Is evidence for late selection due to automatic or attentional processing of stimulus identities?

This study determined whether evidence for late selection is due to attention processing or to processing by an automatic system that is separate from attention (two systems framework; Eriksen, Webb, & Fournier, 1990). The task was a two-choice discrimination of a target that appeared in one of two sequentially cued locations in an eight-letter visual display. Attention was directed to the first cued location (cue 1), and whether identification processing occurred at a different location before the second cue (cue 2) directed attention there was determined. Cue validity varied across two experiments, and critical trials were those in which the target appeared at cue 2. For these trials, the target was preceded by a letter (either identical, neutral, or incompatible) that changed to the target at various time intervals following cue 2. Automatic identification was assumed if theincompatible letter interfered with response to the target when it appeared only before cue 2 onset and independent of cue validity. The incompatible letter appearing only before cue 2 onset interfered with the target when the target occurred equally often at cue 1 and cue 2, but not when the target occurred at cue 1 70% and at cue 2 30% of the time. This disconfirms the two systems framework and suggests that attention is required for spatial form processing and response competition

De novo and inherited variants in ZNF292 underlie a neurodevelopmental disorder with features of autism spectrum disorder

Contains fulltext : 218267.pdf (Publisher’s version ) (Closed access)PURPOSE: Intellectual disability (ID) and autism spectrum disorder (ASD) are genetically heterogeneous neurodevelopmental disorders. We sought to delineate the clinical, molecular, and neuroimaging spectrum of a novel neurodevelopmental disorder caused by variants in the zinc finger protein 292 gene (ZNF292). METHODS: We ascertained a cohort of 28 families with ID due to putatively pathogenic ZNF292 variants that were identified via targeted and exome sequencing. Available data were analyzed to characterize the canonical phenotype and examine genotype-phenotype relationships. RESULTS: Probands presented with ID as well as a spectrum of neurodevelopmental features including ASD, among others. All ZNF292 variants were de novo, except in one family with dominant inheritance. ZNF292 encodes a highly conserved zinc finger protein that acts as a transcription factor and is highly expressed in the developing human brain supporting its critical role in neurodevelopment. CONCLUSION: De novo and dominantly inherited variants in ZNF292 are associated with a range of neurodevelopmental features including ID and ASD. The clinical spectrum is broad, and most individuals present with mild to moderate ID with or without other syndromic features. Our results suggest that variants in ZNF292 are likely a recurrent cause of a neurodevelopmental disorder manifesting as ID with or without ASD