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Daniel Gianola

Publications and source records attributed to Daniel Gianola.

6 recordsLinked to original sources

On marker-assisted prediction of genetic value: beyond the ridge.

Marked-assisted genetic improvement of agricultural species exploits statistical dependencies in the joint distribution of marker genotypes and quantitative traits. An issue is how molecular (e.g., dense marker maps) and phenotypic information (e.g., some measure of yield in plants) is to be used for predicting the genetic value of candidates for selection. Multiple regression, selection index techniques, best linear unbiased prediction, and ridge regression of phenotypes on marker genotypes have been suggested, as well as more elaborate methods. Here, phenotype-marker associations are modeled hierarchically via multilevel models including chromosomal effects, a spatial covariance of marked effects within chromosomes, background genetic variability, and family heterogeneity. Lorenz curves and Gini coefficients are suggested for assessing the inequality of the contribution of different marked effects to genetic variability. Classical and Bayesian methods are presented. The Bayesian approach includes a Markov chain Monte Carlo implementation. The generality and flexibility of the Bayesian method is illustrated when a Lorenz curve is to be inferred.

Animals↗

Combining gene expression and molecular marker information for mapping complex trait genes: a simulation study.

A method for mapping complex trait genes using cDNA microarray and molecular marker data jointly is presented and illustrated via simulation. We introduce a novel approach for simulating phenotypes and genotypes conditionally on real, publicly available, microarray data. The model assumes an underlying continuous latent variable (liability) related to some measured cDNA expression levels. Partial least-squares logistic regression is used to estimate the liability under several scenarios where the level of gene interaction, the gene effect, and the number of cDNA levels affecting liability are varied. The results suggest that: (1) the usefulness of microarray data for gene mapping increases when both the number of cDNA levels in the underlying liability and the QTL effect decrease and when genes are coexpressed; (2) the correlation between estimated and true liability is large, at least under our simulation settings; (3) it is unlikely that cDNA clones identified as significant with partial least squares (or with some other technique) are the true responsible cDNAs, especially as the number of clones in the liability increases; (4) the number of putatively significant cDNA levels increases critically if cDNAs are coexpressed in a cluster (however, the proportion of true causal cDNAs within the significant ones is similar to that in a no-coexpression scenario); and (5) data reduction is needed to smooth out the variability encountered in expression levels when these are analyzed individually.

Chromosome Mapping↗

A Bayesian approach for constructing genetic maps when markers are miscoded.

The advent of molecular markers has created opportunities for a better understanding of quantitative inheritance and for developing novel strategies for genetic improvement of agricultural species, using information on quantitative trait loci (QTL). A QTL analysis relies on accurate genetic marker maps. At present, most statistical methods used for map construction ignore the fact that molecular data may be read with error. Often, however, there is ambiguity about some marker genotypes. A Bayesian MCMC approach for inferences about a genetic marker map when random miscoding of genotypes occurs is presented, and simulated and real data sets are analyzed. The results suggest that unless there is strong reason to believe that genotypes are ascertained without error, the proposed approach provides more reliable inference on the genetic map.

Bayes Theorem↗

Multivariate Bayesian analysis of Gaussian, right censored Gaussian, ordered categorical and binary traits using Gibbs sampling.

A fully Bayesian analysis using Gibbs sampling and data augmentation in a multivariate model of Gaussian, right censored, and grouped Gaussian traits is described. The grouped Gaussian traits are either ordered categorical traits (with more than two categories) or binary traits, where the grouping is determined via thresholds on the underlying Gaussian scale, the liability scale. Allowances are made for unequal models, unknown covariance matrices and missing data. Having outlined the theory, strategies for implementation are reviewed. These include joint sampling of location parameters; efficient sampling from the fully conditional posterior distribution of augmented data, a multivariate truncated normal distribution; and sampling from the conditional inverse Wishart distribution, the fully conditional posterior distribution of the residual covariance matrix. Finally, a simulated dataset was analysed to illustrate the methodology. This paper concentrates on a model where residuals associated with liabilities of the binary traits are assumed to be independent. A Bayesian analysis using Gibbs sampling is outlined for the model where this assumption is relaxed.

Bayes Theorem↗

Longitudinal random effects models for genetic analysis of binary data with application to mastitis in dairy cattle.

A Bayesian analysis of longitudinal mastitis records obtained in the course of lactation was undertaken. Data were 3341 test-day binary records from 329 first lactation Holstein cows scored for mastitis at 14 and 30 days of lactation and every 30 days thereafter. First, the conditional probability of a sequence for a given cow was the product of the probabilities at each test-day. The probability of infection at time t for a cow was a normal integral, with its argument being a function of "fixed" and "random" effects and of time. Models for the latent normal variable included effects of: (1) year-month of test + a five-parameter linear regression function ("fixed", within age-season of calving) + genetic value of the cow + environmental effect peculiar to all records of the same cow + residual. (2) As in (1), but with five parameter random genetic regressions for each cow. (3) A hierarchical structure, where each of three parameters of the regression function for each cow followed a mixed effects linear model. Model 1 posterior mean of heritability was 0.05. Model 2 heritabilities were: 0.27, 0.05, 0.03 and 0.07 at days 14, 60, 120 and 305, respectively. Model 3 heritabilities were 0.57, 0.16, 0.06 and 0.18 at days 14, 60, 120 and 305, respectively. Bayes factors were: 0.011 (Model 1/Model 2), 0.017 (Model 1/Model 3) and 1.535 (Model 2/Model 3). The probability of mastitis for an "average" cow, using Model 2, was: 0.06, 0.05, 0.06 and 0.07 at days 14, 60, 120 and 305, respectively. Relaxing the conditional independence assumption via an autoregressive process (Model 2) improved the results slightly.

Animals↗

Mixture model for inferring susceptibility to mastitis in dairy cattle: a procedure for likelihood-based inference.

A Gaussian mixture model with a finite number of components and correlated random effects is described. The ultimate objective is to model somatic cell count information in dairy cattle and to develop criteria for genetic selection against mastitis, an important udder disease. Parameter estimation is by maximum likelihood or by an extension of restricted maximum likelihood. A Monte Carlo expectation-maximization algorithm is used for this purpose. The expectation step is carried out using Gibbs sampling, whereas the maximization step is deterministic. Ranking rules based on the conditional probability of membership in a putative group of uninfected animals, given the somatic cell information, are discussed. Several extensions of the model are suggested.

Algorithms↗