( Forsyth Institute research with the fla...)New understanding of regeneration gained by Forsyth scientists

Forsyth Institute research with the flatworm, planaria, offers new clues for understanding restoration of body structures. Researchers at The Forsyth Institute have discovered how the worm's cells communicate to correctly repair and regenerate tissue. Forsyth scientists have found that gap-junction (microscopic tunnels directly linking neighboring cells) communication contributes to this signaling. This research, led by Dr. Michael Levin, underlies principles that can potentially offer insight into human regeneration.

The restoration of body structures following injury requires both an initiation of growth and an imposition of the correct morphology upon the regenerating tissue. Understanding this process is crucial for both the basic biology of pattern formation, and for developing novel biomedical approaches. Planaria have powerful regeneration capability that makes them ideal for studying this process. When the worms are cut in half, the bottom section of the worm grows a head and the upper section a tail. Scientists have suspected that the ability of previously adjacent cells (on either side of the cut) to adopt radically different fates, as is the case with planaria where the cells have to decide whether to build a head or a tail, could be due to long-range signaling, which allows the determination of position relative to - and the identity of - remaining tissue.

Michael Levin, PhD., Associate Member of the Staff, said, "This research has important implications for understanding the signaling necessary to build (or re-build) complex structures. By understanding how cells communicate through gap junctional channels we can gain a greater understanding of how we can possibly direct this process in tissues that don't currently regenerate; this has clear applications towards induction of regeneration in biomedical settings." Dr. Levin and his team ultimately hope to gain an understanding of how adult stem cells are controlled by gap-junctional c
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Source:Forsyth Institute

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