Shear heating reconciles thermal models with the metamorphic rock record of subduction.

Some commonly referenced thermal-mechanical models of current subduction zones imply temperatures that are 100-500 °C colder at 30-80-km depth than pressure-temperature conditions determined thermobarometrically from exhumed metamorphic rocks. Accurately inferring subduction zone thermal structure, whether from models or rocks, is crucial for predicting metamorphic reactions and associated fluid release, subarc melting conditions, rheologies, and fault-slip phenomena. Here, we compile surface heat flow data from subduction zones worldwide and show that values are higher than can be explained for a frictionless subduction interface often assumed for modeling. An additional heat source--likely shear heating--is required to explain these forearc heat flow values. A friction coefficient of at least 0.03 and possibly as high as 0.1 in some cases explains these data, and we recommend a provisional average value of 0.05 ± 0.015 for modeling. Even small coefficients of friction can contribute several hundred degrees of heating at depths of 30-80 km. Adding such shear stresses to thermal models quantitatively reproduces the pressure-temperature conditions recorded by exhumed metamorphic rocks. Comparatively higher temperatures generally drive rock dehydration and densification, so, at a given depth, hotter rocks are denser than colder rocks, and harder to exhume through buoyancy mechanisms. Consequently--conversely to previous proposals--exhumed metamorphic rocks might overrepresent old-cold subduction where rocks at the slab interface are wetter and more buoyant than in young-hot subduction zones.

Trace element diffusivities in bone rule out simple diffusive uptake during fossilization but explain in vivo uptake and release.

Diffusion rates of numerous trace elements in bone at 20 °C were determined using laser-ablation inductively coupled plasma mass spectrometry analysis of experimentally induced diffusion profiles. Diffusivities are about 1 order of magnitude slower than current semiquantitative geochemical views and about 1.5 orders of magnitude faster than indirect radiotracer estimates. Intrabone volume diffusion is too slow and too similar among many elements to explain trace element profiles in young fossils and archeological materials. Diffusivity differences among elements do, however, explain disparate biokinetic washout of Sr vs. Ba and of light vs. heavy rare earth elements (REEs). These results improve the understanding of the physical principles underlying biokinetic models and rates and mechanisms of trace element alteration of phosphatic tissues in paleontological, archeological, and crystal-chemical contexts. Recrystallization and transport limitations in soils explain trace element profiles in young fossils better than intrabone volume diffusion alone and imply that diffusion of REE and other trivalent cations is likely controlled by a common charge-compensating species rather than ionic radii or partition coefficients.

Large temperature drop across the Eocene-Oligocene transition in central North America.

The Eocene-Oligocene transition towards a cool climate (approximately 33.5 million years ago) was one of the most pronounced climate events during the Cenozoic era. The marine record of this transition has been extensively studied. However, significantly less research has focused on continental climate change at the time, yielding partly inconsistent results on the magnitude and timing of the changes. Here we use a combination of in vivo stable isotope compositions of fossil tooth enamel with diagenetic stable isotope compositions of fossil bone to derive a high-resolution (about 40,000 years) continental temperature record for the Eocene-Oligocene transition. We find a large drop in mean annual temperature of 8.2 +/- 3.1 degrees C over about 400,000 years, the possibility of a small increase in temperature seasonality, and no resolvable change in aridity across the transition. The large change in mean annual temperature, exceeding changes in sea surface temperatures at comparable latitudes and possibly delayed in time with respect to marine changes by up to 400,000 years, explains the faunal turnover for gastropods, amphibians and reptiles, whereas most mammals in the region were unaffected. Our results are in agreement with modelling studies that attribute the climate cooling at the Eocene-Oligocene transition to a significant drop in atmospheric carbon dioxide concentrations.

Carbon isotope compositions of terrestrial C3 plants as indicators of (paleo)ecology and (paleo)climate.

A broad compilation of modern carbon isotope compositions in all C3 plant types shows a monotonic increase in δ(13)C with decreasing mean annual precipitation (MAP) that differs from previous models. Corrections for temperature, altitude, or latitude are smaller than previously estimated. As corrected for altitude, latitude, and the δ(13)C of atmospheric CO(2), these data permit refined interpretation of MAP, paleodiet, and paleoecology of ecosystems dominated by C3 plants, either prior to 7-8 million years ago (Ma), or more recently at mid- to high latitudes. Twenty-nine published paleontological studies suggest preservational or scientific bias toward dry ecosystems, although wet ecosystems are also represented. Unambiguous isotopic evidence for C4 plants is lacking prior to 7-8 Ma, and hominid ecosystems at 4.4 Ma show no isotopic evidence for dense forests. Consideration of global plant biomass indicates that average δ(13)C of C3 plants is commonly overestimated by approximately 2‰.

Toward a Cenozoic history of atmospheric CO2.

The geological record encodes the relationship between climate and atmospheric carbon dioxide (CO2) over long and short timescales, as well as potential drivers of evolutionary transitions. However, reconstructing CO2 beyond direct measurements requires the use of paleoproxies and herein lies the challenge, as proxies differ in their assumptions, degree of understanding, and even reconstructed values. In this study, we critically evaluated, categorized, and integrated available proxies to create a high-fidelity and transparently constructed atmospheric CO2 record spanning the past 66 million years. This newly constructed record provides clearer evidence for higher Earth system sensitivity in the past and for the role of CO2 thresholds in biological and cryosphere evolution.

Preimplantation development regulatory pathway construction through a text-mining approach.

BACKGROUND: The integration of sequencing and gene interaction data and subsequent generation of pathways and networks contained in databases such as KEGG Pathway is essential for the comprehension of complex biological processes. We noticed the absence of a chart or pathway describing the well-studied preimplantation development stages; furthermore, not all genes involved in the process have entries in KEGG Orthology, important information for knowledge application with relation to other organisms. RESULTS: In this work we sought to develop the regulatory pathway for the preimplantation development stage using text-mining tools such as Medline Ranker and PESCADOR to reveal biointeractions among the genes involved in this process. The genes present in the resulting pathway were also used as seeds for software developed by our group called SeedServer to create clusters of homologous genes. These homologues allowed the determination of the last common ancestor for each gene and revealed that the preimplantation development pathway consists of a conserved ancient core of genes with the addition of modern elements. CONCLUSIONS: The generation of regulatory pathways through text-mining tools allows the integration of data generated by several studies for a more complete visualization of complex biological processes. Using the genes in this pathway as "seeds" for the generation of clusters of homologues, the pathway can be visualized for other organisms. The clustering of homologous genes together with determination of the ancestry leads to a better understanding of the evolution of such process.

The multifunctional RNA-binding protein La is required for mouse development and for the establishment of embryonic stem cells.

The La protein is a target of autoantibodies in patients suffering from Sjögren's syndrome, systemic lupus erythematosus, and neonatal lupus. Ubiquitous in eukaryotes, La functions as a RNA-binding protein that promotes the maturation of tRNA precursors and other nascent transcripts synthesized by RNA polymerase III as well as other noncoding RNAs. La also associates with a class of mRNAs that encode ribosome subunits and precursors to snoRNAs involved in ribosome biogenesis. Thus, it was surprising that La is dispensable in the yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe, the organisms from which it has been characterized most extensively. To determine whether La is essential in mammals and if so, at which developmental stage it is required, mice were created with a disrupted La gene, and the offspring from La+/-intercrosses were analyzed. La-/- offspring were detected at the expected frequency among blastocysts prior to implantation, whereas no nullizygotes were detected after implantation, indicating that La is required early in development. Blastocysts derived from La+/- intercrosses yielded 38 La+/+ and La+/- embryonic stem (ES) cell lines but no La-/- ES cell lines, suggesting that La contributes a critical function toward the establishment or survival of ES cells. Consistent with this, La-/- blastocyst outgrowths revealed loss of the inner cell mass (ICM). The results indicate that in contrast to the situation in yeasts, La is essential in mammals and is one of a limited number of genes required as early as the development of the ICM.

Dp1 is largely dispensable for embryonic development.

E2F/DP complexes activate or repress the transcription of E2F target genes, depending on the association of a pRB family member, thereby regulating cell cycle progression. Whereas the E2F family consists of seven members, the DP family contains only two (Dp1 and Dp2), Dp1 being the more highly expressed member. In contrast to the inactivation of individual E2F family members, we have recently demonstrated that loss of Dp1 results in embryonic lethality by embryonic day 12.5 (E12.5) due to the failure of extraembryonic lineages to develop and replicate DNA properly. To bypass this placental requirement and search for roles of Dp1 in the embryo proper, we generated Dp1-deficient embryonic stem (ES) cells that carry the ROSA26-LacZ marker and injected them into wild-type blastocysts to construct Dp1-deficient chimeras. Surprisingly, we recovered mid- to late gestational embryos (E12.5 to E17.5), in which the Dp1-deficient ES cells contributed strongly to most chimeric tissues as judged by X-Gal (5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside) staining and Western blotting. Importantly, the abundance of DP2 protein does not increase and the expression of an array of cell cycle genes is virtually unchanged in Dp1-deficient ES cells or chimeric E15.5 tissues with the absence of Dp1. Thus, Dp1 is largely dispensable for embryonic development, despite the absolute extraembryonic requirement for Dp1, which is highly reminiscent of the restricted roles for Rb and cyclins E1/E2 in vivo.

Linked canopy, climate, and faunal change in the Cenozoic of Patagonia.

Vegetation structure is a key determinant of ecosystems and ecosystem function, but paleoecological techniques to quantify it are lacking. We present a method for reconstructing leaf area index (LAI) based on light-dependent morphology of leaf epidermal cells and phytoliths derived from them. Using this proxy, we reconstruct LAI for the Cenozoic (49 million to 11 million years ago) of middle-latitude Patagonia. Our record shows that dense forests opened up by the late Eocene; open forests and shrubland habitats then fluctuated, with a brief middle-Miocene regreening period. Furthermore, endemic herbivorous mammals show accelerated tooth crown height evolution during open, yet relatively grass-free, shrubland habitat intervals. Our Patagonian LAI record provides a high-resolution, sensitive tool with which to dissect terrestrial ecosystem response to changing Southern Ocean conditions during the Cenozoic.

Isotopic ordering in eggshells reflects body temperatures and suggests differing thermophysiology in two Cretaceous dinosaurs.

Our understanding of the evolutionary transitions leading to the modern endothermic state of birds and mammals is incomplete, partly because tools available to study the thermophysiology of extinct vertebrates are limited. Here we show that clumped isotope analysis of eggshells can be used to determine body temperatures of females during periods of ovulation. Late Cretaceous titanosaurid eggshells yield temperatures similar to large modern endotherms. In contrast, oviraptorid eggshells yield temperatures lower than most modern endotherms but ∼ 6 °C higher than co-occurring abiogenic carbonates, implying that this taxon did not have thermoregulation comparable to modern birds, but was able to elevate its body temperature above environmental temperatures. Therefore, we observe no strong evidence for end-member ectothermy or endothermy in the species examined. Body temperatures for these two species indicate that variable thermoregulation likely existed among the non-avian dinosaurs and that not all dinosaurs had body temperatures in the range of that seen in modern birds.

Decoupling the spread of grasslands from the evolution of grazer-type herbivores in South America.

The evolution of high-crowned cheek teeth (hypsodonty) in herbivorous mammals during the late Cenozoic is classically regarded as an adaptive response to the near-global spread of grass-dominated habitats. Precocious hypsodonty in middle Eocene (∼38 million years (Myr) ago) faunas from Patagonia, South America, is therefore thought to signal Earth's first grasslands, 20 million years earlier than elsewhere. Here, using a high-resolution, 43-18 million-year record of plant silica (phytoliths) from Patagonia, we show that although open-habitat grasses existed in southern South America since the middle Eocene (∼40 Myr ago), they were minor floral components in overall forested habitats between 40 and 18 Myr ago. Thus, distinctly different, continent-specific environmental conditions (arid grasslands versus ash-laden forests) triggered convergent cheek-tooth evolution in Cenozoic herbivores. Hypsodonty evolution is an important example where the present is an insufficient key to the past, and contextual information from fossils is vital for understanding processes of adaptation.

The acrosomal protein Dickkopf-like 1 (DKKL1) is not essential for fertility.

OBJECTIVE: To determine the role of Dkkl1 on mouse development, viability, and fertility. DESIGN: Prospective experimental study. SETTING: Government research institution. ANIMAL(S): Mice of C57BL/6 and 129X1/SvJ strains, as well as transgenic mice of mixed C57BL/6 and 129X1/SvJ strains were used for the studies. INTERVENTION(S): Mice were constructed that lacked a functional Dkkl1 gene. MAIN OUTCOME MEASURE(S): Deletion of the gene was confirmed by DNA, RNA, and protein analyses; in vivo fertility was examined by continuous mating scheme. RESULT(S): Previous studies have shown that Dkkl1, a gene unique to mammals, is expressed predominantly, if not exclusively, in developing spermatocytes, and the DKKL1 protein accumulates in the acrosome of mature sperm. Subsequent studies (reported in the accompanying article) demonstrate that Dkkl1 also is expressed in the trophectoderm/placental lineage. Taken together, these results strongly suggested that DKKL1 protein is required for terminal differentiation either of trophoblast giant cells or of sperm, both of which are directly involved in fertility. To challenge this hypothesis, conditional targeted mutagenesis was used to ablate the Dkkl1 gene in mice. Surprisingly, Dkkl1 nullizygous embryos developed into viable, fertile adults, despite the fact that they failed to produce any portion of the DKKL1 protein. CONCLUSION(S): DKKL1 is a mammalian-specific acrosomal protein that is not essential either for development or fertility.

The acrosomal protein Dickkopf-like 1 (DKKL1) facilitates sperm penetration of the zona pellucida.

OBJECTIVE: To determine the role of Dkkl1 in mouse development, viability, and fertility. DESIGN: Prospective experimental study. SETTING: Government research institution. ANIMAL(S): Mice of C57BL/6, B6D2F1/J, and 129X1/SvJ strains, as well as transgenic mice of mixed C57BL/6 and 129X1/SvJ strains were used for the studies. INTERVENTION(S): Expression of the Dkkl1 gene was characterized during early mouse development, and the effects of Dkkl1 ablation on reproduction and fertility were characterized in vitro and in vivo. MAIN OUTCOME MEASURE(S): Dkkl1 RNA expression was determined by Northern blotting hybridization as well as quantitative reverse transcriptase-polymerase chain reaction assays. In vitro fertilization assays were used to assess fertility of sperm from male mice lacking functional Dkkl1. RESULT(S): Dkkl1 is a gene unique to mammals that is expressed primarily in developing spermatocytes and its product localized in the acrosome of mature sperm. Here we show that Dkkl1 also is expressed in the trophectoderm/placental lineage. Surprisingly, embryos lacking DKKL1 protein developed into viable, fertile adults. Nevertheless, the ability of sperm that lacked DKKL1 protein to fertilize wild-type eggs was severely compromised in vitro. Because this defect could be overcome either by removal of the zona pellucida or by the presence of wild-type sperm, Dkkl1, either directly or indirectly, facilitates the ability of sperm to penetrate the zona pellucida. Penetration of the zona pellucida by Dkkl1(-) sperm was delayed in vivo as well as in vitro, but the delay in vivo was compensated by other factors during preimplantation development. Accordingly, Dkkl1-/- males offer an in vitro fertilization model for identifying factors that may contribute to infertility. CONCLUSION(S): DKKL1 is a mammalian-specific, acrosomal protein that strongly affects in vitro fertilization, although the effect is attenuated in vivo.

Differentiation of trophoblast stem cells into giant cells is triggered by p57/Kip2 inhibition of CDK1 activity.

Genome endoreduplication during mammalian development is a rare event for which the mechanism is unknown. It first appears when fibroblast growth factor 4 (FGF4) deprivation induces differentiation of trophoblast stem (TS) cells into the nonproliferating trophoblast giant (TG) cells required for embryo implantation. Here we show that RO3306 inhibition of cyclin-dependent protein kinase 1 (CDK1), the enzyme required to enter mitosis, induced differentiation of TS cells into TG cells. In contrast, RO3306 induced abortive endoreduplication and apoptosis in embryonic stem cells, revealing that inactivation of CDK1 triggers endoreduplication only in cells programmed to differentiate into polyploid cells. Similarly, FGF4 deprivation resulted in CDK1 inhibition by overexpressing two CDK-specific inhibitors, p57/KIP2 and p21/CIP1. TS cell mutants revealed that p57 was required to trigger endoreduplication by inhibiting CDK1, while p21 suppressed expression of the checkpoint protein kinase CHK1, thereby preventing induction of apoptosis. Furthermore, Cdk2(-/-) TS cells revealed that CDK2 is required for endoreduplication when CDK1 is inhibited. Expression of p57 in TG cells was restricted to G-phase nuclei to allow CDK activation of S phase. Thus, endoreduplication in TS cells is triggered by p57 inhibition of CDK1 with concomitant suppression of the DNA damage response by p21.

Transcription factor TEAD4 specifies the trophectoderm lineage at the beginning of mammalian development.

Specification of cell lineages in mammals begins shortly after fertilization with formation of a blastocyst consisting of trophectoderm, which contributes exclusively to the placenta, and inner cell mass (ICM), from which the embryo develops. Here we report that ablation of the mouse Tead4 gene results in a preimplantation lethal phenotype, and TEAD4 is one of two highly homologous TEAD transcription factors that are expressed during zygotic gene activation in mouse 2-cell embryos. Tead4(-/-) embryos do not express trophectoderm-specific genes, such as Cdx2, but do express ICM-specific genes, such as Oct4 (also known as Pou5f1). Consequently, Tead4(-/-) morulae do not produce trophoblast stem cells, trophectoderm or blastocoel cavities, and therefore do not implant into the uterine endometrium. However, Tead4(-/-) embryos can produce embryonic stem cells, a derivative of ICM, and if the Tead4 allele is not disrupted until after implantation, then Tead4(-/-) embryos complete development. Thus, Tead4 is the earliest gene shown to be uniquely required for specification of the trophectoderm lineage.

Transcription factor TEAD2 is involved in neural tube closure.

TEAD2, one of the first transcription factors expressed at the beginning of mammalian development, appears to be required during neural development. For example, Tead2 expression is greatest in the dorsal neural crest where it appears to regulate expression of Pax3, a gene essential for brain development. Consistent with this hypothesis, we found that inactivation of the Tead2 gene in mice significantly increased the risk of exencephaly (a defect in neural tube closure). However, none of the embryos exhibited spina bifida, the major phenotype of Pax3 nullizygous embryos, and expression of Pax3 in E11.5 Tead2 nullizygous embryos was normal. Thus, Tead2 plays a role in neural tube closure that is independent of its putative role in Pax3 regulation. In addition, the risk of exencephaly was greatest with Tead2 nullizygous females, and could be suppressed either by folic acid or pifithrin-alpha. These results reveal a maternal genetic contribution to neural tube closure, and suggest that Tead2-deficient mice provide a model for anencephaly, a common human birth defect that can be prevented by folic acid.

DkkL1 (Soggy), a Dickkopf family member, localizes to the acrosome during mammalian spermatogenesis.

Dickkopf-like 1 (DkkL1) is related to the Dickkopf gene family, a group of proteins that are characterized as secreted antagonists of Wingless (Wnt) signal transduction proteins. DkkL1 mRNA is found in preimplantation mouse embryos and in developing neural tissue, but in adults it is found primarily in the testes. In an effort to elucidate its function, the distribution of DkkL1 protein in mouse testis and mature sperm was analyzed by immuno-histochemistry and immuno-blotting techniques. DkkL1 first appeared in the developing spermatocytes in seminiferous tubules as early as Stage XII, coincident with the appearance of DkkL1 mRNA. Surprisingly, however, DkkL1 localized to the developing acrosome in spermatocytes and spermatids and to the acrosome in mature sperm. Furthermore, DkkL1 was N-glycosylated in the testis, but it did not appear to be excreted, and the DkkL1 in mature sperm was no longer N-glycosylated, suggesting that additional post-translational modifications occurred during the final stages of spermatogenesis. These results identify a member of the Dickkopf family as a novel acrosomal protein that may be involved in acrosome assembly or function, a unique role for a secreted signaling molecule.

Dp1 is required for extra-embryonic development.

Release of E2F1/DP1 heterodimers from repression mediated by the retinoblastoma tumor suppressor (pRB) triggers cell cycle entry into S phase, suggesting that E2F1 and DP1 proteins must act in unison, either to facilitate or to suppress cell-cycle progression. In stark contrast to the milder phenotypes that result from inactivation of E2Fs, we report that loss of Dp1 leads to death in utero because of the failure of extra-embryonic development. Loss of Dp1 compromises the trophectoderm-derived tissues - specifically, the expansion of the ectoplacental cone and chorion, and endoreduplication in trophoblast giant cells. Inactivation of p53 is unable to rescue the Dp1-deficient embryonic lethality. Thus, DP1 is absolutely required for extra-embryonic development and consequently embryonic survival, consistent with E2F/DP1 normally acting to promote growth in vivo.