Expressed Likelihood as Motivator: Creating Value through Engaging What's Real.

Our research tested two predictions regarding how likelihood can have motivational effects as a function of how a probability is expressed. We predicted that describing the probability of a future event that could be either A or B using the language of high likelihood ("80% A") rather than low likelihood ("20% B"), i.e., high rather than low expressed likelihood, would make a present activity more real and engaging, as long as the future event had properties relevant to the present activity. We also predicted that strengthening engagement from the high (vs. low) expressed likelihood of a future event would intensify the value of present positive and negative objects (in opposite directions). Both predictions were supported. There was also evidence that this intensification effect from expressed likelihood was independent of the actual probability or valence of the future event. What mattered was whether high versus low likelihood language was used to describe the future event.

APLF promotes the assembly and activity of non-homologous end joining protein complexes.

Non-homologous end joining (NHEJ) is critical for the maintenance of genetic integrity and DNA double-strand break (DSB) repair. NHEJ is regulated by a series of interactions between core components of the pathway, including Ku heterodimer, XLF/Cernunnos, and XRCC4/DNA Ligase 4 (Lig4). However, the mechanisms by which these proteins assemble into functional protein-DNA complexes are not fully understood. Here, we show that the von Willebrand (vWA) domain of Ku80 fulfills a critical role in this process by recruiting Aprataxin-and-PNK-Like Factor (APLF) into Ku-DNA complexes. APLF, in turn, functions as a scaffold protein and promotes the recruitment and/or retention of XRCC4-Lig4 and XLF, thereby assembling multi-protein Ku complexes capable of efficient DNA ligation in vitro and in cells. Disruption of the interactions between APLF and either Ku80 or XRCC4-Lig4 disrupts the assembly and activity of Ku complexes, and confers cellular hypersensitivity and reduced rates of chromosomal DSB repair in avian and human cells, respectively. Collectively, these data identify a role for the vWA domain of Ku80 and a molecular mechanism by which DNA ligase proficient complexes are assembled during NHEJ in mammalian cells, and reveal APLF to be a structural component of this critical DSB repair pathway.