Did clickbait crack the code on virality?

Although clickbait is a ubiquitous tactic in digital media, we challenge the popular belief that clickbait systematically leads to enhanced sharing of online content on social media. Using the Persuasion Knowledge Model, we predict that clickbait tactics may be perceived by some readers as a manipulative attempt, leading to source derogation where the publisher may be perceived as less competent and trustworthy. This, in turn, may reduce some readers' intention to share content. Using a controlled experiment, we confirm that high-emotional headlines are shared more and show evidence that clickbait often leads to inferences of manipulative intent and source derogation. We then use a well-known secondary data set containing 19,386 articles from 27 leading online publishers. We supplement it with Twitter share data, sentiment analysis, topic modeling, and additional control variables. We confirm that, on average, clickbait articles elicit far fewer shares than non-clickbait articles. Our results are stable, with large effect sizes even after controlling for endogenous selection. Supplementary Information: The online version contains supplementary material available at 10.1007/s11747-021-00830-x.

Quorum Sensing Autoinducer(s) and Flagellum Independently Mediate EPS Signaling in Vibrio cholerae Through LuxO-Independent Mechanism.

Vibrio cholerae, the Gram-negative bacterium causing lethal diarrheal disease cholera, forms biofilm on solid surfaces to gain adaptive advantage for successful survival in aquatic reservoirs. Expression of exopolysaccharide (EPS), an extracellular matrix material, has been found critical for biofilm-based environmental persistence. In a subset of epidemic-causing V. cholerae, absence of flagellum but not motility was identified to induce elevated exopolysaccharide expression. Identification of the role played by quorum sensing autoinducer molecules, i.e., cholera autoinducer 1 (CAI-1) and autoinducer 2 (AI-2) as well as central regulator LuxO on EPS expression in the subset was explored. Deletion mutations were introduced in vital genes responsible for synthesizing CAI-1 (cqsA), AI-2 (luxS), flagellum (flaA), LuxO (luxO), flagellar motor (motX), and VpsR (vpsR) in the model strain MO10. Subsequent phenotypic alterations in terms of colony morphology, EPS expression, biofilm formation, and transcription level of relevant genes were analyzed. Autoinducer cross-feeding experiment confirmed the role of autoinducers in EPS signaling. Results reveal that autoinducers and flagellum are the two major EPS signaling units in this subset where one unit becomes predominant for EPS production in absence of the other. Moreover, either unit exerts negative influence on EPS induction by the other. Both the EPS signaling cascades are independent of LuxO contribution and essentially involve sodium-driven flagellar motor and VpsR. A cell density and flagellum-mediated, but LuxO-independent, EPS signaling mechanism is considered to be functional in these organisms that confers their survival fitness.