the promoter methylation timing associated with gene expression dysregulation in the embryo was also identified. Decay Whereas the mutation rate in a given 100-base gene may be 10−7 per generation, epigenes may "mutate" several times per generation or may be fixed for many generations. This raises the question: do changes in epigene frequencies constitute evolution? Rapidly decaying epigenetic effects on phenotypes (i.e. lasting less than three generations) may explain some of the residual variation in phenotypes after genotype and environment are accounted for. However, distinguishing these short-term effects from the effects of the maternal environment on early ontogeny remains a challenge. Contribution to phenotypes The relative importance of genetic and epigenetic inheritance is subject to debate. Though hundreds of examples of epigenetic modification of phenotypes have been published, few studies have been conducted outside of the laboratory setting. Therefore, the interactions of genes and epigenes with the environment cannot be inferred despite the central role of environment in natural selection. Experimental methodologies for manipulating epigenetic mechanisms are nascent (e.g.) and will need rigorous demonstration before studies explicitly testing the relative contributions of genotype, environment, and epigenotype are feasible. In plants Studies concerning transgenerational epigenetic inheritance in plants have been reported as early as the 1950s. One of the earliest and best characterized examples of this is b1 paramutation in maize. The b1 gene encodes a basic helix-loop-helix transcription factor that is involved in the anthocyanin production pathway. When the b1 gene is expressed, the plant accumulates anthocyanin within its tissues, leading to a purple coloration of those tissues. The B-I allele (for B-Intense) has high expression of b1 resulting in the dark pigmentation of the sheath and husk tissues while the B' (pronounced B-prime) allele has low expression of b1 resulting in low pigmentation in those tissues. When homozygous B-I parents are crossed to homozygous B', the resultant F1 offspring all display low pigmentation which is due to gene silencing of b1. Unexpectedly, when F1 plants are self-crossed, the resultant F2 generation all display low pigmentation and have low levels of b1 expression. Furthermore, when any F2 plant (including those that are genetically homozygous for B-I) are crossed to homozygous B-I, the offspring will all display low pigmentation and expression of b1. The lack of darkly pigmented individuals in the F2 progeny is an example of non-Mendelian inheritance and further research has suggested that the B-I allele is converted to