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Procreation trumps survival — even on a cellular level

A newly discovered biological mechanism channels a mother’s available energy — in the form of fat — straight to the reproductive system during stressful times, protecting future offspring at the cost of the mother’s health.

USC’s Sean Curran observed the phenomenon in the worm species C. elegans, but the cellular mechanisms associated with it also exist in humans, raising the possibility that we may share this trait as well.

When an organism is exposed to external stresses such as famine, a protein that protects cells called SKN-1 is activated. In addition to stress resistance, activation of SKN-1 also drives the reallocation of lipids from the organism’s soma, or bodily cells, to its germline, or reproductive system, Curran found.


Once there, the fats fuel the development of oocytes, or egg cells, making successful reproduction easier; however, the animal itself faces a higher likelihood of a shortened lifespan. (Most C. elegans are hermaphrodites — Curran is still exploring whether the phenomenon also occurs with the male portion of the worm’s reproductive system.)

When the organism again obtains nutrients, the presence of omega-3 and -6 fatty acids stop the travel of fats into the reproductive cells, bringing the animal’s ability to resist environmental stressors back to normal.

“SKN-1 plays essential roles in survival to stress at all stages in life; however, SKN-1 activation mutants are not long-lived. This is incredibly surprising and confusing at the same time since these animals should be stress resistant,” said Curran, an assistant professor with joint appointments at the USC Davis School of Gerontology and the USC Dornsife College of Letters, Arts and Sciences. “Our study shows that the reason constitutively active SKN-1 doesn’t confer longevity is because of the movement of lipids from the soma to the germline to promote the necessity of reproduction.”

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