Antagonistic Regulation Of LINE-1/Alu Elements And Their Repressor Apobec3B In Cellular Senescence
Our bodies are made of trillions of cells, and as we age, some of these cells enter a state called senescence, often referred to as “zombie cells.” These senescent cells stop dividing and accumulate in tissues, contributing to aging and age-related diseases. A significant portion of our DNA is made up of fascinating segments called transposable elements, or “jumping genes,” such as LINE-1 and Alu elements. Normally, these elements are kept in check, remaining quiet and inactive. However, in senescent cells, these jumping genes become active. When these elements “jump” around our genome, they can cause DNA damage and instability, which further fuels the aging process and related inflammation. Recent research has shed light on a key player in this process: a protein called APOBEC3B. This protein usually acts as a guardian, suppressing the activity of LINE-1 and Alu elements. However, findings indicate that in senescent cells, the levels of APOBEC3B are significantly reduced. This reduction in APOBEC3B means less control over these jumping genes, allowing them to become more active. The increased activity of these elements then leads to more DNA damage, contributing to the hallmarks of aging. Understanding this intricate relationship could pave the way for new strategies to combat aging and age-related diseases by targeting the regulation of these mobile genetic elements or the APOBEC3B protein.