Basic Taste Stimuli Elicit Unique Responses in Facial Skin Blood Flow

Facial expression changes characteristically with the emotions induced by basic tastes in humans. We tested the hypothesis that the five basic tastes also elicit unique responses in facial skin blood flow. Facial skin blood flow was measured using laser speckle flowgraphy in 16 healthy subjects before and during the application of basic taste stimuli in the oral cavity for 20 s. The skin blood flow in the eyelid increased in response to sweet and umami taste stimuli, while that in the nose decreased in response to a bitter stimulus. There was a significant correlation between the subjective hedonic scores accompanying these taste stimuli and the above changes in skin blood flow. These results demonstrate that sweet, umami, and bitter tastes induce unique changes in facial skin blood flow that reflect subjective hedonic scores

Sweet, umami, and bitter stimuli were significantly correlated with hedonic rating and blood flow in specific facial skin regions.

<p>Sweet (a) and umami (b) stimuli were significantly correlated with hedonic rating and eyelid skin blood flow (sweet: r = 0.60, n = 41; umami: r = 0.57, n = 44). Bitter (c) stimuli were significantly correlated with hedonic rating and nose skin blood flow (r = 0.52, n = 38).</p

Changes in facial skin blood-flow distribution in a subject before (Pre) and during (Stimulus) gustatory stimulation.

<p>The colored bar on the right side indicates the blood flow magnitude, with the red and blue colors indicating higher and lower blood flows, respectively. The white ellipses in the six facial regions represent the target areas where blood flow was measured. Sweet (a) and umami (b) stimuli characteristically increased eyelid skin blood flow, while bitter (c) stimuli decreased nose skin blood flow.</p

The tested concentrations for each taste substance.

<p>MSG: monosodium glutamate.</p

Binding of a novel SMG-1–Upf1–eRF1–eRF3 complex (SURF) to the exon junction complex triggers Upf1 phosphorylation and nonsense-mediated mRNA decay

Nonsense-mediated mRNA decay (NMD) is a surveillance mechanism that degrades mRNA containing premature termination codons (PTCs). In mammalian cells, recognition of PTCs requires translation and depends on the presence on the mRNA with the splicing-dependent exon junction complex (EJC). While it is known that a key event in the triggering of NMD is phosphorylation of the trans-acting factor, Upf1, by SMG-1, the relationship between Upf1 phosphorylation and PTC recognition remains undetermined. Here we show that SMG-1 binds to the mRNA-associated components of the EJC, Upf2, Upf3b, eIF4A3, Magoh, and Y14. Further, we describe a novel complex that contains the NMD factors SMG-1 and Upf1, and the translation termination release factors eRF1 and eRF3 (SURF). Importantly, an association between SURF and the EJC is required for SMG-1-mediated Upf1 phosphorylation and NMD. Thus, the SMG-1-mediated phosphorylation of Upf1 occurs on the association of SURF with EJC, which provides the link between the EJC and recognition of PTCs and triggers NMD