Lamin chromatin binding is modulated by interactions of different LAP2α domains with lamins and chromatin.

Lamins A and C are components of the lamina at the nuclear periphery and associate with heterochromatin. A distinct, relatively mobile pool of lamin A/C in the nuclear interior associates with euchromatic regions and with lamin-associated polypeptide 2α (LAP2α). Here we show that phosphorylation-dependent impairment of lamin assembly had no effect on its chromatin association, while LAP2α depletion was sufficient to increase chromatin association of lamins.

LAP2alpha maintains a mobile and low assembly state of A-type lamins in the nuclear interior.

Lamins form stable filaments at the nuclear periphery in metazoans. Unlike B-type lamins, lamins A and C localize also in the nuclear interior, where they interact with lamin-associated polypeptide 2 alpha (LAP2α). Using antibody labeling, we previously observed a depletion of nucleoplasmic A-type lamins in mouse cells lacking LAP2α.

Exploring the Relationship of a Gamified Assessment with Performance.

Our study explores the validity of a game-based assessment method assessing candidates' soft skills. Using self-reported measures of performance, (job performance, Organizational Citizenship Behaviors (OCBs), and Great Point Average (GPA), we examined the criterion-related and incremental validity of a game-based assessment, above and beyond the effect of cognitive ability and personality. Our findings indicate that a game-based assessment measuring soft skills (adaptability, flexibility, resilience and decision making) can predict self-reported job and academic performance.

Nucleoplasmic lamins define growth-regulating functions of lamina-associated polypeptide 2α in progeria cells.

A-type lamins are components of the peripheral nuclear lamina but also localize in the nuclear interior in a complex with lamina-associated polypeptide (LAP) 2α. Loss of LAP2α and nucleoplasmic lamins in wild-type cells increases cell proliferation, but in cells expressing progerin (a mutant lamin A that causes Hutchinson-Gilford progeria syndrome), low LAP2α levels result in proliferation defects. Here, the aim was to understand the molecular mechanism governing how relative levels of LAP2α, progerin and nucleoplasmic lamins affect cell proliferation.

Stage-Specific Changes in Plasmodium Metabolism Required for Differentiation and Adaptation to Different Host and Vector Environments.

Malaria parasites (Plasmodium spp.) encounter markedly different (nutritional) environments during their complex life cycles in the mosquito and human hosts. Adaptation to these different host niches is associated with a dramatic rewiring of metabolism, from a highly glycolytic metabolism in the asexual blood stages to increased dependence on tricarboxylic acid (TCA) metabolism in mosquito stages.