Social groups and polarization of aesthetic values from symmetry and complexity.

When deciding what images we prefer, our brain must weigh many aesthetic variables, such as symmetry and complexity. To date, aesthetic research has mainly focused on investigating one variable at a time. In this article, we use symmetry and complexity to study the problem of multi aesthetic-variable interactions. For symmetry and complexity, there are two simple interaction hypotheses. The independence hypothesis proposes that the evaluation of aesthetic variables is mutually independent. Meanwhile, Birkhoff's aesthetic-measure hypothesis predicts that people prefer images high in symmetry and low in complexity, and dislike the opposite. To test these hypotheses, we generated images that systematically varied in levels of symmetry and complexity. We then compared the subjects' preference maps to identify regions of likes and dislikes. Unlike the predictions from these hypotheses, we found that most, but not all subjects, formed two distinct natural clusters, termed "islands," in terms of likes and dislikes. We also found that people with more art exposure were less likely to belong to an island. If someone did belong to an island, their gender influenced which cluster they belonged to. We discuss alternate hypotheses, possible mechanisms for the occurrence of islands, and their possible social implications.

Decreasing mutant ATXN1 nuclear localization improves a spectrum of SCA1-like phenotypes and brain region transcriptomic profiles.

Spinocerebellar ataxia type 1 (SCA1) is a dominant trinucleotide repeat neurodegenerative disease characterized by motor dysfunction, cognitive impairment, and premature death. Degeneration of cerebellar Purkinje cells is a frequent and prominent pathological feature of SCA1. We previously showed that transport of ATXN1 to Purkinje cell nuclei is required for pathology, where mutant ATXN1 alters transcription. To examine the role of ATXN1 nuclear localization broadly in SCA1-like disease pathogenesis, CRISPR-Cas9 was used to develop a mouse with an amino acid alteration (K772T) in the nuclear localization sequence of the expanded ATXN1 protein. Characterization of these mice indicates that proper nuclear localization of mutant ATXN1 contributes to many disease-like phenotypes including motor dysfunction, cognitive deficits, and premature lethality. RNA sequencing analysis of genes with expression corrected to WT levels in Atxn1175QK772T/2Q mice indicates that transcriptomic aspects of SCA1 pathogenesis differ between the cerebellum, brainstem, cerebral cortex, hippocampus, and striatum.