The return of subducted continental crust in Samoan lavas

Substantial quantities of terrigenous sediments are known to enter the mantle at subduction zones, but little is known about their fate in the mantle. Subducted sediment may be entrained in buoyantly upwelling plumes and returned to the Earth's surface at hotspots, but the proportion of recycled sediment in the mantle is small, and clear examples of recycled sediment in hotspot lavas are rare. Here we report remarkably enriched 87Sr/86Sr and 143Nd/144Nd isotope signatures in Samoan lavas from three dredge locations on the underwater flanks of Savai'i island, Western Samoa. The submarine Savai'i lavas represent the most extreme 87Sr/86Sr isotope compositions reported for ocean island basalts to date. The data are consistent with the presence of a recycled sediment component (with a composition similar to the upper continental crust) in the Samoan mantle. Trace-element data show affinities similar to those of the upper continental crust--including exceptionally low Ce/Pb and Nb/U ratios--that complement the enriched 87Sr/86Sr and 143Nd/144Nd isotope signatures. The geochemical evidence from these Samoan lavas significantly redefines the composition of the EM2 (enriched mantle 2; ref. 9) mantle endmember, and points to the presence of an ancient recycled upper continental crust component in the Samoan mantle plume.     

Quantifying the evolutionary dynamics of language

Human language is based on grammatical rules. Cultural evolution allows these rules to change over time. Rules compete with each other: as new rules rise to prominence, old ones die away. To quantify the dynamics of language evolution, we studied the regularization of English verbs over the past 1,200 years. Although an elaborate system of productive conjugations existed in English's proto-Germanic ancestor, Modern English uses the dental suffix, '-ed', to signify past tense. Here we describe the emergence of this linguistic rule amidst the evolutionary decay of its exceptions, known to us as irregular verbs. We have generated a data set of verbs whose conjugations have been evolving for more than a millennium, tracking inflectional changes to 177 Old-English irregular verbs. Of these irregular verbs, 145 remained irregular in Middle English and 98 are still irregular today. We study how the rate of regularization depends on the frequency of word usage. The half-life of an irregular verb scales as the square root of its usage frequency: a verb that is 100 times less frequent regularizes 10 times as fast. Our study provides a quantitative analysis of the regularization process by which ancestral forms gradually yield to an emerging linguistic rule.     

Reproductive biology of the endangered wattled curassow (Crax globulosa; Galliformes: Cracidae) in the Juruá River Basin,Western Brazilian Amazonia

The reproductive biology of Crax globulosa is virtually unknown, this knowledge comprised of only a few anecdotal notes. We found nine nests of Crax globulosa in the middle section of the Juruá River, western Brazilian Amazon, during the dry season. Nests averaged 22.5 m from water and 13.3 m above the ground. We observed two nest types: five made of twigs, leaves and vines, and four within a bromeliad. All nests contained two eggs, but six (67%) were subsequently predated. A female tagged with a transmitter nested twice during the same breeding season. A chick was monitored together with its parents for > 10 months. In addition to hunting and habitat loss, nest predation could be another threat to this endangered species.     

Mutations in ORC1, encoding the largest subunit of the origin recognition complex, cause microcephalic primordial dwarfism resembling Meier-Gorlin syndrome

Studies into disorders of extreme growth failure (for example, Seckel syndrome and Majewski osteodysplastic primordial dwarfism type II) have implicated fundamental cellular processes of DNA damage response signaling and centrosome function in the regulation of human growth. Here we report that mutations in ORC1, encoding a subunit of the origin recognition complex, cause microcephalic primordial dwarfism resembling Meier-Gorlin syndrome. We establish that these mutations disrupt known ORC1 functions including pre-replicative complex formation and origin activation. ORC1 deficiency perturbs S-phase entry and S-phase progression. Additionally, we show that Orc1 depletion in zebrafish is sufficient to markedly reduce body size during rapid embryonic growth. Our data suggest a model in which ORC1 mutations impair replication licensing, slowing cell cycle progression and consequently impeding growth during development, particularly at times of rapid proliferation. These findings establish a novel mechanism for the pathogenesis of microcephalic dwarfism and show a surprising but important developmental impact of impaired origin licensing.     

Mutations in the gene encoding the 3'-5' DNA exonuclease TREX1 cause Aicardi-Goutières syndrome at the AGS1 locus

Aicardi-Goutières syndrome (AGS) presents as a severe neurological brain disease and is a genetic mimic of the sequelae of transplacentally acquired viral infection. Evidence exists for a perturbation of innate immunity as a primary pathogenic event in the disease phenotype. Here, we show that TREX1, encoding the major mammalian 3' --> 5' DNA exonuclease, is the AGS1 gene, and AGS-causing mutations result in abrogation of TREX1 enzyme activity. Similar loss of function in the Trex1(-/-) mouse leads to an inflammatory phenotype. Our findings suggest an unanticipated role for TREX1 in processing or clearing anomalous DNA structures, failure of which results in the triggering of an abnormal innate immune response.     

Hes-1 regulates the excitatory fate of neural progenitors through modulation of <Emphasis Type="Italic">Tlx3 (HOX11L2)</Emphasis> expression

Tlx3 (HOX11L2) is regarded as one of the selector genes in excitatory versus inhibitory fate specification of neurons in distinct regions of the nervous system. Expression of Tlx3 in a post-mitotic immature neuron favors a glutamatergic over GABAergic fate. The factors that regulate Tlx3 have immense importance in the fate specification of glutamatergic neurons. Here, we have shown that Notch target gene, Hes-1, negatively regulates Tlx3 expression, resulting in decreased generation of glutamatergic neurons. Down-regulation of Hes-1 removed the inhibition on Tlx3 promoter, thus promoting glutamatergic differentiation. Promoter–protein interaction studies with truncated/mutated Hes-1 protein suggested that the co-repressor recruitment mediated through WRPW domain of Hes-1 has contributed to the repressive effect. Our results clearly demonstrate a new and unique role for canonical Notch signaling through Hes-1, in neurotransmitter/subtype fate specification of neurons in addition to its known functional role in proliferation/maintenance of neural progenitors.