Clustering with partial information

The Correlation Clustering problem, also known as the Cluster Editing problem, seeks to edit a given graph by adding and deleting edges to obtain a collection of vertex-disjoint cliques, such that the editing cost is minimized. The Edge Clique Partitioning problem seeks to partition the edges of a given graph into edge-disjoint cliques, such that the number of cliques is minimized. Both problems are known to be NP-hard, and they have been previously studied with respect to approximation and fixed parameter tractability. In this paper we study these two problems in a more general setting that we term fuzzy graphs, where the input graphs may have missing information, meaning that whether or not there is an edge between some pairs of vertices of the input graph can be undecided. For fuzzy graphs the Correlation Clustering and Edge Clique Partitioning problems have previously been studied only with respect to approximation. Here we give parameterized algorithms based on kernelization for both problems. We prove that the Correlation Clustering problem is fixed-parameter tractable on fuzzy graphs when parameterized by (k,r), where k is the editing cost and r is the minimum number of vertices required to cover the undecided edges. In particular we show that it has a polynomial-time reduction to a problem kernel on O(k² + r) vertices. We provide an analogous result for the Edge Clique Partitioning problem on fuzzy graphs. Using (k,r) as parameters, where k bounds the size of the partition, and r is the minimum number of vertices required to cover the undecided edges, we describe a polynomial-time kernelization to a problem kernel on O(k⁴‧3r) vertices. This implies fixed-parameter tractability for this parameterization. Furthermore we also show that parameterizing only by the number of cliques k, is not enough to obtain fixed-parameter tractability. The problem remains, in fact, NP-hard for each fixed k > 2

Identifiers for the 21st century: How to design, provision, and reuse persistent identifiers to maximize utility and impact of life science data.

In many disciplines, data are highly decentralized across thousands of online databases (repositories, registries, and knowledgebases). Wringing value from such databases depends on the discipline of data science and on the humble bricks and mortar that make integration possible; identifiers are a core component of this integration infrastructure. Drawing on our experience and on work by other groups, we outline 10 lessons we have learned about the identifier qualities and best practices that facilitate large-scale data integration. Specifically, we propose actions that identifier practitioners (database providers) should take in the design, provision and reuse of identifiers. We also outline the important considerations for those referencing identifiers in various circumstances, including by authors and data generators. While the importance and relevance of each lesson will vary by context, there is a need for increased awareness about how to avoid and manage common identifier problems, especially those related to persistence and web-accessibility/resolvability. We focus strongly on web-based identifiers in the life sciences; however, the principles are broadly relevant to other disciplines

Fine-mapping of 150 breast cancer risk regions identifies 191 likely target genes

International audienceGenome-wide association studies have identified breast cancer risk variants in over 150 genomic regions, but the mechanisms underlying risk remain largely unknown. These regions were explored by combining association analysis with in silico genomic feature annotations. We defined 205 independent risk-associated signals with the set of credible causal variants in each one. In parallel, we used a Bayesian approach (PAINTOR) that combines genetic association, linkage disequilibrium and enriched genomic features to determine variants with high posterior probabilities of being causal. Potentially causal variants were significantly over-represented in active gene regulatory regions and transcription factor binding sites. We applied our INQUSIT pipeline for prioritizing genes as targets of those potentially causal variants, using gene expression (expression quantitative trait loci), chromatin interaction and functional annotations. Known cancer drivers, transcription factors and genes in the developmental, apoptosis, immune system and DNA integrity checkpoint gene ontology pathways were over-represented among the highest-confidence target genes