Magma-maintained rift segmentation at continental rupture in the 2005 Afar dyking episode

Seafloor spreading centres show a regular along-axis segmentation thought to be produced by a segmented magma supply in the passively upwelling mantle. On the other hand, continental rifts are segmented by large offset normal faults, and many lack magmatism. It is unclear how, when and where the ubiquitous segmented melt zones are emplaced during the continental rupture process. Between 14 September and 4 October 2005, 163 earthquakes (magnitudes greater than 3.9) and a volcanic eruption occurred within the approximately 60-km-long Dabbahu magmatic segment of the Afar rift, a nascent seafloor spreading centre in stretched continental lithosphere. Here we present a three-dimensional deformation field for the Dabbahu rifting episode derived from satellite radar data, which shows that the entire segment ruptured, making it the largest to have occurred on land in the era of satellite geodesy. Simple elastic modelling shows that the magmatic segment opened by up to 8 m, yet seismic rupture can account for only 8 per cent of the observed deformation. Magma was injected along a dyke between depths of 2 and 9 km, corresponding to a total intrusion volume of approximately 2.5 km3. Much of the magma appears to have originated from shallow chambers beneath Dabbahu and Gabho volcanoes at the northern end of the segment, where an explosive fissural eruption occurred on 26 September 2005. Although comparable in magnitude to the ten year (1975-84) Krafla events in Iceland, seismic data suggest that most of the Dabbahu dyke intrusion occurred in less than a week. Thus, magma intrusion via dyking, rather than segmented normal faulting, maintains and probably initiated the along-axis segmentation along this sector of the Nubia-Arabia plate boundary.     

Lithium isotope evidence for subduction-enriched mantle in the source of mid-ocean-ridge basalts

'Recycled' crustal materials, returned from the Earth's surface to the mantle by subduction, have long been invoked to explain compositional heterogeneity in the upper mantle. Yet increasingly, problems have been noted with this model. The debate can be definitively addressed using stable isotope ratios, which should only significantly vary in primitive, mantle-derived materials as a consequence of recycling. Here we present data showing a notable range in lithium isotope ratios in basalts from the East Pacific Rise, which correlate with traditional indices of mantle heterogeneity (for example, 143Nd/144Nd ratios). Such co-variations of stable and radiogenic isotopes in melts from a normal ridge segment provide critical evidence for the importance of recycled material in generating chemical heterogeneity in the upper mantle. Contrary to many models, however, the elevated lithium isotope ratios of the 'enriched' East Pacific Rise lavas imply that subducted ocean crust is not the agent of enrichment. Instead, we suggest that fluid-modified mantle, which is enriched during residency in a subduction zone, is mixed back into the upper mantle to cause compositional variability.     

iASPP oncoprotein is a key inhibitor of p53 conserved from worm to human

We have previously shown that ASPP1 and ASPP2 are specific activators of p53; one mechanism by which wild-type p53 is tolerated in human breast carcinomas is through loss of ASPP activity. We have further shown that 53BP2, which corresponds to a C-terminal fragment of ASPP2, acts as a dominant negative inhibitor of p53 (ref. 1). Hence, an inhibitory form of ASPP resembling 53BP2 could allow cells to bypass the tumor-suppressor functions of p53 and the ASPP proteins. Here, we characterize such a protein, iASPP (inhibitory member of the ASPP family), encoded by PPP1R13L in humans and ape-1 in Caenorhabditis elegans. iASPP is an evolutionarily conserved inhibitor of p53; inhibition of iASPP by RNA-mediated interference or antisense RNA in C. elegans or human cells, respectively, induces p53-dependent apoptosis. Moreover, iASPP is an oncoprotein that cooperates with Ras, E1A and E7, but not mutant p53, to transform cells in vitro. Increased expression of iASPP also confers resistance to ultraviolet radiation and to cisplatin-induced apoptosis. iASPP expression is upregulated in human breast carcinomas expressing wild-type p53 and normal levels of ASPP. Inhibition of iASPP could provide an important new strategy for treating tumors expressing wild-type p53.     

UK pharmaceuticals: a matter of Life

A British anti-abortion organization, Life, has challenged the legality of an abortion clinic's prescribing of post-coital hormone treatment (PCHT), the so-called "morning-after pill." Life contends that, contrary to its classification by the Department of Health and Social Security, PCHT is an abortifacient rather than a contraceptive. Even if Life wins the case, successful prosecution of the abortion clinic appears unlikely because British law would require proof of intention to procure miscarriage.     

Structural basis for the regulated protease and chaperone function of DegP

All organisms have to monitor the folding state of cellular proteins precisely. The heat-shock protein DegP is a protein quality control factor in the bacterial envelope that is involved in eliminating misfolded proteins and in the biogenesis of outer-membrane proteins. Here we describe the molecular mechanisms underlying the regulated protease and chaperone function of DegP from Escherichia coli. We show that binding of misfolded proteins transforms hexameric DegP into large, catalytically active 12-meric and 24-meric multimers. A structural analysis of these particles revealed that DegP represents a protein packaging device whose central compartment is adaptable to the size and concentration of substrate. Moreover, the inner cavity serves antagonistic functions. Whereas the encapsulation of folded protomers of outer-membrane proteins is protective and might allow safe transit through the periplasm, misfolded proteins are eliminated in the molecular reaction chamber. Oligomer reassembly and concomitant activation on substrate binding may also be critical in regulating other HtrA proteases implicated in protein-folding diseases.     

The decline and fate of an iron-induced subarctic phytoplankton bloom

Iron supply has a key role in stimulating phytoplankton blooms in high-nitrate low-chlorophyll oceanic waters. However, the fate of the carbon fixed by these blooms, and how efficiently it is exported into the ocean's interior, remains largely unknown. Here we report on the decline and fate of an iron-stimulated diatom bloom in the Gulf of Alaska. The bloom terminated on day 18, following the depletion of iron and then silicic acid, after which mixed-layer particulate organic carbon (POC) concentrations declined over six days. Increased particulate silica export via sinking diatoms was recorded in sediment traps at depths between 50 and 125 m from day 21, yet increased POC export was not evident until day 24. Only a small proportion of the mixed-layer POC was intercepted by the traps, with more than half of the mixed-layer POC deficit attributable to bacterial remineralization and mesozooplankton grazing. The depletion of silicic acid and the inefficient transfer of iron-increased POC below the permanent thermocline have major implications both for the biogeochemical interpretation of times of greater iron supply in the geological past, and also for proposed geo-engineering schemes to increase oceanic carbon sequestration.