Unlike humans, planarian flatworms have the remarkable ability to regrow any missing body part, making them an ideal model with which to study the molecular basis of regeneration.
Over the years scientists have learned that planarians mount recovery responses that differ depending on the severity of the injury they suffer. For example, a worm with a cut or a puncture wound reacts at the cellular and molecular levels quite differently from one that loses its head or tail. What has remained unclear, however, is just exactly how these responses are triggered.
Whitehead Institute Member Peter Reddien and two of his former graduate students, Michael Gaviño and Danielle Wenemoser, address this longstanding question this week in the journal eLife, revealing a fascinating interplay of signals between two wound-induced genes.
According to the work of Gavino, Wenemoser, and Reddien, regeneration initiation in planarians is regulated by the expression of the genes Smed-follistatin (or fst) and Smed-activin-1 and -2 (or act-1 and act-2), that together act like a switch. After a planarian is wounded, the type of injury determines the level fst expression——the more extreme the loss of tissue, the higher the level of fst expressed. At puncture wounds, fst expression is low, and regeneration is inhibited. However, following amputation, which results in major loss of tissue, fst levels rise and in turn inhibit Activin proteins, allowing regeneration to begin.
To the researchers’ surprise, this interaction only affects regeneration and healing related to injury. Normal maintenance and cell turnover throughout the planarian body continue unaffected when fst is inhibited, even though these activities rely on the same neoblast cell population that creates new tissue during regeneration.
Read more at: Phys.org