6,684 research outputs found
The evolution of genetic architectures underlying quantitative traits
In the classic view introduced by R. A. Fisher, a quantitative trait is
encoded by many loci with small, additive effects. Recent advances in QTL
mapping have begun to elucidate the genetic architectures underlying vast
numbers of phenotypes across diverse taxa, producing observations that
sometimes contrast with Fisher's blueprint. Despite these considerable
empirical efforts to map the genetic determinants of traits, it remains poorly
understood how the genetic architecture of a trait should evolve, or how it
depends on the selection pressures on the trait. Here we develop a simple,
population-genetic model for the evolution of genetic architectures. Our model
predicts that traits under moderate selection should be encoded by many loci
with highly variable effects, whereas traits under either weak or strong
selection should be encoded by relatively few loci. We compare these
theoretical predictions to qualitative trends in the genetics of human traits,
and to systematic data on the genetics of gene expression levels in yeast. Our
analysis provides an evolutionary explanation for broad empirical patterns in
the genetic basis of traits, and it introduces a single framework that unifies
the diversity of observed genetic architectures, ranging from Mendelian to
Fisherian.Comment: Minor changes in the text; Added supplementary materia
Protein Mobility in the Cytoplasm of Escherichia coli
The rate of protein diffusion in bacterial cytoplasm may constrain a variety of cellular functions and limit the rates of many biochemical reactions in vivo. In this paper, we report noninvasive measurements of the apparent diffusion coefficient of green fluorescent protein (GFP) in the cytoplasm of Escherichia coli. These measurements were made in two ways: by photobleaching of GFP fluorescence and by photoactivation of a red-emitting fluorescent state of GFP (M. B. Elowitz, M. G. Surette, P. E. Wolf, J. Stock, and S. Leibler, Curr. Biol. 7:809-812, 1997). The apparent diffusion coefficient, Da, of GFP in E. coli DH5alpha was found to be 7.7 ± 2.5 ”m^2/s. A 72-kDa fusion protein composed of GFP and a cytoplasmically localized maltose binding protein domain moves more slowly, with Da of 2.5 ± 0.6 ”m^2/s. In addition, GFP mobility can depend strongly on at least two factors: first, Da is reduced to 3.6 ± 0.7 ”m^2/s at high levels of GFP expression; second, the addition to GFP of a small tag consisting of six histidine residues reduces Da to 4.0 ± 2.0 ”m^2/s. Thus, a single effective cytoplasmic viscosity cannot explain all values of Da reported here. These measurements have implications for the understanding of intracellular biochemical networks
Spontaneous coronary artery dissection: cases at the CHUV between 2012 and 2014
Introduction
Spontaneous coronary artery dissection (SCAD) is a rare entity. It consists of the separation of the several layers of the coronary arteries, with or without an intimal flap1-3. In other words, at this time two physiopathological processes are identified: the first one is the rupture of the intimal and often the medial layers, as well as the engulfment of blood in that false lumen witch then compress the true lumen leading to a ischemia of the coronary artery's territory. The second one implies a probable rupture of the vasa vasorum, which leads to an intra-Âââmural hematoma, without rupture of the coronary artery's layers. In that situation there is no communication between the true and the false lumen1,2,4,5. Some studies include SCAD patients with underlying artheromtous disease, but commonly SCAD is considered as a synonym for a non-Âââ atherosclerotic coronary arterie's dissection1-4,6
- âŠ