Energy efficiency trade-offs drive nucleotide usage in transcribed regions

Efficient nutrient usage is a trait under universal selection. A substantial part of cellular resources is spent on making nucleotides. We thus expect preferential use of cheaper nucleotides especially in transcribed sequences, which are often amplified thousand-fold compared with genomic sequences. To test this hypothesis, we derive a mutation-selection-drift equilibrium model for nucleotide skews (strand-specific usage of 'A' versus 'T' and 'G' versus 'C'), which explains nucleotide skews across 1,550 prokaryotic genomes as a consequence of selection on efficient resource usage. Transcription-related selection generally favours the cheaper nucleotides 'U' and 'C' at synonymous sites. However, the information encoded in mRNA is further amplified through translation. Due to unexpected trade-offs in the codon table, cheaper nucleotides encode on average energetically more expensive amino acids. These trade-offs apply to both strand-specific nucleotide usage and GC content, causing a universal bias towards the more expensive nucleotides 'A' and 'G' at non-synonymous coding sites

Non-neutral processes drive the nucleotide composition of non-coding sequences in Drosophila

The nature of the forces affecting base composition is a key question in genome evolution. There is uncertainty as to whether differences in the GC contents of non-coding sequences reflect differences in mutational bias, or in the intensity of selection or biased gene conversion. We have used a polymorphism dataset for non-coding sequences on the X chromosome of Drosophila simulans to examine this question. The proportion of GC→AT versus AT→GC polymorphic mutations in a locus is correlated with its GC content. This implies the action of forces that favour GC over AT base pairs, which are apparently strongest in GC-rich sequences

Superconductivity from correlated hopping

We consider a chain described by a next-nearest-neighbor hopping combined with a nearest-neighbor spin flip. In two dimensions this three-body term arises from a mapping of the three-band Hubbard model for CuO$_2$ planes to a generalized $t-J$ model and for large O-O hopping favors resonance-valence-bond superconductivity of predominantly $d$-wave symmetry. Solving the ground state and low-energy excitations by analytical and numerical methods we find that the chain is a Luther-Emery liquid with correlation exponent $K_{\rho} = (2-n)^2/2$, where $n$ is the particle density.Comment: 10 pages, RevTeX 3.0 + 2 PostScript figs. Accepted for publication in Phys.Rev.

Pairing Correlations in a Generalized Hubbard Model for the Cuprates

Using numerical diagonalization of a 4x4 cluster, we calculate on-site s, extended s and d pairing correlation functions (PCF) in an effective generalized Hubbard model for the cuprates, with nearest-neighbor correlated hopping and next nearest-neighbor hopping t'. The vertex contributions (VC) to the PCF are significantly enhanced, relative to the t-t'-U model. The behavior of the PCF and their VC, and signatures of anomalous flux quantization, indicate superconductivity in the d-wave channel for moderate doping and in the s-wave channel for high doping and small U.Comment: 5 pages, 5 figure

Optimal trapping wavelengths of Cs2_2 molecules in an optical lattice

The present paper aims at finding optimal parameters for trapping of Cs$_2$ molecules in optical lattices, with the perspective of creating a quantum degenerate gas of ground-state molecules. We have calculated dynamic polarizabilities of Cs$_2$ molecules subject to an oscillating electric field, using accurate potential curves and electronic transition dipole moments. We show that for some particular wavelengths of the optical lattice, called "magic wavelengths", the polarizability of the ground-state molecules is equal to the one of a Feshbach molecule. As the creation of the sample of ground-state molecules relies on an adiabatic population transfer from weakly-bound molecules created on a Feshbach resonance, such a coincidence ensures that both the initial and final states are favorably trapped by the lattice light, allowing optimized transfer in agreement with the experimental observation

Quantifying atherogenic lipoproteins for lipid-lowering strategies : Consensus-based recommendations from EAS and EFLM

The joint consensus panel of the European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) recently addressed present and future challenges in the laboratory diagnostics of atherogenic lipoproteins. Total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, and calculated non-HDL cholesterol (= total - HDL cholesterol) constitute the primary lipid panel for estimating risk of atherosclerotic cardiovascular disease (ASCVD) and can be measured in the nonfasting state. LDL cholesterol is the primary target of lipid-lowering therapies. For on-treatment follow-up, LDL cholesterol shall be measured or calculated by the same method to attenuate errors in treatment decisions due to marked between-method variations. Lipoprotein(a)-cholesterol is part of measured or calculated LDL cholesterol and should be estimated at least once in all patients at risk of ASCVD, especially in those whose LDL cholesterol decline poorly upon statin treatment. Residual risk of ASCVD even under optimal LDL-lowering treatment should be also assessed by non-HDL cholesterol or apolipoprotein B, especially in patients with mild-to-moderate hypertriglyceridemia (2-10 mmol/L). Non-HDL cholesterol includes the assessment of remnant lipoprotein cholesterol and shall be reported in all standard lipid panels. Additional apolipoprotein B measurement can detect elevated LDL particle numbers often unidentified on the basis of LDL cholesterol alone. Reference intervals of lipids, lipoproteins, and apolipoproteins are reported for European men and women aged 20-100 years. However, laboratories shall flag abnormal lipid values with reference to therapeutic decision thresholds.Peer reviewe

Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM

The joint consensus panel of the European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) recently addressed present and future challenges in the laboratory diagnostics of atherogenic lipoproteins. Total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDLC), LDL cholesterol (LDLC), and calculated non-HDLC (=total - HDLC) constitute the primary lipid panel for estimating risk of atherosclerotic cardiovascular disease (ASCVD) and can be measured in the nonfasting state. LDLC is the primary target of lipid-lowering therapies. For on-treatment follow-up, I.DLC shall be measured or calculated by the same method to attenuate errors in treatment decisions due to marked between-method variations. Lipoprotein(a) [Lp(a)]-cholesterol is part of measured or calculated LDLC and should be estimated at least once in all patients at risk of ASCVD, especially in those whose LDLC declines poorly upon statin treatment. Residual risk of ASCVD even under optimal LDL-lowering treatment should be also assessed by non-HDLC or apolipoprotein B (apoB), especially in patients with mild-to-moderate hypertriglyceridemia (2-10 mmol/L). Non-HDLC includes the assessment of remnant lipoprotein cholesterol and shall be reported in all standard lipid panels. Additional apoB measurement can detect elevated LDL particle (LDLP) numbers often unidentified on the basis of LDLC alone. Reference intervals of lipids, lipoproteins, and apolipoproteins are reported for European men and women aged 20-100 years. How-ever, laboratories shall flag abnormal lipid values with reference to therapeutic decision thresholds.Afdeling Klinische Chemie en Laboratoriumgeneeskunde (AKCL

Similar gene expression profiles do not imply similar tissue functions

Although similarities in gene expression among tissues are commonly inferred to reflect functional constraints, this has never been formally tested. Furthermore, it is unclear which evolutionary processes are responsible for the observed similarities. When examining genomewide expression data in mouse, we found that patterns of expression similarity between tissues extend to genes that are unlikely to function in the tissues. Thus, ectopic expression can seem coordinated across tissues. This indicates that knowledge of gene expression patterns per se is insufficient to infer gene function. Ectopic expression is possibly explained as expression leakage, caused by spreading of chromatin modifications or the transcription apparatus into neighboring genes

Adaptive evolution of complex innovations through stepwise metabolic niche expansion

Contains fulltext : 172832.pdf (publisher's version ) (Open Access)A central challenge in evolutionary biology concerns the mechanisms by which complex metabolic innovations requiring multiple mutations arise. Here, we propose that metabolic innovations accessible through the addition of a single reaction serve as stepping stones towards the later establishment of complex metabolic features in another environment. We demonstrate the feasibility of this hypothesis through three complementary analyses. First, using genome-scale metabolic modelling, we show that complex metabolic innovations in Escherichia coli can arise via changing nutrient conditions. Second, using phylogenetic approaches, we demonstrate that the acquisition patterns of complex metabolic pathways during the evolutionary history of bacterial genomes support the hypothesis. Third, we show how adaptation of laboratory populations of E. coli to one carbon source facilitates the later adaptation to another carbon source. Our work demonstrates how complex innovations can evolve through series of adaptive steps without the need to invoke non-adaptive processes