Humor Works in Funny Ways: Examining Satirical Tone as a Key Determinant in Political Humor Message Processing

This multi-experiment study builds upon extant political entertainment theory, testing whether satire type (horatian versus juvenalian) cues varying processing mechanisms (message discounting versus resource allocation), and if consequential differences to argument scrutiny levels or message persuasiveness result. Using novel stimuli (e.g., animated cartoons, study one) and real-world late-night political satire (The Daily Show and The Colbert Report, study two), results suggest that satire type was a key antecedent in political humor message processing. Additionally, the varying mechanisms had differential effects on political argument scrutiny levels and message persuasiveness

Satirical narrative processing: Examining the roles of character liking and media enjoyment on narrative-consistent attitudes

This study uses online survey data (n=127) with an embedded media manipulation to examine relationships between character liking, media enjoyment, and narrative consistent attitudes with late-night political comedian, Stephen Colbert’s satirical campaign finance narrative. The data offer empirical support for the notion that narratively structured political satire processing models should consider relevant entertainment psychology and narrative persuasion concepts such as how audiences respond to the main characters and the role enjoyment plays in the process. Using structural equation modeling, media enjoyment significantly mediated the relationship between character liking and narrative consistent attitude formation (about the antagonist), but appears to have functioned as a suppressor variable. Competing models are offered in an Online Appendix

Targeted resequencing identifies PTCH1 as a major contributor to ocular developmental anomalies and extends the SOX2 regulatory network

International audienceOcular developmental anomalies (ODA) such as Anophthalmia/Microphthalmia (AM) or anterior segment dysgenesis (ASD) have an estimated combined prevalence of 3.7 in 10,000 births. Mutations in SOX2 are the most frequent contributors to severe ODA, yet account for a minority of the genetic drivers. To identify novel ODA loci, we conducted targeted high-throughput sequencing of 407 candidate genes in an initial cohort of 22 sporadic ODA patients. Patched 1 (PTCH1), an inhibitor of sonic hedgehog (SHH) signaling, harbored an enrichment of rare heterozygous variants in comparison to either controls, or to the other candidate genes (four missense and one frameshift); targeted resequencing of PTCH1 in a second cohort of 48 ODA patients identified two additional rare nonsynonymous changes. Using multiple transient models and a CRISPR/Cas9 mutant, we show physiologically relevant phenotypes altering SHH signaling and eye development upon abrogation of ptch1 in zebrafish which in vivo complementation assays using these models showed that all six patient missense mutations affect SHH signaling. Finally, through transcriptomic and ChIP analyses, we show that SOX2 binds to an intronic domain of the PTCH1 locus to regulate PTCH1 expression, findings that were validated both in vitro and in vivo. Together, these results demonstrate that PTCH1 mutations contribute to as much as 10% of ODA, identify the SHH signaling pathway as a novel effector of SOX2 activity during human ocular development, and indicate that ODA is likely the result of overactive SHH signaling in humans harboring mutations in either PTCH1 or SOX2