Genetic Relationships of Crown Rust Resistance, Grain Yield, Test Weight, and Seed Weight in Oat

Integrating selection for agronomic performance and quantitative resistance to crown rust, caused by Puccinia coronata Corda var. avenae W.P. Fraser & Ledingham, in oat (Avena sativa L.) requires an understanding of their genetic relationships. This study was conducted to investigate the genetic relationships of crown rust resistance, grain yield, test weight, and seed weight under both inoculated and fungicide-treated conditions. A Design II mating was performed between 10 oat lines with putative partial resistance to crown rust and nine lines with superior grain yield and grain quality potential. Progenies from this mating were evaluated in both crown rust-inoculated and fungicide-treated plots in four Iowa environments to estimate genetic effects and phenotypic correlations between crown rust resistance and grain yield, seed weight, and test weight under either infection or fungicide-treated conditions. Lines from a random-mated population derived from the same parents were evaluated in three Iowa environments to estimate heritabilities of, and genetic correlations between, these traits. Resistance to crown rust, as measured by area under the disease progress curve (AUDPC), was highly heritable (H = 0.89 on an entry-mean basis), and was favorably correlated with grain yield, seed weight, and test weight measured in crown rust-inoculated plots. AUDPC was unfavorably correlated or uncorrelated with grain yield, test weight, and seed weight measured in fungicide-treated plots. To improve simultaneously crown rust resistance, grain yield, and seed weight under both lower and higher levels of crown rust infection, an optimum selection index can be developed with the genetic parameters estimated in this stud

The effects of artificial selection on the maize genome

Domestication promotes rapid phenotypic evolution through artificial selection. We investigated the genetic history by which the wild grass teosinte (Zea mays ssp. parviglumis) was domesticated into modern maize (Z. mays ssp. mays). Analysis of single-nucleotide polymorphisms in 774 genes indicates that 2 to 4% of these genes experienced artificial selection. The remaining genes retain evidence of a population bottleneck associated with domestication. Candidate selected genes with putative function in plant growth are clustered near quantitative trait loci that contribute to phenotypic differences between maize and teosinte. If we assume that our sample of genes is representative, ∼1200 genes throughout the maize genome have been affected by artificial selection

A unified mixed model method for association mapping that accounts for multiple levels of relatedness

As population structure can result in spurious associations, it has constrained the use of association studies in human and plant genetics. Association mapping, however, holds great promise if true signals of functional association can be separated from the vast number of false signals generated by population structure1,2. We have developed a unified mixed-model approach to account for multiple levels of relatedness simultaneously as detected by random genetic markers. We applied this new approach to two samples: a family-based sample of 14 human families, for quantitative gene expression dissection, and a sample of 277 diverse maize inbred lines with complex familial relationships and population structure, for quantitative trait dissection. Our method demonstrates improved control of both type I and type II error rates over other methods. As this new method crosses the boundary between family-based and structured association samples, it provides a powerful complement to currently available methods for association mapping

Calcium in the heart: when it's good, it's very very good, but when it's bad, it's horrid

Ca(2+) increases in the heart control both contraction and transcription. To accommodate a short-term increased cardiovascular demand, neurohormonal modulators acting on the cardiac pacemaker and individual myocytes induce an increase in frequency and magnitude of myocyte contraction respectively. Prolonged, enhanced function results in hypertrophic growth of the heart, which is initially also associated with greater Ca(2+) signals and cardiac contraction. As a result of disease, however, hypertrophy progresses to a decompensated state and Ca(2+) signalling capacity and cardiac output are reduced. Here, the role that Ca(2+) plays in the induction of hypertrophy as well as the impact that cardiac hypertrophy and failure has on Ca(2+) fluxes will be discussed