When do descriptive regularities become prescriptive norms? We examined children's and adults' use of group regularities to make prescriptive judgments, employing novel groups that engaged in morally neutral behaviors. Participants were introduced to conforming or non-conforming individuals. Children negatively evaluated non-conformity, with negative evaluations declining with age. These effects were replicable across competitive and cooperative intergroup contexts and stemmed from reasoning about group regularities rather than reasoning about individual regularities. These data provide new insights into children's group concepts and have (...) important implications for understanding the development of stereotyping and norm enforcement. (shrink)

Psychological essentialism is a folk theory characterized by the belief that a causal internal essence or force gives rise to the common outward behaviors or attributes of a category's members. In two studies, we investigated whether 4- to 7-year-old children evidenced essentialist reasoning about heart transplants by asking them to predict whether trading hearts with an individual would cause them to take on the donor's attributes. Control conditions asked children to consider the effects of trading money with an individual. Results (...) indicated that children reasoned according to essentialism, predicting more transfer of attributes in the transplant condition versus the non-bodily money control. Children also endorsed essentialist transfer of attributes even when they did not believe that a transplant would change the recipient's category membership. This finding runs counter to predictions from a strong interpretation of the “minimalist” position, an alternative to essentialism. (shrink)

The gain of a selective advantage in cancer as well as the establishment of complex traits during evolution require multiple genetic alterations, but how these mutations accumulate over time is currently unclear. There is increasing evidence that a mutator phenotype perpetuates the development of many human cancers. While in some cases the increased mutation rate is the result of a genetic disruption of DNA repair and replication or environmental exposures, other evidence suggests that endogenous DNA damage induced by AID/APOBEC cytidine (...) deaminases can result in transient localized hypermutation generating simultaneous, closely spaced (i.e. “clustered”) multiple mutations. Here, we discuss mechanisms that lead to mutation cluster formation, the biological consequences of their formation in cancer and evidence suggesting that APOBEC mutagenesis can also occur genome‐wide. This raises the possibility that dysregulation of these enzymes may enable rapid malignant transformation by increasing mutation rates without the loss of fitness associated with permanent mutators. (shrink)

Somatic mutations arising in human skin cancers are heterogeneously distributed across the genome, meaning that certain genomic regions (e.g., heterochromatin or transcription factor binding sites) have much higher mutation densities than others. Regional variations in mutation rates are typically not a consequence of selection, as the vast majority of somatic mutations in skin cancers are passenger mutations that do not promote cell growth or transformation. Instead, variations in DNA repair activity, due to chromatin organization and transcription factor binding, have been (...) proposed to be a primary driver of mutational heterogeneity in melanoma. However, as discussed in this review here, recent studies indicate that chromatin organization and transcription factor binding also significantly modulate the rate at which UV lesions form in DNA. The authors propose that local variations in lesion susceptibility may be an important driver of mutational hotspots in melanoma and other skin cancers, particularly at binding sites for ETS transcription factors. (shrink)