural complexity and prey survivorship. Specifically, volume and spatial arrangement of oysters as well as prey density were manipulated, and the survivorship of prey (grass shrimp, Palaemonetes pugio) in the presence of a predator (wild red drum, Sciaenops ocellatus) was quantified. We found that the presence of structure increased prey survivorship, and that increasing complexity of this structure further increased survivorship, but only to a point. This agrees with the theory that structural complexity may influence predator-prey dynamics, but that a threshold exists with diminishing returns. These results held true even when prey density was scaled to structural complexity, or the amount of “predator-free space” was manipulated within our created reef mesocosms. The presence of structure and its complexity (oyster shell volume) were more important in facilitating prey survivorship than perceived refugia or density-dependent prey effects. A more accurate indicator of refugia might require “predator-free space” measures that also account for the available area within the structure itself (i.e., volume) and not just on the surface of a structure. Creating experiments that better mimic natural conditions and test a wider range of “predator-free space” are suggested to better understand the role of structural complexity in oyster reefs and other complex habitats

Occupying Cave-Sites: A Case Study from Azokh 1 Cave (Southern Caucasus)

peer reviewedThe Caucasus is an important intercontinental passageway for fauna and hominin dispersal from Africa to Eurasia. Numerous Pleistocene sites emphasise the importance of this region for the study of human evolution and hominin ‘Out of Africa’ dispersals. The Azokh 1 site in the Southern Caucasus provides a stratigraphic sequence, the renewed excavations of which have shown the presence of well-contextualised lithic and faunal assemblages dated between 300 and 100 ka associated with hominin remains (Homo heidelbergensis and Homo neanderthalensis) also found in the site. Faunal assemblages are dominated by cave bear (Ursus spelaeus) remains resulting from their hibernation at the rear of the cave. Recent taphonomic studies indicate the in-situ exploitation of some of these remains. Other faunal remains, mainly herbivore, some showing signs of human activity, were most likely introduced into the cave by hominins. The study of lithic artefacts suggests an incomplete operative chain for all raw materials with a general absence of knapping debris, unknapped cobbles/pebbles, rare cores and refits. Techno-typologically, these assemblages display characteristics that link them to Late Acheulean or Early Mousterian and Levallois Mousterian traditions. The faunal and lithic assemblages originate from the rear of the cave. Research results, including some preliminary data on lithic use-wear, along with analyses of spatial distribution and post-depositional modification, indicate that occupation of the cave was short and seasonal in character. Cave bears were an important factor affecting the duration of hominin occupation of the cave. The characteristics of the lithic assemblages suggest mobile toolkits, with some isolated evidence of in situ knapping and retouching activities

Defining the Functional Domain of Programmed Cell Death 10 through Its Interactions with Phosphatidylinositol-3,4,5-Trisphosphate

Cerebral cavernous malformations (CCM) are vascular abnormalities of the central nervous system predisposing blood vessels to leakage, leading to hemorrhagic stroke. Three genes, Krit1 (CCM1), OSM (CCM2), and PDCD10 (CCM3) are involved in CCM development. PDCD10 binds specifically to PtdIns(3,4,5)P3 and OSM. Using threading analysis and multi-template modeling, we constructed a three-dimensional model of PDCD10. PDCD10 appears to be a six-helical-bundle protein formed by two heptad-repeat-hairpin structures (α1–3 and α4–6) sharing the closest 3D homology with the bacterial phosphate transporter, PhoU. We identified a stretch of five lysines forming an amphipathic helix, a potential PtdIns(3,4,5)P3 binding site, in the α5 helix. We generated a recombinant wild-type (WT) and three PDCD10 mutants that have two (Δ2KA), three (Δ3KA), and five (Δ5KA) K to A mutations. Δ2KA and Δ3KA mutants hypothetically lack binding residues to PtdIns(3,4,5)P3 at the beginning and the end of predicted helix, while Δ5KA completely lacks all predicted binding residues. The WT, Δ2KA, and Δ3KA mutants maintain their binding to PtdIns(3,4,5)P3. Only the Δ5KA abolishes binding to PtdIns(3,4,5)P3. Both Δ5KA and WT show similar secondary and tertiary structures; however, Δ5KA does not bind to OSM. When WT and Δ5KA are co-expressed with membrane-bound constitutively-active PI3 kinase (p110-CAAX), the majority of the WT is co-localized with p110-CAAX at the plasma membrane where PtdIns(3,4,5)P3 is presumably abundant. In contrast, the Δ5KA remains in the cytoplasm and is not present in the plasma membrane. Combining computational modeling and biological data, we propose that the CCM protein complex functions in the PI3K signaling pathway through the interaction between PDCD10 and PtdIns(3,4,5)P3

Two million years of flaking stone and the evolutionary efficiency of stone tool technology

Temporal variability in flaking stone has been used as one of the currencies for hominin behavioural and biological evolution. This variability is usually traced through changes in artefact forms and techniques of production, resulting overall in unilineal and normative models of hominin adaptation. Here, we focus on the fundamental purpose of flaking stone—the production of a sharp working edge—and model this behaviour over evolutionary time to reassess the evolutionary efficiency of stone tool technology. Using more than 19,000 flakes from 81 assemblages spanning two million years, we show that greater production of sharp edges was followed by increased variability in this behaviour. We propose that a diachronic increase in this variability was related to a higher intensity of interrelations between different behaviours involving the use and management of stone resources that gave fitness advantages in particular environmental contexts. The long-term trends identified in this study inform us that the evolutionary efficiency of stone tool technology was not inherently in advanced tool forms and production techniques, but emerged within the contingencies of hominin interaction with local environments

Experimental Design and Experimental Inference in Stone Artifact Archaeology

Lithic researchers rely heavily on experimentation to infer past behaviors and activities based on stone artifacts. This paper explores the analogical nature of archaeological inference and the relationship between experimental design and inference validity in stone artifact experimentation. We show that actualistic flintknapping lacks vital aspects of scientific experimentation, and thus has inherent inferential issues of analogical adequacy and confidence. It is argued that a greater emphasis on hypothesis construction and variable control is needed in order to establish sound referential linkages upon which constructive analogic inferences about the past can be built

Systems biology and proteomic analysis of cerebral cavernous malformation

Cerebral cavernous malformations (CCM) are vascular anomalies caused by mutations in genes encoding KRIT1, OSM and PDCD10 proteins causing hemorrhagic stroke. We examine proteomic change of loss of CCM gene expression. Using human umbilical vein endothelial cells, label-free differential protein expression analysis with multidimensional liquid chromatography/tandem mass spectrometry was applied to three CCM protein knockdown cell lines and two control cell lines: ProteomeXchange identifier PXD000362. Principle component and cluster analyses were used to examine the differentially expressed proteins associated with CCM. The results from the five cell lines revealed 290 and 192 differentially expressed proteins (p < 0.005 and p < 0.001, respectively). Most commonly affected proteins were cytoskeleton-associated proteins, in particular myosin-9. Canonical genetic pathway analysis suggests that CCM may be a result of defective cell–cell interaction through dysregulation of cytoskeletal associated proteins. CONCLUSION: The work explores signaling pathways that may elucidate early detection and novel therapy for CCM