On the purported presence of fossilized collagen fibres in an ichthyosaur and a theropod dinosaur

Since the discovery of exceptionally preserved theropod dinosaurs with soft tissues in China in the 1990s, there has been much debate about the nature of filamentous structures observed in some specimens. Sinosauropteryx was the first non‐avian theropod to be described with these structures, and remains one of the most studied examples. Despite a general consensus that the structures represent feathers or feather homologues, a few identify them as degraded collagen fibres derived from the skin. This latter view has been based on observations of low‐quality images of Sinosauropteryx, as well as the suggestion that because superficially similar structures are seen in Jurassic ichthyosaurs they cannot represent feathers. Here, we highlight issues with the evidence put forward in support of this view, showing that integumentary structures have been misinterpreted based on sedimentary features and preparation marks, and that these errors have led to incorrect conclusions being drawn about the existence of collagen in Sinosauropteryx and the ichthyosaur Stenopterygius. We find that there is no evidence to support the idea that the integumentary structures seen in the two taxa are collagen fibres, and confirm that the most parsimonious interpretation of fossilized structures that look like feather homologues in Sinosauropteryx is that they are indeed the remains of feather homologues.     

Effect of salt shock on stability of lambdaimm434 lysogens

The affinities of the bacteriophage 434 repressor for its various binding sites depend on the type and/or concentration of monovalent cations. The ability of bacteriophage 434 repressor to govern the lysis-lysogeny decision depends on the DNA binding activities of the phage's cI repressor protein. We wished to determine whether changes in the intracellular ionic environment influence the lysis-lysogeny decision of the bacteriophage lambda(imm434). Our findings show that the ionic composition within bacterial cells varies with the cation concentration in the growth media. When lambda(imm434) lysogens were grown to mid-log or stationary phase and subsequently incubated in media with increasing monovalent salt concentrations, we observed a salt concentration-dependent increase in the frequency of bacteriophage spontaneous induction. We also found that the frequency of spontaneous induction varied with the type of monovalent cation in the medium. The salt-dependent increase in phage production was unaffected by a recA mutation. These findings indicate that the salt-dependent increase in phage production is not caused by activation of the SOS pathway. Instead, our evidence suggests that salt stress induces this lysogenic bacteriophage by interfering with 434 repressor-DNA interactions. We speculate that the salt-dependent increase in spontaneous induction is due to a direct effect on the repressor's affinity for DNA. Regardless of the precise mechanism, our findings demonstrate that salt stress can regulate the phage lysis-lysogeny switch.     

An Escherichia coli MutY mutant without the six-helix barrel domain is a dimer in solution and assembles cooperatively into multisubunit complexes with DNA

Escherichia coli MutY is an adenine and weak guanine DNA glycosylase involved in reducing the mutagenic effects of 7,8-dihydro-8-oxoguanine (GO). MutY contains three structural domains: an iron-sulfur module, a six-helix barrel module with the helix-hairpin-helix motif, and a C-terminal domain. Here, we demonstrate that the mutant MutY(Delta26-134), which lacks the six-helix barrel domain, cannot complement the mutator phenotype of a mutY mutant in vivo. However, the mutant can still bind DNA and has weak catalytic activity at high enzyme concentrations. The mutant is a dimer in solution and assembled into two and multiple (up to five) complexes with 20- and 44-bp DNA fragments, respectively, in a concentration-dependent manner. Higher order complexes with DNA substrates containing A/GO mismatches were formed at lower protein concentrations than with the A/G mismatch and homoduplex DNA. Measurement of equilibrium binding using fluorescence anisotropy showed that the mutant protein retains some specificity for A/GO-containing DNA substrates and that the binding event is highly cooperative. This is consistent with the MutY structure determined, which indicates that GO specificity is contributed by both the six-helix barrel and C-terminal domains. The nonspecific binding of MutY(Delta26-134) to DNA suggests a model in which the specific binding of mismatched DNA by MutY involves sequential interactions, in which one MutY molecule scans the DNA and enhances binding of another MutY molecule to the A/GO mismatch.     

Non-regulatory CD8+CD45RO+CD25+ T-lymphocytes may compensate for the loss of antigen-inexperienced CD8+CD45RA+ T-cells in old age

The age-related decline in immune system functions is responsible for the increased prevalence of infectious diseases and the low efficacy of vaccination in elderly individuals. In particular, the number of peripheral naive T-cells declines throughout life and they exhibit severe functional defects at advanced age. However, we have recently identified a non-regulatory CD8+CD45RO+ CD25+ T-cell subset that occurs in a subgroup of healthy elderly individuals, who still exhibit an intact humoral immune response following influenza vaccination. Here, we demonstrate that CD8+CD45RO+CD25+ T-cells share phenotypic and functional characteristics with naive CD8+CD45RA+CD28+ T-cells from young individuals, despite their expression of CD45RO. CD8+CD45RO+ CD25+ T-cells also have long telomeres and upon antigenic challenge, they efficiently expand in vitro and differentiate into functional effector cells. The expanded population also maintains a diverse T-cell receptor repertoire. In conclusion, CD8+CD45RO+CD25+ T-cells from elderly individuals compensate for the loss of functional naive T-cells and may therefore be used as a marker of immunological competence in old age.     

Oxidative stress attenuates NO-induced modulation of sympathetic neurotransmission in the mesenteric arterial bed of spontaneously hypertensive rats

Current evidence suggests that hyperactivity of the sympathetic nervous system and endothelial dysfunction are important factors in the development and maintenance of hypertension. Under normal conditions the endothelial mediator nitric oxide (NO) negatively modulates the activity of the norepinephrine portion of sympathetic neurotransmission, thereby placing a "brake" on the vasoconstrictor ability of this transmitter. This property of NO is diminished in the isolated, perfused mesenteric arterial bed taken from the spontaneously hypertensive rat (SHR), resulting in greater nerve-stimulated norepinephrine and lower neuropeptide Y (NPY) overflow from this mesenteric preparation compared with that of the normotensive Wistar-Kyoto rat (WKY). We hypothesized that increased oxidative stress in the SHR contributes to the dysfunction in the NO modulation of sympathetic neurotransmission. Here we demonstrate that the antioxidant N-acetylcysteine reduced nerve-stimulated norepinephrine and increased NPY overflow in the mesenteric arterial bed taken from the SHR. Furthermore, this property of N-acetylcysteine was prevented by inhibiting nitric oxide synthase with N(omega)-nitro-l-arginine methyl ester, demonstrating that the effect of N-acetylcysteine was due to the preservation of NO from oxidation. Despite a reduction in norepinephrine overflow, the nerve-stimulated perfusion pressure response in the SHR mesenteric bed was not altered by the inclusion of N-acetylcysteine. Studies including the Y(1) antagonist BIBO 3304 with N-acetylcysteine demonstrated that this preservation of the perfusion pressure response was due to elevated NPY overflow. These results demonstrate that the reduction in the bioavailability of NO as a result of elevated oxidative stress contributes to the increase in norepinephrine overflow from the SHR mesenteric sympathetic neuroeffector junction.     

The early Eocene birds of the Messel fossil site: a 48 million‐year‐old bird community adds a temporal perspective to the evolution of tropical avifaunas

Birds play an important role in studies addressing the diversity and species richness of tropical ecosystems, but because of the poor avian fossil record in all extant tropical regions, a temporal perspective is mainly provided by divergence dates derived from calibrated molecular analyses. Tropical ecosystems were, however, widespread in the Northern Hemisphere during the early Cenozoic, and the early Eocene German fossil site Messel in particular has yielded a rich avian fossil record. The Messel avifauna is characterized by a considerable number of flightless birds, as well as a high diversity of aerial insectivores and the absence of large arboreal birds. With about 70 currently known species in 42 named genus‐level and at least 39 family‐level taxa, it approaches extant tropical biotas in terms of species richness and taxonomic diversity. With regard to its taxonomic composition and presumed ecological characteristics, the Messel avifauna is more similar to the Neotropics, Madagascar, and New Guinea than to tropical forests in continental Africa and Asia. Because the former regions were geographically isolated during most of the Cenozoic, their characteristics may be due to the absence of biotic factors, especially those related to the diversification of placental mammals, which impacted tropical avifaunas in Africa and Asia. The crown groups of most avian taxa that already existed in early Eocene forests are species‐poor. This does not support the hypothesis that the antiquity of tropical ecosystems is key to the diversity of tropical avifaunas, and suggests that high diversification rates may be of greater significance.     

High variability and non-neutral evolution of the mammalian <Emphasis Type="Italic">avpr1a</Emphasis> gene

Background  

The arginine-vasopressin 1a receptor has been identified as a key determinant for social behaviour in Microtus voles, humans and other mammals. Nevertheless, the genetic bases of complex phenotypic traits like differences in social and mating behaviour among species and individuals remain largely unknown. Contrary to previous studies focusing on differences in the promotor region of the gene, we investigate here the level of functional variation in the coding region (exon 1) of this locus.