Pre-existing visual preference for white dot patterns in estrildid finches: a comparative study of a multi-species experiment.

The diverse characteristics of animal signal designs can be explained by the sensory bias hypothesis, which suggests that natural selection shapes sensory bias and preferences associated with signal design. Traditionally, this hypothesis has focused on female sensory biases and male sexual traits. However, considering shared sensory systems between males and females in non-sexual contexts, existing sensory bias possibly contributes to the evolution of shared social and sexual traits. Our previous studies on the family Estrildidae supported this idea. An evolutionary relationship probably existed between diet and white dot plumage, and a species of estrildid finches showed a visual preference for white dot patterns. To investigate this further, we examined hunger-related visual preferences using phylogenetic comparative methods and behavioural experiments. Specifically, we compared the gazing responses of 12 species of estrildids to monochromatic printed white dot and stripe patterns, considering their phylogenetic relationships. The results support our idea that the common estrildid ancestor had a hunger-related visual preference for white dot patterns. Subject species generally preferred white dots to stripes. Furthermore, males and females showed a similar preference towards dots. Our findings provide insights into the role of sensory bias in the evolution of mutual ornamentation.

Star finches Neochmia ruficauda have a visual preference for white dot patterns: a possible case of trypophilia.

Many animals have polka dot patterns on their body surface, some of which are known to have signalling functions; however, their evolutionary origins remain unclear. Dot patterns can trigger a fear response (trypophobia) in humans and are known to function as aposematic signals in non-human animals, suggesting that dots may deserve attention for biological reasons. Interestingly in many birds, plumage dot patterns serve for social/sexual signalling. To understand their evolution, we have focused on the sensory bias hypothesis, which predicts the role of pre-existing sensory preference driven by natural selection in shaping signal design. Our previous phylogenetic comparative study supported the hypothesis and showed that diet-driven visual preference promoted the evolution of plumage patterns, as there was an evolutionary correlation between termite-eating (white roundish gregarious prey) and the presence of plumage dot patterns in species of the family Estrildidae. This suggests that these species possess an intrinsic preference for dots. To test this, we compared the responses of an Estrildid species with dot plumage pattern (star finch Neochmia ruficauda) towards simultaneously presented monochrome-printed white dot vs white stripe patterns under both food-deprived and -supplied conditions. Overall, star finches preferred dots to stripes. They showed foraging-like behaviours almost only toward dots when hungry and gazed at dots frequently even when food was available, suggesting both hunger-related and hunger-neutral dot preferences. These results are rather surprising, given how strongly the subjects were attracted to abstract dot patterns without organic structure, but provided good support for the sensory bias hypothesis.

Cold-sensitive phenotypes of a yeast null mutant of ARV1 support its role as a GPI flippase.

Glycosylphosphatidylinositol (GPI) is synthesized in the endoplasmic reticulum (ER) and added onto proteins to form GPI-anchored proteins. Among the many proteins involved in this process, ACAT-related enzyme-2 required for viability 1 (Arv1) is a candidate, functioning as a flippase that translocates GPI intermediates from the cytoplasmic side into the luminal side of the ER membranes. Here, we show that the deletion of the ARV1 gene in yeast leads to cold-sensitive defects in cell growth and GPI anchor synthesis. Furthermore, complementation assays show that the overexpression of a missense human ARV1-G189R mutant does not completely restore the cold-sensitive phenotypes of the yeast arv1 mutant. Our results support the proposed role of Arv1 in GPI anchor synthesis and suggest that ARV1-linked human diseases result from defective GPI anchor synthesis.