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Retinotopic adaptation reveals distinct categories of causal perception.

ABSTRACT: We can perceive not only low-level features of events such as color and motion, but also seemingly higher-level properties such as causality. A prototypical example of causal perception is the 'launching effect': one object (A) moves toward a stationary second object (B) until they are adjacent, at which point A stops and B starts moving in the same direction. Beyond these motions themselves - and regardless of any higher-level beliefs - this display induces a vivid visual impression of causality, wherein A is seen to cause B's motion. Do such percepts reflect a unitary category of visual processing, or might there be multiple distinct forms of causal perception? While launching is often simply equated with causal perception, researchers have sometimes described other phenomena such as 'triggering' (in which B moves faster than A) and 'entraining' (in which A continues to move alongside B). We used psychophysical methods to determine whether these labels really carve visual processing at its joints, and how putatively different forms of causal perception relate to each other. Previous research demonstrated retinotopically specific adaptation to causality: exposure to causal launching makes subsequent ambiguous events in that same location more likely to be seen as non-causal 'passing'. Here, after replicating this effect, we show that exposure to triggering also yields retinotopically specific adaptation for subsequent ambiguous launching displays, but that exposure to entraining does not. Collectively, these results reveal that visual processing distinguishes some (but not all) types of causal interactions.

SUBMITTER: Kominsky JF

PROVIDER: S-EPMC7484022 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:One of the key questions about genomic alterations in cancer is whether they are functional in the sense of contributing to the selective advantage of tumor cells. The frequency with which an alteration occurs might reflect its ability to increase cancer cell growth, or alternatively, enhanced instability of a locus may increase the frequency with which it is found to be aberrant in tumors, regardless of oncogenic impact. Here we've addressed this on a genome-wide scale for cancer-associated focal deletions, which are known to pinpoint both tumor suppressor genes (tumor suppressors) and unstable loci. Based on DNA copy number analysis of over one-thousand human cancers representing ten different tumor types, we observed five loci with focal deletion frequencies above 5%, including the A2BP1 gene at 16p13.3 and the MACROD2 gene at 20p12.1. However, neither RNA expression nor functional studies support a tumor suppressor role for either gene. Further analyses suggest instead that these are sites of increased genomic instability and that they resemble common fragile sites (CFS). Genome-wide analysis revealed properties of CFS-like recurrent deletions that distinguish them from deletions affecting tumor suppressor genes, including their isolation at specific loci away from other genomic deletion sites, a considerably smaller deletion size, and dispersal throughout the affected locus rather than assembly at a common site of overlap. Additionally, CFS-like deletions have less impact on gene expression and are enriched in cell lines compared to primary tumors. We show that loci affected by CFS-like deletions are often distinct from known common fragile sites. Indeed, we find that each tumor tissue type has its own spectrum of CFS-like deletions, and that colon cancers have many more CFS-like deletions than other tumor types. We present simple rules that can pinpoint focal deletions that are not CFS-like and more likely to affect functional tumor suppressors.

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Retinotopic adaptation reveals distinct categories of causal perception.

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