The psychophysiology of Mastermind: Characterizing response times and blinking in a high-stakes television game show.

Television game shows have proven to be a valuable resource for studying human behavior under conditions of high stress and high stakes. However, previous work has focused mostly on choices-ignoring much of the rich visual information that is available on screen. Here, we take a first step to extracting more of this information by investigating the response times and blinking of contestants in the BBC show Mastermind. In Mastermind, contestants answer rapid-fire quiz questions while a camera slowly zooms in on their faces. By labeling contestants' behavior and blinks from 25 episodes, we asked how accuracy, response times, and blinking varied over the course of the game. For accuracy and response times, we tested whether contestants responded more accurately and more slowly after an error-exhibiting the "post-error increase in accuracy" and "post-error slowing" which has been repeatedly observed in the lab. For blinking, we tested whether blink rates varied according to the cognitive demands of the game-decreasing during periods of cognitive load, such as when pondering a response, and increasing at event boundaries in the task, such as the start of a question. In contrast to the lab, evidence for post-error changes in accuracy and response time was weak, with only marginal effects observed. In line with the lab, blinking varied over the course of the game much as we predicted. Overall, our findings demonstrate the potential of extracting dynamic signals from game shows to study the psychophysiology of behavior in the real world.

The bacterial metalloprotease NleD selectively cleaves mitogen-activated protein kinases that have high flexibility in their activation loop.

Microbial pathogens often target the host mitogen-activated protein kinase (MAPK) network to suppress host immune responses. We previously identified a bacterial type III secretion system effector, termed NleD, a metalloprotease that inactivates MAPKs by specifically cleaving their activation loop. Here, we show that NleDs form a growing family of virulence factors harbored by human and plant pathogens as well as insect symbionts. These NleDs disable specifically Jun N-terminal kinases (JNKs) and p38s that are required for host immune response, whereas extracellular signal-regulated kinase (ERK), which is essential for host cell viability, remains intact. We investigated the mechanism that makes ERK resistant to NleD cleavage. Biochemical and structural analyses revealed that NleD exclusively targets activation loops with high conformational flexibility. Accordingly, NleD cleaved the flexible loops of JNK and p38 but not the rigid loop of ERK. Our findings elucidate a compelling mechanism of native substrate proteolysis that is promoted by entropy-driven specificity. We propose that such entropy-based selectivity is a general attribute of proteolytic enzymes.