A mechanism for the segregation of age in mammalian neural stem cells

See allHide authors and affiliations

Science  18 Sep 2015:
Vol. 349, Issue 6254, pp. 1334-1338
DOI: 10.1126/science.aac9868

You are currently viewing the abstract.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Youthful damage limitation in stem cells

Every day brings more risk of damage to stem cells, which could have consequences for the whole organism. Moore et al. observed that dividing neural stem cells in rodents establish a diffusion barrier that restricts damaged proteins to one daughter cell, leaving the other with intact molecules. But with age this diffusion barrier weakens, so that replicating stem cells of older animals are less able to exclude damaged proteins than are the stem cells of younger rodents.

Science, this issue p. 1334


Throughout life, neural stem cells (NSCs) generate neurons in the mammalian brain. Using photobleaching experiments, we found that during cell division in vitro and within the developing mouse forebrain, NSCs generate a lateral diffusion barrier in the membrane of the endoplasmic reticulum, thereby promoting asymmetric segregation of cellular components. The diffusion barrier weakens with age and in response to impairment of lamin-associated nuclear envelope constituents. Weakening of the diffusion barrier disrupts asymmetric segregation of damaged proteins, a product of aging. Damaged proteins are asymmetrically inherited by the nonstem daughter cell in embryonic and young adult NSC divisions, whereas in the older adult brain, damaged proteins are more symmetrically distributed between progeny. Thus, these data identify a mechanism of how damage that accumulates with age is asymmetrically distributed during somatic stem cell division.

View Full Text

Stay Connected to Science