The Mu transposon system of maize is highly active, with each of the ∼50–100 copies transposing on average once each generation. The approximately one dozen distinct Mu transposons contain highly similar ∼215 bp terminal inverted repeats (TIRs) and generate 9-bp target site duplications (TSDs) upon insertion. Using a novel genome walking strategy that uses these conserved TIRs as primer binding sites, Mu insertion sites were amplified from Mu stocks and sequenced via 454 technology. 94% of ∼965,000 reads carried Mu TIRs, demonstrating the specificity of this strategy. Among these TIRs, 21 novel Mu TIRs were discovered, revealing additional complexity of the Mu transposon system. The distribution of >40,000 non-redundant Mu insertion sites was strikingly non-uniform, such that rates increased in proportion to distance from the centromere. An identified putative Mu transposase binding consensus site does not explain this non-uniformity. An integrated genetic map containing more than 10,000 genetic markers was constructed and aligned to the sequence of the maize reference genome. Recombination rates (cM/Mb) are also strikingly non-uniform, with rates increasing in proportion to distance from the centromere. Mu insertion site frequencies are strongly correlated with recombination rates. Gene density does not fully explain the chromosomal distribution of Mu insertion and recombination sites, because pronounced preferences for the distal portion of chromosome are still observed even after accounting for gene density. The similarity of the distributions of Mu insertions and meiotic recombination sites suggests that common features, such as chromatin structure, are involved in site selection for both Mu insertion and meiotic recombination. The finding that Mu insertions and meiotic recombination sites both concentrate in genomic regions marked with epigenetic marks of open chromatin provides support for the hypothesis that open chromatin enhances rates of both Mu insertion and meiotic recombination.

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Objective This study aimed to determine the effects of diet‐induced paternal obesity on cognitive function in mice offspring. Methods Male mice (F0) were randomized to receive either a control diet (10 kcal% fat) or a high‐fat diet (HFD; 60 kcal% fat) for 10 weeks before being mated with normal females to generate F1 offspring. Male F1 offspring were mated with normal females to generate F2 offspring. Behavioral tests were used to assess cognitive functions in F1 and F2 offspring. Reduced representation bisulfite sequencing was used to the explore mechanisms of epigenetic inheritance. Results HFD‐induced paternal obesity resulted in cognitive impairments in F1 offspring, potentially due, at least in part, to increased methylation of the BDNF gene promoter, which was inherited from F0 spermatozoa. BDNF/tyrosine receptor kinase B signaling was associated with cognitive impairments in HFD‐fed F1 offspring. However, there were no significant changes in F2 offspring. Conclusions The findings provide evidence of intergenerational effects of paternal obesity on cognitive function in offspring occurring via epigenetic spermatozoan modifications.

Most companies maintain warranty databases for purposes of nancial reporting and warranty expense forecasting. In some cases, there are attempts to extract engineering information (e.g., on the reliability of components) from such databases. Another important application is to use warranty data to detect potentially serious eld reliability problems as early as possible. When a serious problem arises, the existence of the problem will eventually be obvious. Early detection of serious problems through the use of sensitive statistical methods, allowing early action to mitigate potential reliability problems, could save large amounts of money and product goodwill. This article describes a detection procedure that has been designed for this purpose. In addition to the statistical decision rules, we suggest graphical tools for illustrating and describing the particular information in the data that caused the potential problem to be agged. The methods are illustrated using data from an automobile warranty database.

Wu and Hamada recommend selecting resolution IV designs with the maximum number of clear two-factor interactions (2FIs), called MaxC2 designs. In this paper, we develop a method by using graphical representations, combinatorial and group-theoretic arguments to prove if a given design is a MaxC2 design. In particular, we show that all known minimum aberration designs with resolution IV are MaxC2 designs (except in six cases) and that the second 2 9−4 , 2 13−7 , 2 16−10 and 2 17−11 designs given in Wu and Hamada are MaxC2 designs. The method also enables us to identify new MaxC2 designs that are too large to be verified by computer search.