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June 12, 2007 ͉ vol. 104 ͉ no. 24 ͉ 9913–10294 In This Issue Proceedings of the National Academy ofPNAS Sciences of the United States of America www.pnas.org 9964 Oldest human decorations 10057 Posttranscriptional regulation problems in fragile X 10110 Systematic mapping of genomic breakpoints 10199 Nitric oxide may decrease the severity of Escherichia coli infections 10288 Emissions accelerating faster than economy ANTHROPOLOGY CELL BIOLOGY Oldest human decorations Posttranscriptional regulation problems Besides anatomical differences, cultural innovations have also in fragile X played a large role in human development. Abdeljalil Fragile X syndrome, the leading heritable form of mental retarda- Bouzouggar et al. have discovered relics of one of these inno- tion, is mainly caused by a mutation in the FMR1 gene and the vations: human-made shell beads from Morocco that may be resulting loss of its encoded protein FMRP. Yinqun Huang and the oldest objects used purely as decoration or ornaments. colleagues previously found that FMRP, which is highly expressed The 82,000-year-old beads in the brain and testes and likely involved in brain development indicate that humans were and synaptic plasticity, interacts with a nuclear mRNA export making purely symbolic ob- protein, NXF2, in mouse brain jects in Africa 40,000 years and testes. Meiqin Zhang et al. before they did in Europe. report additional functional The authors discovered the characteristics of this interac- shells at the Grotte des Pi- tion. The authors found that geons at Taforalt, a cave site the ubiquitously expressed in eastern Morocco. A dozen mRNA nuclear export factor Ancient shell beads from eastern of the shells were perforated NXF1, a close relative of Morocco. in their centers, showed signs NXF2, is a likely in vivo reg- of being suspended or hung, ulatory target of both FMRP and appeared to have been covered in red ochre, similar to and NXF2 in neurons. Expres- other less well dated African beads. These symbolic, decora- sion of NXF2 destabilized tive objects are considered early signs of modern human be- NXF1 mRNA. This effect was havior and material culture, which serve as markers of when abolished by reducing expres- and where major shifts in human behavior occurred. Similar sion of FMRP, suggesting that beads have been found at sites from Algeria, Israel, and FMRP and NXF2 together reg- South Africa and are probably contemporaneous or slightly ulate the stability of NXF1 more recent than the beads found at Taforalt. The authors mRNA. Although numerous Model for FMRP/NXF2-mediated say that bead making in Africa was a widespread practice, studies support the role of gene expression. which was spread between cultures of different stone technol- FMRP in mRNA transport and ogy by exchange or by long-distance social networks, at that translation, this study establishes a third role of FMRP as an time. — P.D. mRNA stability modulator. The findings may be crucial for understanding and ameliorating the pathogenesis of fragile X ‘‘82,000-year-old shell beads from North Africa and implications for syndrome. — M.M. the origins of modern human behavior’’ by Abdeljalil Bouzouggar, Nick Barton, Marian Vanhaeren, Francesco d’Errico, Simon Collcutt, ‘‘Fragile X mental retardation protein FMRP and the RNA export Tom Higham, Edward Hodge, Simon Parfitt, Edward Rhodes, Jean-Luc factor NXF2 associate with and destabilize Nxf1 mRNA in neuronal Schwenninger, Chris Stringer, Elaine Turner, Steven Ward, Abdelkrim cells’’ by Meiqin Zhang, Qiaoqiao Wang, and Yingqun Huang (see Moutmir, and Abdelhamid Stambouli (see pages 9964–9969) pages 10057–10062) www.pnas.org͞cgi͞doi͞10.1073͞iti2407104 PNAS ͉ June 12, 2007 ͉ vol. 104 ͉ no. 24 ͉ 9913–9914 Downloaded by guest on September 25, 2021 damaging agents such as the GENETICS antibiotic mitomycin C, and decreased Stx mRNA expres- Systematic mapping of genomic breakpoints sion and Stx-phage release. Mutations in single DNA nucleotides are one path by which NO worked regardless of microevolution may occur. Another path is copy number varia- whether it was chemically or tion (CNV), in which genes are duplicated, often more than cellularly derived. The authors once, or deleted, wholly or partially. CNV is responsible for suggest that agents that in- phenotypic variation in humans, but not much is known about crease NO may protect indi- the frequency of CNV occurrence or how it is inherited. Jan viduals from developing hemolytic syndromes, limiting Transition A Transition B Korbel et al. report a system- Bacteriophage purified from EHEC the severity of EHEC infec- culture supernatant. Duplication Normal Deletion atic algorithm to identify DNA breakpoints, the loca- tion. — F.A. Transition A’ Transition B’ tions at which whole or partial ‘‘Nitric oxide inhibits Shiga-toxin synthesis by enterohemorrhagic Hidden Markov Model architec- genes are copied or deleted Escherichia coli’’ by Marjolaine Vareille, Thibaut de Sablet, Thomas ture and parameters. when CNV occurs. ‘‘Break- Hindre´, Christine Martin, and Alain P. Gobert (see pages 10199– Pointer’’ is an approach based 10204) on a Hidden Markov Model that combines DNA sequence in- formation with hybridization data to narrow in on breakpoints SUSTAINABILITY SCIENCE in a subject’s genome. The authors trained Break-Pointer using a small number of gold standards to establish parameters, be- Emissions accelerating faster fore testing the system on chromosome 22 and the -globin lo- than economy cus on chromosome 11, in which mutations can cause the blood disease -thalassemia. In DNA from two healthy subjects and Carbon dioxide released to the atmosphere is the main culprit in human-induced global warming. Typically, developed coun- eight with genomic disorders, the authors were able to identify 8000 -1 tries are identified as the main CO Emissions (MtC y ) D3 232 putative CNVs, including two disease-associated deletions. 7000 2 D2 source of CO2 as a result of The authors expect that training and refinement of the model 6000 India will result in precise genome-wide mapping of breakpoints. — the burning of fossil fuels and 5000 China 4000 FSU other industrialized processes. D1 K.M. 3000 Japan An analysis by Michael Rau- 2000 EU ‘‘Systematic prediction and validation of breakpoints associated with 1000 pach et al. shows that develop- USA copy-number variants in the human genome’’ by Jan O. Korbel, 0 ing countries are quickly 2 8 0 2 4 90 92 94 96 9 9 9 9 99 00 00 00 Alexander Eckehart Urban, Fabian Grubert, Jiang Du, Thomas E. 1980 198 1984 1986 1988 1 1 1 1 1 2 2 2 catching up in CO2 emissions. Royce, Peter Starr, Guoneng Zhong, Beverly S. Emanuel, Sherman Ϫ1 The authors studied regional Fossil-fuel CO2 emissions (MtC y ), M. Weissman, Michael Snyder, and Mark B. Gerstein (see pages for nine regions. 10110–10115) trends in emissions, energy use, and population and eco- MICROBIOLOGY nomic 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 Nitric oxide may decrease the severity of than predicted because emissions and energy use are growing Escherichia coli infections faster than the gross domestic product (GDP) of many coun- Enterohemorrhagic Escherichia coli (EHEC) is one of the most tries. No countries are decreasing their percentage of reliance common causes of food-borne illness in North America and Eu- on fossil carbon as an energy source. In addition, developing rope. Infection occurs by ingesting contaminated meat, milk, or countries show significantly increased recent rates of growth in water. EHEC colonizes the large intestine and can induce emissions. Developing economies, together forming 80% of the symptoms that range from bloody diarrhea to life-threatening world’s population, accounted for 73% of the global growth in complications such as hemolytic–uremic syndrome (HUS) and emissions in 2004. However, these economies accounted for renal failure. Marjolaine Vareille et al. have found that nitric only 41% of emissions themselves and only 23% of emis- oxide (NO) helps mitigate host/EHEC interactions, preventing sions since the start of the Industrial Revolution around HUS development. A key immunological messenger that causes 1800. — T.H.D. vasodilation, NO inhibited the production of Shiga-toxin (Stx), ‘‘Global and regional drivers of accelerating CO2 emissions’’ by the main EHEC virulence factor, which is encoded by a gene Michael R. Raupach, Gregg Marland, Philippe Ciais, Corinne Le carried by a lambda bacteriophage. The signaling molecule sup- Que´re´, Josep G. Canadell, Gernot Klepper, and Christopher B. Field pressed the bacteria’s SOS response, typically induced by DNA- (see pages 10288–10293) 9914 ͉ www.pnas.org͞cgi͞doi͞10.1073͞iti2407104 Downloaded by guest on September 25, 2021.