Efficient Bayesian Inference for Generalized Bradley-Terry Models

The Bradley-Terry model is a popular approach to describe probabilities of the possible outcomes when elements of a set are repeatedly compared with one another in pairs. It has found many applications including animal behaviour, chess ranking and multiclass classification. Numerous extensions of the basic model have also been proposed in the literature including models with ties, multiple comparisons, group comparisons and random graphs. From a computational point of view, Hunter (2004) has proposed efficient iterative MM (minorization-maximization) algorithms to perform maximum likelihood estimation for these generalized Bradley-Terry models whereas Bayesian inference is typically performed using MCMC (Markov chain Monte Carlo) algorithms based on tailored Metropolis-Hastings (M-H) proposals. We show here that these MM\ algorithms can be reinterpreted as special instances of Expectation-Maximization (EM) algorithms associated to suitable sets of latent variables and propose some original extensions. These latent variables allow us to derive simple Gibbs samplers for Bayesian inference. We demonstrate experimentally the efficiency of these algorithms on a variety of applications

Dissecting high-dimensional phenotypes with bayesian sparse factor analysis of genetic covariance matrices.

Quantitative genetic studies that model complex, multivariate phenotypes are important for both evolutionary prediction and artificial selection. For example, changes in gene expression can provide insight into developmental and physiological mechanisms that link genotype and phenotype. However, classical analytical techniques are poorly suited to quantitative genetic studies of gene expression where the number of traits assayed per individual can reach many thousand. Here, we derive a Bayesian genetic sparse factor model for estimating the genetic covariance matrix (G-matrix) of high-dimensional traits, such as gene expression, in a mixed-effects model. The key idea of our model is that we need consider only G-matrices that are biologically plausible. An organism's entire phenotype is the result of processes that are modular and have limited complexity. This implies that the G-matrix will be highly structured. In particular, we assume that a limited number of intermediate traits (or factors, e.g., variations in development or physiology) control the variation in the high-dimensional phenotype, and that each of these intermediate traits is sparse - affecting only a few observed traits. The advantages of this approach are twofold. First, sparse factors are interpretable and provide biological insight into mechanisms underlying the genetic architecture. Second, enforcing sparsity helps prevent sampling errors from swamping out the true signal in high-dimensional data. We demonstrate the advantages of our model on simulated data and in an analysis of a published Drosophila melanogaster gene expression data set