Obstacle avoidance movement-related motor cortical activity with cognitive task.

Lack of attention to obstacles on the floor or walking path may cause trip and fall accidents. The preparatory activity in the motor cortex to the perturbation associated with obstacle avoidance movements with cognitive task is still unclear. The purpose of this study was to investigate the motor cortical activity involved in the preparation and execution of concurrent obstacle avoidance movement and cognitive task.

EVI1 and GATA2 misexpression induced by inv(3)(q21q26) contribute to megakaryocyte-lineage skewing and leukemogenesis.

Chromosomal rearrangements between 3q21 and 3q26 elicit high-risk acute myeloid leukemia (AML), which is often associated with elevated platelet and megakaryocyte (Mk) numbers. The 3q rearrangements reposition a GATA2 enhancer near the EVI1 (or MECOM) locus, which results in both EVI1 overexpression and GATA2 haploinsufficiency. However, the mechanisms explaining how the misexpression of these 2 genes individually contribute to leukemogenesis are unknown.

GATA2 haploinsufficiency accelerates EVI1-driven leukemogenesis.

Chromosomal rearrangements between 3q21 and 3q26 induce inappropriate expression by recruiting a -distal hematopoietic enhancer (G2DHE) to the proximity of the gene, leading to myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). The acquisition of G2DHE by the gene reciprocally deprives this enhancer of 1 of the 2 alleles, resulting in a loss-of-function genetic reduction in abundance. Because haploinsufficiency is strongly associated with MDS and AML, we asked whether misexpression and haploinsufficiency both contributed to the observed leukemogenesis by using a 3q21q26 mouse model that recapitulates the G2DHE-driven misexpression, but in this case, it was coupled to a heterozygous germ line deletion.