In This Issue
ANTHROPOLOGY
Oldest human decorations
Besides anatomical differences, cultural innovations have also played a large role in human development. Abdeljalil Bouzouggar et al. have discovered relics of one of these innovations: human-made shell beads from Morocco that may be the oldest objects used purely as decoration or ornaments. The 82,000-year-old beads indicate that humans were making purely symbolic objects in Africa 40,000 years before they did in Europe. The authors discovered the shells at the Grotte des Pigeons at Taforalt, a cave site in eastern Morocco. A dozen of the shells were perforated in their centers, showed signs of being suspended or hung, and appeared to have been covered in red ochre, similar to other less well dated African beads. These symbolic, decorative objects are considered early signs of modern human behavior and material culture, which serve as markers of when and where major shifts in human behavior occurred. Similar beads have been found at sites from Algeria, Israel, and South Africa and are probably contemporaneous or slightly more recent than the beads found at Taforalt. The authors say that bead making in Africa was a widespread practice, which was spread between cultures of different stone technology by exchange or by long-distance social networks, at that time. — P.D.
Ancient shell beads from eastern Morocco.
“82,000-year-old shell beads from North Africa and implications for the origins of modern human behavior” by Abdeljalil Bouzouggar, Nick Barton, Marian Vanhaeren, Francesco d'Errico, Simon Collcutt, Tom Higham, Edward Hodge, Simon Parfitt, Edward Rhodes, Jean-Luc Schwenninger, Chris Stringer, Elaine Turner, Steven Ward, Abdelkrim Moutmir, and Abdelhamid Stambouli (see pages 9964–9969)
CELL BIOLOGY
Posttranscriptional regulation problems in fragile X
Fragile X syndrome, the leading heritable form of mental retardation, is mainly caused by a mutation in the FMR1 gene and the resulting loss of its encoded protein FMRP. Yinqun Huang and colleagues previously found that FMRP, which is highly expressed in the brain and testes and likely involved in brain development and synaptic plasticity, interacts with a nuclear mRNA export protein, NXF2, in mouse brain and testes. Meiqin Zhang et al. report additional functional characteristics of this interaction. The authors found that the ubiquitously expressed mRNA nuclear export factor NXF1, a close relative of NXF2, is a likely in vivo regulatory target of both FMRP and NXF2 in neurons. Expression of NXF2 destabilized NXF1 mRNA. This effect was abolished by reducing expression of FMRP, suggesting that FMRP and NXF2 together regulate the stability of NXF1 mRNA. Although numerous studies support the role of FMRP in mRNA transport and translation, this study establishes a third role of FMRP as an mRNA stability modulator. The findings may be crucial for understanding and ameliorating the pathogenesis of fragile X syndrome. — M.M.
Model for FMRP/NXF2-mediated gene expression.
“Fragile X mental retardation protein FMRP and the RNA export factor NXF2 associate with and destabilize Nxf1 mRNA in neuronal cells” by Meiqin Zhang, Qiaoqiao Wang, and Yingqun Huang (see pages 10057–10062)
GENETICS
Systematic mapping of genomic breakpoints
Mutations in single DNA nucleotides are one path by which microevolution may occur. Another path is copy number variation (CNV), in which genes are duplicated, often more than once, or deleted, wholly or partially. CNV is responsible for phenotypic variation in humans, but not much is known about the frequency of CNV occurrence or how it is inherited. Jan Korbel et al. report a systematic algorithm to identify DNA breakpoints, the locations at which whole or partial genes are copied or deleted when CNV occurs. “Break-Pointer” is an approach based on a Hidden Markov Model that combines DNA sequence information with hybridization data to narrow in on breakpoints in a subject's genome. The authors trained Break-Pointer using a small number of gold standards to establish parameters, before testing the system on chromosome 22 and the β-globin locus on chromosome 11, in which mutations can cause the blood disease β-thalassemia. In DNA from two healthy subjects and eight with genomic disorders, the authors were able to identify 232 putative CNVs, including two disease-associated deletions. The authors expect that training and refinement of the model will result in precise genome-wide mapping of breakpoints. — K.M.
Hidden Markov Model architecture and parameters.
“Systematic prediction and validation of breakpoints associated with copy-number variants in the human genome” by Jan O. Korbel, Alexander Eckehart Urban, Fabian Grubert, Jiang Du, Thomas E. Royce, Peter Starr, Guoneng Zhong, Beverly S. Emanuel, Sherman M. Weissman, Michael Snyder, and Mark B. Gerstein (see pages 10110–10115)
MICROBIOLOGY
Nitric oxide may decrease the severity of Escherichia coli infections
Enterohemorrhagic Escherichia coli (EHEC) is one of the most common causes of food-borne illness in North America and Europe. Infection occurs by ingesting contaminated meat, milk, or water. EHEC colonizes the large intestine and can induce symptoms that range from bloody diarrhea to life-threatening complications such as hemolytic–uremic syndrome (HUS) and renal failure. Marjolaine Vareille et al. have found that nitric oxide (NO) helps mitigate host/EHEC interactions, preventing HUS development. A key immunological messenger that causes vasodilation, NO inhibited the production of Shiga-toxin (Stx), the main EHEC virulence factor, which is encoded by a gene carried by a lambda bacteriophage. The signaling molecule suppressed the bacteria's SOS response, typically induced by DNA-damaging agents such as the antibiotic mitomycin C, and decreased Stx mRNA expression and Stx-phage release. NO worked regardless of whether it was chemically or cellularly derived. The authors suggest that agents that increase NO may protect individuals from developing hemolytic syndromes, limiting the severity of EHEC infection. — F.A.
Bacteriophage purified from EHEC culture supernatant.
“Nitric oxide inhibits Shiga-toxin synthesis by enterohemorrhagic Escherichia coli” by Marjolaine Vareille, Thibaut de Sablet, Thomas Hindré, Christine Martin, and Alain P. Gobert (see pages 10199–10204)
SUSTAINABILITY SCIENCE
Emissions accelerating faster than economy
Carbon dioxide released to the atmosphere is the main culprit in human-induced global warming. Typically, developed countries are identified as the main source of CO2 as a result of the burning of fossil fuels and other industrialized processes. An analysis by Michael Raupach et al. shows that developing countries are quickly catching up in CO2 emissions. The authors studied regional trends in emissions, energy use, and population and economic growth to determine patterns that affect CO2 emission and, ultimately, global warming. The analysis showed that, since 2000, CO2 emissions worldwide have increased more rapidly than predicted because emissions and energy use are growing faster than the gross domestic product (GDP) of many countries. No countries are decreasing their percentage of reliance on fossil carbon as an energy source. In addition, developing countries show significantly increased recent rates of growth in emissions. Developing economies, together forming 80% of the world's population, accounted for 73% of the global growth in emissions in 2004. However, these economies accounted for only 41% of emissions themselves and only 23% of emis-sions since the start of the Industrial Revolution around 1800. — T.H.D.
Fossil-fuel CO2 emissions (MtC y−1), for nine regions.
“Global and regional drivers of accelerating CO2 emissions” by Michael R. Raupach, Gregg Marland, Philippe Ciais, Corinne Le Quéré, Josep G. Canadell, Gernot Klepper, and Christopher B. Field (see pages 10288–10293)
