Coral reefs drilled offshore of Barbados provide the first continuous and detailed record of sea level change during the last deglaciation. The sea level was 121 ± 5 metres below present level during the last glacial maximum. The deglacial sea level rise was not monotonic; rather, it was marked by two intervals of rapid rise. Varying rates of melt-water discharge to the North Atlantic surface ocean dramatically affected North Atlantic deep-water production and oceanic oxygen isotope chemistry. A global oxygen isotope record for ocean water has been calculated from the Barbados sea level curve, allowing separation of the ice volume component common to all oxygen isotope records measured in deep-sea cores.

A 17,000-year glacio-eustatic sea level record: influence of glacial melting rates on the Younger Dryas event and deep-ocean circulation

Oxygen isotope records of five stalagmites from Hulu Cave near Nanjing bear a remarkable resemblance to oxygen isotope records from Greenland ice cores, suggesting that East Asian Monsoon intensity changed in concert with Greenland temperature between 11,000 and 75,000 years before the present (yr. B.P.). Between 11,000 and 30,000 yr. B.P., the timing of changes in the monsoon, as established with 230Th dates, generally agrees with the timing of temperature changes from the Greenland Ice Sheet Project Two (GISP2) core, which supports GISP2's chronology in this interval. Our record links North Atlantic climate with the meridional transport of heat and moisture from the warmest part of the ocean where the summer East Asian Monsoon originates.

http://science.sciencemag.org/content/sci/294/5550/2345.full.pdf

A High-Resolution Absolute-Dated Late Pleistocene Monsoon Record from Hulu Cave, China

G protein-coupled receptors (GPCRs) are seven transmembrane proteins that form the largest single family of integral membrane receptors. GPCRs transduce information provided by extracellular stimuli into intracellular second messengers via their coupling to heterotrimeric G proteins and the subsequent regulation of a diverse variety of effector systems. Agonist activation of GPCRs also initiates processes that are involved in the feedback desensitization of GPCR responsiveness, the internalization of GPCRs, and the coupling of GPCRs to heterotrimeric G protein-independent signal transduction pathways. GPCR desensitization occurs as a consequence of G protein uncoupling in response to phosphorylation by both second messenger-dependent protein kinases and G protein-coupled receptor kinases (GRKs). GRK-mediated receptor phosphorylation promotes the binding of beta-arrestins, which not only uncouple receptors from heterotrimeric G proteins but also target many GPCRs for internalization in clathrin-coated vesicles. beta-Arrestin-dependent endocytosis of GPCRs involves the direct interaction of the carboxyl-terminal tail domain of beta-arrestins with both beta-adaptin and clathrin. The focus of this review is the current and evolving understanding of the contribution of GRKs, beta-arrestins, and endocytosis to GPCR-specific patterns of desensitization and resensitization. In addition to their role as GPCR-specific endocytic adaptor proteins, beta-arrestins also serve as molecular scaffolds that foster the formation of alternative, heterotrimeric G protein-independent signal transduction complexes. Similar to what is observed for GPCR desensitization and resensitization, beta-arrestin-dependent GPCR internalization is involved in the intracellular compartmentalization of these protein complexes.

Evolving Concepts in G Protein-Coupled Receptor Endocytosis: The Role in Receptor Desensitization and Signaling

A high-resolution, absolute-dated Holocene and deglacial Asian monsoon record from Dongge Cave, China

Bcl-2 is an oncogenic protein that acts by inhibiting programmed cell death. The mechanisms used by this and related anti-apoptotic proteins to protect cells from cytotoxic stimuli are now emerging, with the discovery that Bcl-2 can function both as an ion channel and as an adaptor or docking protein.

Double identity for proteins of the Bcl-2 family

238U234U230Th232Th systematics and the precise measurement of time over the past 500,000 years

238U,234U and232Th in seawater

The development of mass spectrometric techniques for determination of ^(230)Th abundance has made it possible to reduce analytical errors in ^(238)U-^(234)U-^(230)Th dating of corals even with very small samples. Samples of 6 x 10^8 atoms of ^(230)Th can be measured to an accuracy of ±3 percent (2σ) and 3 x 10^(10) atoms of ^(230)Th can be measured to an accuracy of ±0.2 percent. The time range over which useful age data on corals can be obtained now ranges from about 50 to about 500,000 years. For young corals, this approach may be preferable to ^(14)C dating. The precision with which the age of a coral can now be determined should make it possible to critically test the Milankovitch hypothesis concerning Pleistocene climate fluctuations. Analyses of a number of corals that grew during the last interglacial period yield ages of 122,000 to 130,000 years. The ages coincide with, or slightly postdate, the summer solar insolation high at 65°N latitude which occurred 128,000 years ago. This supports the idea that changes in Pleistocene climate can be the result of variations in the distribution of solar insolation caused by changes in the geometry of the earth's orbit and rotation axis.

http://science.sciencemag.org/content/sci/236/4808/1547.full.pdf

Precise Timing of the Last Interglacial Period from Mass Spectrometric Determination of Thorium-230 in Corals

Arrestins are soluble cytoplasmic proteins that bind to G-protein-coupled receptors, thus switching off activation of the G protein and terminating the signalling pathway that triggers the cellular response. Although visual arrestin has been shown to quench the catalytic activity of photoexcited, phosphorylated rhodopsin in a reconstituted system, its role in the intact rod cell remains unclear because phosphorylation alone reduces the catalytic activity of rhodopsin. Here we have recorded photocurrents of rods from transgenic mice in which one or both copies of the arrestin gene were disrupted. Photoresponses were unaffected when arrestin expression was halved, indicating that arrestin binding is not rate limiting for recovery of the rod photoresponse, as it is in Drosophila . With arrestin absent, the flash response displayed a rapid partial recovery followed by a prolonged final phase. This behaviour indicates that an arrestin-independent mechanism initiates the quench of rhodopsin's catalytic activity and that arrestin completes the quench. The intensity dependence of the photoresponse in rods lacking arrestin further suggests that, although arrestin is required for normal signal termination, it does not participate directly in light adaptation.

Prolonged photoresponses in transgenic mouse rods lacking arrestin

Although biochemical experiments suggest that rhodopsin and other receptors coupled to heterotrimeric guanosine triphosphate-binding proteins (G proteins) are inactivated by phosphorylation near the carboxyl (COOH)-terminus and the subsequent binding of a capping protein, little is known about the quenching process in vivo. Flash responses were recorded from rods of transgenic mice in which a fraction of the rhodopsin molecules lacked the COOH-terminal phosphorylation sites. In the single photon regime, abnormally prolonged responses, attributed to activation of individual truncated rhodopsins, occurred interspersed with normal responses. The occurrence of the prolonged responses suggests that phosphorylation is required for normal shutoff. Comparison of normal and prolonged single photon responses indicated that rhodopsin begins to be quenched before the peak of the electrical response and that quenching limits the response amplitude.

http://science.sciencemag.org/content/sci/267/5196/374.full.pdf

Jeannie Chen

Papers

238U234U230Th232Th systematics and the precise measurement of time over the past 500,000 years

238U,234U and232Th in seawater

Precise Timing of the Last Interglacial Period from Mass Spectrometric Determination of Thorium-230 in Corals

Prolonged photoresponses in transgenic mouse rods lacking arrestin

Mechanisms of rhodopsin inactivation in vivo as revealed by a COOH-terminal truncation mutant