What Color Is Your Anger? Assessing Color-Emotion Pairings in English Speakers

Do English-speakers think about anger as “red” and sadness as “blue”? Some theories of emotion suggests that color(s)—like other biologically-derived signals- should be reliably paired with an emotion, and that colors should differentiate across emotions. We assessed consistency and specificity for color-emotion pairings among English-speaking adults. In study 1, participants (n = 73) completed an online survey in which they could select up to three colors from 23 colored swatches (varying hue, saturation, and light) for each of ten emotion words. In study 2, different participants (n = 52) completed a similar online survey except that we added additional emotions and colors (which better sampled color space). Participants in both studies indicated the strength of the relationship between a selected color(s) and the emotion. In study 1, four of the ten emotions showed consistency, and about one-third of the colors showed specificity, yet agreement was low-to-moderate among raters even in these cases. When we resampled our data, however, none of these effects were likely to replicate with statistical confidence. In study 2, only two of 20 emotions showed consistency, and three colors showed specificity. As with the first study, no color-emotion pairings were both specific and consistent. In addition, in study 2, we found that saturation and lightness, and to a lesser extent hue, predicted color-emotion agreement rather than perceived color. The results suggest that previous studies which report emotion-color pairings are likely best thought of experiment-specific. The results are discussed with respect to constructionist theories of emotion

Whole-Exome Sequencing Identifies Homozygous AFG3L2 Mutations in a Spastic Ataxia-Neuropathy Syndrome Linked to Mitochondrial m-AAA Proteases

We report an early onset spastic ataxia-neuropathy syndrome in two brothers of a consanguineous family characterized clinically by lower extremity spasticity, peripheral neuropathy, ptosis, oculomotor apraxia, dystonia, cerebellar atrophy, and progressive myoclonic epilepsy. Whole-exome sequencing identified a homozygous missense mutation (c.1847G>A; p.Y616C) in AFG3L2, encoding a subunit of an m-AAA protease. m-AAA proteases reside in the mitochondrial inner membrane and are responsible for removal of damaged or misfolded proteins and proteolytic activation of essential mitochondrial proteins. AFG3L2 forms either a homo-oligomeric isoenzyme or a hetero-oligomeric complex with paraplegin, a homologous protein mutated in hereditary spastic paraplegia type 7 (SPG7). Heterozygous loss-of-function mutations in AFG3L2 cause autosomal-dominant spinocerebellar ataxia type 28 (SCA28), a disorder whose phenotype is strikingly different from that of our patients. As defined in yeast complementation assays, the AFG3L2Y616C gene product is a hypomorphic variant that exhibited oligomerization defects in yeast as well as in patient fibroblasts. Specifically, the formation of AFG3L2Y616C complexes was impaired, both with itself and to a greater extent with paraplegin. This produced an early-onset clinical syndrome that combines the severe phenotypes of SPG7 and SCA28, in additional to other “mitochondrial” features such as oculomotor apraxia, extrapyramidal dysfunction, and myoclonic epilepsy. These findings expand the phenotype associated with AFG3L2 mutations and suggest that AFG3L2-related disease should be considered in the differential diagnosis of spastic ataxias