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Michael Bastiani

Professor of Biology

B.S. University of California, San Diego

Ph.D. University of California, Davis

Research

References

bastiani@bioscience.utah.edu

 

Research

Neuronal regeneration after axotomy has been studied in humans and other vertebrate model systems for over 100 years and yet we still do not have a comprehensive molecular model nor an effective treatment to induce regeneration. Surprisingly, the powerful genetic model systems used so successfully to study body pattern formation, programmed cell death,  neural development and many other important biological problems have not been used to study neuronal regeneration.  This was obviously not an oversight by scientists.  Rather, it has been difficult to devise a robust screening assay for neural regeneration in either D. melanogaster or C. elegans.  Recently, Hammarlund, Jorgensen, and myself made an observation that now makes it possible to screen for genes required for regeneration in C. elegans.  We discovered that embryonic neurons lacking  b-spectrin  develop normally (normal growth cone motility, pathfinding, and target recognition), but after hatching undergo movement-induced axotomy followed by regeneration.  This is a robust phenotype,with most commissural axons in each animal breaking and regenerating before the animal reaches adulthood.  There is a progressive failure of regeneration as each cycle of axotomy and regeneration takes place so that the adult displays a severely abnormal nervous system.  This well-characterized regeneration phenotype in C. elegans mimics the phenotype of mammalian neurons in response to axotomy.  We are using RNAi knockdown to assay the function of every gene in the worm genome in the process of neuronal regeneration. 

References