X-ray Fluorescence and Neutron Activation Analysis of Obsidian from the Red Sea Coast of Eritrea

The strategic location of Eritrea along the Red Sea coast and the Horn of Africa makes it an important place to study human prehistory over a long span of time. However, recurrent political instability and the environmental adversity in the region have hindered comprehensive archaeological investigation. Paleolithic research in Eritrea began after the country obtained independence from Ethiopia in 1991. Geological survey in the Abdur area, along the Gulf of Zula coast (Figure 1), identified Paleolithic artifacts embedded in reef limestone dating to ~ 125 Ka BP (Walter et al., 2000). Based on this evidence, human coastal adaptation during the Late Pleistocene has been proposed. To explore the archaeological potential of the region, surveys and excavations were recently initiated along the Gulf of Zula and Buri Peninsula portions of the Red Sea coast. The survey documented a series of prehistoric sites from coastal and inland contexts featuring Acheulian, Middle Stone Age (MSA) and Later Stone Age (LSA) artifacts (Beyin and Shea, 2007). The Acheulian and MSA Lithic assemblages include highly deflated surface scatters of handaxes, prepared core products and retouched points made on locally available materials such as basalt, shale, and rhyolite. These assemblages however, lack secured stratigraphic contexts and obtaining radiometric dating is problematical. Excavations at three sites, Asfet, Misse East and Gelalo NW (Figure 1) in 2006 produced archaeological deposits of LSA affinity with mollusk shell association. A large quantity of debitage, blades, bladelets, backed tools and microliths characterize the lithic artifacts. A few of the artifacts are shown in Figure 2. The LSA bearing archaeological strata have been dated to the Early Holocene by 14C (AMS)

The Otterbein Miscellany - June 1984

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Self-oligomerization regulates stability of survival motor neuron protein isoforms by sequestering an SCF^Slmb degron

Spinal muscular atrophy (SMA) is caused by homozygous mutations in human SMN1. Expression of a duplicate gene (SMN2) primarily results in skipping of exon 7 and production of an unstable protein isoform, SMNΔ7. Although SMN2 exon skipping is the principal contributor to SMA severity, mechanisms governing stability of survival motor neuron (SMN) isoforms are poorly understood. We used a Drosophila model system and label-free proteomics to identify the SCFSlmb ubiquitin E3 ligase complex as a novel SMN binding partner. SCFSlmb interacts with a phosphor degron embedded within the human and fruitfly SMN YG-box oligomerization domains. Substitution of a conserved serine (S270A) interferes with SCFSlmb binding and stabilizes SMNΔ7. SMA-causing missense mutations that block multimerization of full-length SMN are also stabilized in the degron mutant background. Overexpression of SMNΔ7S270A, but not wild-type (WT) SMNΔ7, provides a protective effect in SMA model mice and human motor neuron cell culture systems. Our findings support a model wherein the degron is exposed when SMN is monomeric and sequestered when SMN forms higher-order multimers