Alongside smartphones, coffee shops, and bars, we all also need properly functioning stem cells to survive and prosper. Indeed, the stem cell theory of aging posits that the malfunctioning of stem cells in our later years, and not all that caffeine and alcohol, is the major cause of human aging. So how do we keep our stem cells young and functional for so long and what goes wrong?
A recent study, covered here at EpiGenie, demonstrated that when a stem cell divides, the stem cell copy keeps the keeps all the new pristine cellular components while the other more differentiated cell receives the old/damaged components. The authors suggest that by sorting components, the stem cell compartment can maintain optimal functionality over time. This makes perfect sense, but what controls this sorting mechanism and what changes over time?
A new study by Sebastian Jessberger has taken inspiration from work on budding yeast, which demonstrated a role for the endoplasmic reticulum (ER) in sorting cellular components, and has now shown that in a rat model:
- Both in vitro and in vivo, neural stem cells (NSCs) also form a “barrier” within their ER membrane.
- This barrier mediates the uneven sorting of cellular components before cell division.
- Stem cells receiving new cellular components are highly proliferative.
- Daughter cells receiving old/damaged components are less proliferative and in a more differentiated state.
- However, the study also found that the ER barrier strength reduces with age.
- This represses sorting and produces NSCs with old cellular components and lower proliferation.
- Lamins, the nuclear envelope component that become part of the ER during cell division, control barrier strength.
- Expression of a mutant lamin (Progerin), which causes a premature aging syndrome, weakens the barrier in young NSCs and inhibits component sorting.
Like many of the things which make up modern life, it seems that neural stem cells need shiny new parts to function properly and a lamin-mediated ER barrier helps them to achieve this. The next question is why lamin-mediated sorting fails during aging, and furthermore, whether we can pharmacologically target and alter this mechanism to keep our stem cells forever young!
So take note, get rid of those old dog-eared papers, and move this “younger” study to the top of the pile – Science, September 2015.