The phenotype is a major determinant of individual fitness, often mediated through associated variation in behaviour or performance (Arnold, 1983; Kingsolver & Huey, 2003), and is usually the foundation of evolu-

, evolutionary mechanisms where the same genes are used multiple times in the process of building a phenotype. Such gene reuse allows compact representations of very complex phenotypes. Development is a natural choice for implementing indirect encodings, if only because nature itself uses this very process

Phenotypic plasticity is an environmentally based change in the phenotype. Understanding the evolution of adaptive phenotypic plasticity has been hampered by dissenting opinions on the merits of different methods of description, on the underlying genetic mechanisms, and on the way that plasticity

thaliana inbred lines

on transcript abundance, revealing that at least 12% of transcripts show a significant tissue-specific expression bias. By identifying candidate functional variants at 718 quantitative trait loci we show that the molecular nature of functional variants and their position relative to genes vary according

Cellular phenotypes are determined by the differential activity of networks linking coregulated genes. Available methods for the reverse engineering of such networks from genome-wide expression profiles have been successful only in the analysis of lower eukaryotes with simple genomes. Using a new

that are unpredictable at the generational level. Moreover, while evolution operates on the genotype, learning affects the phenotype and phenotypic changes cannot directly modify the genotype. Recently, the study of artificial neural networks that are subjected both to an evolutionary and a lifetime learning process

In nature, phenotypic variability is highly structured with respect to correlations between different phenotypic traits. In this paper we argue that this structuredness can be understood as the outcome of an adaptive process of phenotypic exploration distributions, similar to the adaptation

Cr mice are homozygous for a mutant Lps allele (Lpsd/d) that confers hyporesponsiveness to LPS challenge, and therefore exhibit natural tolerance to its lethal effects. Genetic and physical mapping of 1,345 backcross progeny segregating this mutant phenotype confined Lps to a 0.9-cM interval spanning 1

Biologists often compare average phenotypes of groups of species defined cladistically or on behavioral, ecological, or physiological criteria (e.g., carnivores vs. herbivores, social vs. nonsocial species, endotherms vs. ectotherms). Hypothesis testing typically is accomplished via analysis