Calculations of the Knight Shift Anomalies in Heavy Electron Materials

We have studied the Knight shift $K(\vec r, T)$ and magnetic susceptibility $\chi(T)$ of heavy electron materials, modeled by the infinite U Anderson model with the NCA method. A systematic study of $K(\vec r, T)$ and $\chi(T)$ for different Kondo temperatures $T_0$ (which depends on the hybridization width $\Gamma$) shows a low temperature anomaly (nonlinear relation between $K$ and $\chi$) which increases as the Kondo temperature $T_0$ and distance $r$ increase. We carried out an incoherent lattice sum by adding the $K(\vec r)$ of a few hundred shells of rare earth atoms around a nucleus and compare the numerically calculated results with the experimental results. For CeSn_3, which is a concentrated heavy electron material, both the ^{119}Sn NMR Knight shift and positive muon Knight shift are studied. Also, lattice coherence effects by conduction electron scattering at every rare earth site are included using the average-T matrix approximation. Also NMR Knight shifts for YbCuAl and the proposed quadrupolar Kondo alloy Y_{0.8}U_{0.2}Pd_{3} are studied.Comment: 31 pages of RevTex, 22 Postscript figures, submmitted to PRB, some figures are delete

Identifying the favored mutation in a positive selective sweep.

Most approaches that capture signatures of selective sweeps in population genomics data do not identify the specific mutation favored by selection. We present iSAFE (for "integrated selection of allele favored by evolution"), a method that enables researchers to accurately pinpoint the favored mutation in a large region (∼5 Mbp) by using a statistic derived solely from population genetics signals. iSAFE does not require knowledge of demography, the phenotype under selection, or functional annotations of mutations

Artificial reefs: from ecological processes to fishing enhancement tools

info:eu-repo/semantics/publishedVersio

Genome-wide Identity-by-Descent Sharing among CEPH Siblings

The concept of genetic identity–by–descent (IBD) has markedly advanced our understanding of the genetic similarity among relatives and triggered a number of developments in epidemiological genetics. However, no empirical measure of this relatedness throughout the whole human genome has yet been published. Analyzing highly polymorphic genetic variations from the Centre d’études du polymorphisme humain (CEPH) database, we report the first genome–wide estimation of the mean and variation in IBD sharing among siblings. From 1,522 microsatellite markers spaced at an average of 2.3 cM on 498 sibling pairs, we estimated a mean of 0.4994 and a standard deviation of 0.0395. In order to account for the impact of varying chromosomal lengths and recombination rates, the analysis was also performed at the chromosomal and marker levels and for paternal and maternal DNA separately. Based on the variation, we estimate an “effective number of segregating loci” of around 80 for sibling pairs over the whole genome (i.e., the number of loci that would yield the same standard deviation in IBD sharing if all loci were segregating independently). Finally, we briefly assess the impact of genotyping errors on IBD estimations, compare our results to published theoretical and simulated expectations, and discuss some implications of our findings

Modelling survival and allele complementation in the evolution of genomes with polymorphic loci

We have simulated the evolution of sexually reproducing populations composed of individuals represented by diploid genomes. A series of eight bits formed an allele occupying one of 128 loci of one haploid genome (chromosome). The environment required a specific activity of each locus, this being the sum of the activities of both alleles located at the corresponding loci on two chromosomes. This activity is represented by the number of bits set to zero. In a constant environment the best fitted individuals were homozygous with alleles’ activities corresponding to half of the environment requirement for a locus (in diploid genome two alleles at corresponding loci produced a proper activity). Changing the environment under a relatively low recombination rate promotes generation of more polymorphic alleles. In the heterozygous loci, alleles of different activities complement each other fulfilling the environment requirements. Nevertheless, the genetic pool of populations evolves in the direction of a very restricted number of complementing haplotypes and a fast changing environment kills the population. If simulations start with all loci heterozygous, they stay heterozygous for a long time

Multiple groups of endogenous epsilon-like retroviruses conserved across primates

Several types of cancer in fish are caused by retroviruses, including those responsible for major outbreaks of disease, such as walleye dermal sarcoma virus and salmon swim bladder sarcoma virus. These viruses form a phylogenetic group often described as the epsilonretrovirus genus. Epsilon-like retroviruses have become endogenous retroviruses (ERVs) on several occasions, integrating into germ line cells to become part of the host genome, and sections of fish and amphibian genomes are derived from epsilon-like retroviruses. However, epsilon-like ERVs have been identified in very few mammals. We have developed a pipeline to screen full genomes for ERVs, and using this pipeline, we have located over 800 endogenous epsilon-like ERV fragments in primate genomes. Genomes from 32 species of mammals and birds were screened, and epsilon-like ERV fragments were found in all primate and tree shrew genomes but no others. These viruses appear to have entered the genome of a common ancestor of Old and New World monkeys between 42 million and 65 million years ago. Based on these results, there is an ancient evolutionary relationship between epsilon-like retroviruses and primates. Clearly, these viruses had the potential to infect the ancestors of primates and were at some point a common pathogen in these hosts. Therefore, this result raises questions about the potential of epsilonretroviruses to infect humans and other primates and about the evolutionary history of these retroviruses. IMPORTANCE: Epsilonretroviruses are a group of retroviruses that cause several important diseases in fish. Retroviruses have the ability to become a permanent part of the DNA of their host by entering the germ line as endogenous retroviruses (ERVs), where they lose their infectivity over time but can be recognized as retroviruses for millions of years. Very few mammals are known to have epsilon-like ERVs; however, we have identified over 800 fragments of endogenous epsilon-like ERVs in the genomes of all major groups of primates, including humans. These viruses seem to have circulated and infected primate ancestors 42 to 65 million years ago. We are now interested in how these viruses have evolved and whether they have the potential to infect modern humans or other primates

Analysis of Qa-1bPeptide Binding Specificity and the Capacity of Cd94/Nkg2a to Discriminate between Qa-1–Peptide Complexes

The major histocompatibility complex class Ib protein, Qa-1b, serves as a ligand for murine CD94/NKG2A natural killer (NK) cell inhibitory receptors. The Qa-1b peptide-binding site is predominantly occupied by a single nonameric peptide, Qa-1 determinant modifier (Qdm), derived from the leader sequence of H-2D and L molecules. Five anchor residues were identified in this study by measuring the peptide-binding affinities of substituted Qdm peptides in experiments with purified recombinant Qa-1b. A candidate peptide-binding motif was determined by sequence analysis of peptides eluted from Qa-1 that had been folded in the presence of random peptide libraries or pools of Qdm derivatives randomized at specific anchor positions. The results indicate that Qa-1b can bind a diverse repertoire of peptides but that Qdm has an optimal primary structure for binding Qa-1b. Flow cytometry experiments with Qa-1b tetramers and NK target cell lysis assays demonstrated that CD94/NKG2A discriminates between Qa-1b complexes containing peptides with substitutions at nonanchor positions P4, P5, or P8. Our findings suggest that it may be difficult for viruses to generate decoy peptides that mimic Qdm and raise the possibility that competitive replacement of Qdm with other peptides may provide a novel mechanism for activation of NK cells

Spatially explicit models of dynamic histories: examination of the genetic consequences of Pleistocene glaciation and recent climate change on the American Pika

A central goal of phylogeography is to identify and characterize the processes underlying divergence. One of the biggest impediments currently faced is how to capture the spatiotemporal dynamic under which a species evolved. Here, we described an approach that couples species distribution models (SDMs), demographic and genetic models in a spatiotemporally explicit manner. Analyses of American Pika ( Ochotona princeps ) from the sky islands of the central Rocky Mountains of North America are used to provide insights into key questions about integrative approaches in landscape genetics, population genetics and phylogeography. This includes (i) general issues surrounding the conversion of time‐specific SDMs into simple continuous, dynamic landscapes from past to current, (ii) the utility of SDMs to inform demographic models with deme‐specific carrying capacities and migration potentials as well as (iii) the contribution of the temporal dynamic of colonization history in shaping genetic patterns of contemporary populations. Our results support that the inclusion of a spatiotemporal dynamic is an important factor when studying the impact of distributional shifts on patterns of genetic data. Our results also demonstrate the utility of SDMs to generate species‐specific predictions about patterns of genetic variation that account for varying degrees of habitat specialization and life history characteristics of taxa. Nevertheless, the results highlight some key issues when converting SDMs for use in demographic models. Because the transformations have direct effects on the genetic consequence of population expansion by prescribing how habitat heterogeneity and spatiotemporal variation is related to the species‐specific demographic model, it is important to consider alternative transformations when studying the genetic consequences of distributional shifts.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/92413/1/j.1365-294X.2012.05640.x.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/92413/2/MEC_5640_sm_FigureS3.pd

The reference human nuclear mitochondrial sequences compilation validated and implemented on the UCSC genome browser

<p>Abstract</p> <p>Background</p> <p>Eukaryotic nuclear genomes contain fragments of mitochondrial DNA called NumtS (Nuclear mitochondrial Sequences), whose mode and time of insertion, as well as their functional/structural role within the genome are debated issues. Insertion sites match with chromosomal breaks, revealing that micro-deletions usually occurring at non-homologous end joining <it>loci </it>become reduced in presence of NumtS. Some NumtS are involved in recombination events leading to fragment duplication. Moreover, NumtS are polymorphic, a feature that renders them candidates as population markers. Finally, they are a cause of contamination during human mtDNA sequencing, leading to the generation of false heteroplasmies.</p> <p>Results</p> <p>Here we present RHNumtS.2, the most exhaustive human NumtSome catalogue annotating 585 NumtS, 97% of which were here validated in a European individual and in HapMap samples. The NumtS complete dataset and related features have been made available at the UCSC Genome Browser. The produced sequences have been submitted to INSDC databases. The implementation of the RHNumtS.2 tracks within the UCSC Genome Browser has been carried out with the aim to facilitate browsing of the NumtS tracks to be exploited in a wide range of research applications.</p> <p>Conclusions</p> <p>We aimed at providing the scientific community with the most exhaustive overview on the human NumtSome, a resource whose aim is to support several research applications, such as studies concerning human structural variation, diversity, and disease, as well as the detection of false heteroplasmic mtDNA variants. Upon implementation of the NumtS tracks, the application of the BLAT program on the UCSC Genome Browser has now become an additional tool to check for heteroplasmic artefacts, supported by data available through the NumtS tracks.</p