Differences in the early stages of motor learning between visual-motor illusion and action observation.

The visual-motor illusion (VMI) induces a kinesthetic illusion by watching one's physically-moving video while the body is at rest. It remains unclear whether the early stages (immediately to one hour later) of motor learning are promoted by VMI. This study investigated whether VMI changes the early stages of motor learning in healthy individuals. Thirty-six participants were randomly assigned to two groups: the VMI or action observation condition. Each condition was performed with the left hand for 20 min. The VMI condition induced a kinesthetic illusion by watching one's ball-rotation task video. The action observation condition involved watching the same video as the VMI condition but did not induce a kinesthetic illusion. The ball-rotation task and brain activity during the task were measured pre, post1 (immediately), and post2 (after 1 h) in both conditions, and brain activity was measured using functional near-infrared spectroscopy. The rate of the ball-rotation task improved significantly at post1 and post2 in the VMI condition than in the action observation condition. VMI condition lowers left dorsolateral prefrontal cortex and right premotor area activity from post1 to pre compared to the action observation condition. In conclusion, VMI effectively aids early stages of motor learning in healthy individuals.

AKT signaling is associated with epigenetic reprogramming via the upregulation of TET and its cofactor, alpha-ketoglutarate during iPSC generation.

BACKGROUND: Phosphoinositide-3 kinase (PI3K)/AKT signaling participates in cellular proliferation, survival and tumorigenesis. The activation of AKT signaling promotes the cellular reprogramming including generation of induced pluripotent stem cells (iPSCs) and dedifferentiation of primordial germ cells (PGCs). Previous studies suggested that AKT promotes reprogramming by activating proliferation and glycolysis. Here we report a line of evidence that supports the notion that AKT signaling is involved in TET-mediated DNA demethylation during iPSC induction. METHODS: AKT signaling was activated in mouse embryonic fibroblasts (MEFs) that were transduced with OCT4, SOX2 and KLF4. Multiomics analyses were conducted in this system to examine the effects of AKT activation on cells undergoing reprogramming. RESULTS: We revealed that cells undergoing reprogramming with artificially activated AKT exhibit enhanced anabolic glucose metabolism and accordingly increased level of cytosolic α-ketoglutarate (αKG), which is an essential cofactor for the enzymatic activity of the 5-methylcytosine (5mC) dioxygenase TET. Additionally, the level of TET is upregulated. Consistent with the upregulation of αKG production and TET, we observed a genome-wide increase in 5-hydroxymethylcytosine (5hmC), which is an intermediate in DNA demethylation. Moreover, the DNA methylation level of ES-cell super-enhancers of pluripotency-related genes is significantly decreased, leading to the upregulation of associated genes. Finally, the transduction of TET and the administration of cell-permeable αKG to somatic cells synergistically enhance cell reprogramming by Yamanaka factors. CONCLUSION: These results suggest the possibility that the activation of AKT during somatic cell reprogramming promotes epigenetic reprogramming through the hyperactivation of TET at the transcriptional and catalytic levels.