ommunication (GJC). As reported in the November 15 issue of Developmental Biology, Dr. Levin's research team cloned and characterized the expression of twelve members of the innexin gene family during planarian regeneration. Innexins are proteins which make up gap junctions, and their expression was detected throughout the worms and in regeneration blastemas, undifferentiated cells from which an organ or body part develops, consistent with a role in long-range signaling relevant to specification of blastema positional identity.
Dr. Levin and Taisaku Nogi closed down the gap junctions to determine the impact on regeneration. As a result, the planaria often grew back two heads rather than a head and tail. The loss of GJC function had a direct impact on the regeneration process; without this communication the planaria cells at the posterior end became re-specified and formed a normal head, complete with brain, eyes, etc.. This is an example of a high-level "master" control signal. "If we can learn how to send appropriate signals through gap junctions, we may be able to tell the system to make a complex structure as needed." said Levin.
Michael Levin, PhD. is an Associate Member of the Staff in The Forsyth Institute Department of Cytokine Biology. Through experimental approaches and mathematical modeling, Dr. Levin and his team examine the processes governing large-scale pattern formation and biological information storage during animal embryogenesis. The lab's investigations are directed toward understanding the mechanisms of signaling between cells and tissues that allows a biological system to reliably generate and maintain a complex morphology. The Levin team studies these processes in the context of embryonic development and regeneration, with a particular focus on the biophysics of cell behavior.
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