DNA Methylation, Cellular Stress Response and Expression of Inner Nuclear Membrane Proteins

• Main Author: Levesque, Steve
• Other Authors: Paulin-Levasseur, Micheline
• Language: en
• Published: Université d'Ottawa / University of Ottawa 2011
• Subjects: Epigenetics; DNA methylation; Nuclear stress bodies; Inner nuclear membrane (INM); Lamin A; Lamin B; Emerin; Satellite III (Sat III); Stress response; Heat shock (HS); 2H12; Lamina associated polypeptide 2 (Lap2); Fibrillarin; Laminopathies; Hutchinson Gilford Progeria Syndrome (HGPS)
• Online Access: http://hdl.handle.net/10393/19949; http://dx.doi.org/10.20381/ruor-4565

Hutchinson-Gilford Progeria Syndrome is described as a series of mutations within the lamin A gene leading to the accumulation of progerin in the nucleus, contributing to premature aging and affecting the epigenetic control. Epigenetic control, such as DNA methylation, relies on DNA methyltransferase enzymes. In human cells, heat shock (HS) leads to the formation of nuclear stress bodies (nSBs); ribonucleoprotein aggregates of Sat III RNA and RNA-binding proteins. The objectives of this study were to determine if epigenetic status induces varying responses to HS and assess the variability of nuclear proteins in similar conditions. Results show epigenetic modifications do not prevent a stress response; however the extent may be affected. In addition the functions of most nuclear antigens were not affected. It is most likely the sum of interactions at the inner nuclear membrane and nuclear lamina interface that result in nuclear strength pertaining to lamin A.