Calibration of cognitive tests to address the reliability paradox for decision-conflict tasks

Standard, well-established cognitive tasks that produce reliable effects in group comparisons also lead to unreliable measurement when assessing individual differences. This reliability paradox has been demonstrated in decision-conflict tasks such as the Simon, Flanker, and Stroop tasks, which measure various aspects of cognitive control. We aim to address this paradox by implementing carefully calibrated versions of the standard tests with an additional manipulation to encourage processing of conflicting information, as well as combinations of standard tasks. Over five experiments, we show that a Flanker task and a combined Simon and Stroop task with the additional manipulation produced reliable estimates of individual differences in under 100 trials per task, which improves on the reliability seen in benchmark Flanker, Simon, and Stroop data. We make these tasks freely available and discuss both theoretical and applied implications regarding how the cognitive testing of individual differences is carried out.</p

Listening to the silent genes: Transgene silencing, gene regulation and pathogen control.

By capitalizing on the initially puzzling observations of unpredictable transgene silencing and variable expression, plant scientists have pioneered research into a novel type of epigenetic regulation, termed homology-dependent gene silencing. This silencing process has implications for natural mechanisms of gene expression in plants and other eukaryotes, and has branched out into studies of reversible DNA modifications; RNA metabolism, transport and processing; and host responses to plant viruses, viroids and transposable elements. The analysis of transgene silencing systems has enriched our understanding of other epigenetic phenomena, including paramutation, as well as heterosis and genome evolution. This research is also highly relevant to the biotechnology industry, which is interested in avoiding unwanted transgene silencing in genetically engineered lines and in exploiting various types of silencing to inactivate specific genes. Homology-dependent gene silencing can also be used in high-throughput approaches for functional genomics

Gene silencing mediated by promoter homology occurs at the level of transcription and results in meiotically heritable alterations in methylation and gene activity

International audienc

RNA-Directed Transcriptional Gene Silencing and Activation in Human Cells

The overt loss or uncontrolled gain of gene expression is found at some level in virtually every malady afflicting humans. From cancer to HIV-1, the uncontrolled expression or loss of gene expression is prevalent in human diseases. Approaches toward the specific control of gene expression at the transcriptional level could have the potential to revert or reduce disease pathologies. Over the last several years, researchers have developed methodologies that utilize small antisense non-coding RNAs to specifically silence transcription. Only recently has the endogenous molecular pathway usurped by the introduction of these small RNAs to regulate transcription in human cells been defined. Observations suggest that long antisense non-coding RNAs function as the endogenous epigenetic regulators of transcription in human cells, thus explaining why small antisense RNAs were observed early on to silence transcription via directed epigenetic changes at the target loci. The mechanism of action whereby small regulatory RNAs can either turn gene transcription on or off will be discussed as evidence that one day it may be possible to develop therapeutics to regulate gene transcription and ameliorate particular disease conditions