Evidence of developmental escape from transcriptional gene silencing in MESSI retrotransposons.

Transposable elements (TEs) are ubiquitous genomic features. 'Copy-and-paste' long-terminal-repeat (LTR) retrotransposons have been particularly successful during evolution of the plant kingdom, representing a substantial proportion of genomes. For survival in copious numbers, these TEs may have evolved replicative mobilization strategies that circumvented hosts' epigenetic silencing.

High-frequency recombination between members of an LTR retrotransposon family during transposition bursts.

Retrotransposons containing long terminal repeats (LTRs) form a substantial fraction of eukaryotic genomes. The timing of past transposition can be estimated by quantifying the accumulation of mutations in initially identical LTRs. This way, retrotransposons are divided into young, potentially mobile elements, and old that moved thousands or even millions of years ago.

Developmental Restriction of Retrotransposition Activated in by Environmental Stress.

Retrotransposons (RTs) can rapidly increase in copy number due to periodic bursts of transposition. Such bursts are mutagenic and thus potentially deleterious. However, certain transposition-induced gain-of-function or regulatory mutations may be of selective advantage.

Recurrent evolution of heat-responsiveness in Brassicaceae COPIA elements.

Background: The mobilization of transposable elements (TEs) is suppressed by host genome defense mechanisms. Recent studies showed that the cis-regulatory region of Arabidopsis thaliana COPIA78/ONSEN retrotransposons contains heat-responsive elements (HREs), which cause their activation during heat stress. However, it remains unknown whether this is a common and potentially conserved trait and how it has evolved.

Modulation of endothelial cell migration via manipulation of adhesion site growth using nanopatterned surfaces.

Orthogonally functionalized nanopatterend surfaces presenting discrete domains of fibronectin ranging from 92 to 405 nm were implemented to investigate the influence of limiting adhesion site growth on cell migration. We demonstrate that limiting adhesion site growth to small, immature adhesions using sub-100 nm patterns induced cells to form a significantly increased number of smaller, more densely packed adhesions that displayed few interactions with actin stress fibers. Human umbilical vein endothelial cells exhibiting these traits displayed highly dynamic fluctuations in spreading and a 4.