Catálogo de publicaciones - revistas

<jats:p> Organic carbon (OC) from multiple sources can be delivered contemporaneously to aquatic sediments. The influence of different OC inputs on carbon-14–based sediment chronologies is illustrated in the carbon-14 ages of purified, source-specific (biomarker) organic compounds from near-surface sediments underlying two contrasting marine systems, the Black Sea and the Arabian Sea. In the Black Sea, isotopic heterogeneity of <jats:italic>n</jats:italic> -alkanes indicated that OC was contributed from both fossil and contemporary sources. Compounds reflecting different source inputs to the Arabian Sea exhibit a 10,000-year range in conventional carbon-14 ages. Radiocarbon measurements of biomarkers of marine photoautotrophy enable sediment chronologies to be constructed independent of detrital OC influences. </jats:p>

<jats:p> The sizes of major sources and sinks of atmospheric methane (CH <jats:sub>4</jats:sub> ), an important greenhouse gas, are poorly known. CH <jats:sub>4</jats:sub> from north Siberian lakes contributes ∼1.5 teragrams CH <jats:sub>4</jats:sub> year <jats:sup>−1</jats:sup> to observed winter increases in atmospheric CH <jats:sub>4</jats:sub> concentration at high northern latitudes. CH <jats:sub>4</jats:sub> emitted from these lakes in winter had a radiocarbon age of 27,200 years and was derived largely from Pleistocene-aged carbon. </jats:p>

<jats:p>Satellite altimetry was used to identify and characterize Pacific intraplate seamounts. The gravimetric amplitudes of seamounts appear to be related to the age difference between the sea floor and seamounts; by inverting this relation, pseudo ages can be obtained for undated seamounts. These pseudo ages imply that excursions in seamount volcanism generally correlate with times of formation of large oceanic plateaus.</jats:p>

<jats:p> Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by the widespread development of distinctive tumors termed hamartomas. TSC-determining loci have been mapped to chromosomes 9q34 ( <jats:italic>TSC1</jats:italic> ) and 16p13 ( <jats:italic>TSC2</jats:italic> ). The <jats:italic>TSC1</jats:italic> gene was identified from a 900-kilobase region containing at least 30 genes. The 8.6-kilobase <jats:italic>TSC1</jats:italic> transcript is widely expressed and encodes a protein of 130 kilodaltons (hamartin) that has homology to a putative yeast protein of unknown function. Thirty-two distinct mutations were identified in <jats:italic>TSC1</jats:italic> , 30 of which were truncating, and a single mutation (2105delAAAG) was seen in six apparently unrelated patients. In one of these six, a somatic mutation in the wild-type allele was found in a TSC-associated renal carcinoma, which suggests that hamartin acts as a tumor suppressor. </jats:p>

<jats:p> In addition to the RNA polymerases (RNAPs) transcribing the nuclear genes, eukaryotic cells also require RNAPs to transcribe the genes of the mitochondrial genome and, in plants, of the chloroplast genome. The plant <jats:italic>Arabidopsis thaliana</jats:italic> was found to contain two nuclear genes similar to genes encoding the mitochondrial RNAP from yeast and RNAPs of bacteriophages T7, T3, and SP6. The putative transit peptides of the two polymerases were capable of targeting fusion proteins to mitochondria and chloroplasts, respectively, in vitro. The results indicate that the mitochondrial RNAP in plants is a bacteriophage-type enzyme. A gene duplication event may have generated the second RNAP, which along with the plastid-encoded eubacteria-like RNAP could transcribe the chloroplast genome. </jats:p>

<jats:p>Repeated administration of morphine sensitizes animals to the stimulant and rewarding properties of the drug. It also selectively increases expression of GluR1 (an AMPA glutamate receptor subunit) in the ventral tegmental area, a midbrain region implicated in morphine action. By viral-mediated gene transfer, a causal relation is shown between these behavioral and biochemical adaptations: Morphine's stimulant and rewarding properties are intensified after microinjections of a viral vector expressing GluR1 into the ventral tegmental area. These results confirm the importance of AMPA receptors in morphine action and demonstrate specific locomotor and motivational adaptations resulting from altered expression of a single localized gene product.</jats:p>

<jats:p>TRAIL, also called Apo2L, is a cytotoxic protein that induces apoptosis of many transformed cell lines but not of normal tissues, even though its death domain–containing receptor, DR4, is expressed on both cell types. An antagonist decoy receptor (designated as TRID for TRAIL receptor without an intracellular domain) that may explain the resistant phenotype of normal tissues was identified. TRID is a distinct gene product with an extracellular TRAIL-binding domain and a transmembrane domain but no intracellular signaling domain. TRID transcripts were detected in many normal human tissues but not in most cancer cell lines examined. Ectopic expression of TRID protected mammalian cells from TRAIL-induced apoptosis, which is consistent with a protective role. Another death domain–containing receptor for TRAIL (designated as death receptor–5), which preferentially engaged a FLICE (caspase-8)–related death protease, was also identified.</jats:p>

<jats:p>TRAIL (also called Apo2L) belongs to the tumor necrosis factor family, activates rapid apoptosis in tumor cells, and binds to the death-signaling receptor DR4. Two additional TRAIL receptors were identified. The receptor designated death receptor 5 (DR5) contained a cytoplasmic death domain and induced apoptosis much like DR4. The receptor designated decoy receptor 1 (DcR1) displayed properties of a glycophospholipid-anchored cell surface protein. DcR1 acted as a decoy receptor that inhibited TRAIL signaling. Thus, a cell surface mechanism exists for the regulation of cellular responsiveness to pro-apoptotic stimuli.</jats:p>

<jats:p>Computational studies suggest that acquisition of a motor skill involves learning an internal model of the dynamics of the task, which enables the brain to predict and compensate for mechanical behavior. During the hours that follow completion of practice, representation of the internal model gradually changes, becoming less fragile with respect to behavioral interference. Here, functional imaging of the brain demonstrates that within 6 hours after completion of practice, while performance remains unchanged, the brain engages new regions to perform the task; there is a shift from prefrontal regions of the cortex to the premotor, posterior parietal, and cerebellar cortex structures. This shift is specific to recall of an established motor skill and suggests that with the passage of time, there is a change in the neural representation of the internal model and that this change may underlie its increased functional stability.</jats:p>

<jats:p> Fate determination in <jats:italic>Drosophila</jats:italic> embryos is evidenced by the appearance of mitotic domains. To identify fate or fates of cells, individual cells in mitotic domains 2, 8, and 15 were marked and monitored through development. Comparison of the different fates indicated that domain boundaries are cell fate boundaries. Cells were marked by expression of GAL4-dependent transgenes after photoactivation of a caged GAL4VP16 analog that had its DNA binding activity inhibited with a photolabile blocking reagent. Caged GAL4VP16 was also used to induce gene expression in <jats:italic>Xenopus</jats:italic> embryos. Thus, photoactivated gene expression is a versatile tool for spatiotemporal control of gene expression. </jats:p>