We define a new class of coloured graphical models, called regulatory graphs. These graphs have their own distinctive formal semantics and can directly represent typical qualitative hypotheses about regulatory processes like those described by various biological mechanisms. They admit an embellishment into classes of probabilistic statistical models and so standard Bayesian methods of model selection can be used to choose promising candidate explanations of regulation. Regulation is modelled by the existence of a deterministic relationship between the longitudinal series of observations labelled by the receiving vertex and the donating one. This class contains longitudinal cluster models as a degenerate graph. Edge colours directly distinguish important features of the mechanism like inhibition and excitation and graphs are often cyclic. With appropriate distributional assumptions, because the regulatory relationships map onto each other through a group structure, it is possible to define a conditional conjugate analysis. This means that even when the model space is huge it is nevertheless feasible, using a Bayesian MAP search, to a discover regulatory network with a high Bayes Factor score. We also show that, like the class of Bayesian Networks, regulatory graphs also admit a formal but distinctive causal algebra. The topology of the graph then represents collections of hypotheses about the predicted effect of controlling the process by tearing out message passers or forcing them to transmit certain signals. We illustrate our methods on a microarray experiment measuring the expression of thousands of genes as a longitudinal series where the scientific interest lies in the circadian regulation of these plants.

This paper considers inference of causal structure in a class of graphical models called conditional DAGs. These are directed acyclic graph (DAG) models with two kinds of variables, primary and secondary. The secondary variables are used to aid in the estimation of the structure of causal relationships between the primary variables. We prove that, under certain assumptions, such causal structure is identifiable from the joint observational distribution of the primary and secondary variables. We give causal semantics for the model class, put forward a score-based approach for estimation and establish consistency results. Empirical results demonstrate gains compared with formulations that treat all variables on an equal footing, or that ignore secondary variables. The methodology is motivated by applications in biology that involve multiple data types and is illustrated here using simulated data and in an analysis of molecular data from the Cancer Genome Atlas.

The search for a useful explanatory model based on a Bayesian Network (BN) now has a long and successful history. However, when the dependence structure between the variables of the problem is asymmetric then this cannot be captured by the BN. The Chain Event Graph (CEG) provides a richer class of models which incorporates these types of dependence structures as well as retaining the property that conclusions can be easily read back to the client. We demonstrate on a real health study how the CEG leads us to promising higher scoring models and further enables us to make more refined conclusions than can be made from the BN. Further we show how these graphs can express causal hypotheses about possible interventions that could be enforced.