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Penn researchers find potential in yeast for selecting Lou Gehrig's disease drugs
Date:4/17/2008

ys in the nucleus, but in ALS and FTD it somehow gets sequestered into the cells cytoplasm, where it forms clumps. When we put TDP-43 in yeast cells at normal human levels, it remained in the nucleus, explains Gitler. However, when it was expressed at higher levels, thereby overwhelming the quality control systems of the cell, TDP-43 clumped in the cytoplasm. At even higher levels, TDP-43 became toxic to the yeast cells, making them unable to grow. This experiment suggests, for the first time, that TDP-43 clumps can be a direct cause of cell toxicity.

In earlier studies at Penn, researchers found fragments of TDP-43 that were abundant in the clumps found in the post-mortem tissue of ALS and FTD patients. Knowing this, Gitler and colleagues chopped TDP-43 into many fragments to find the segments that are responsible for clumping and toxicity. They found a very similar segment that was also toxic to yeast cells. Designs of future drugs will depend on what part of the TDP-43 protein needs to be disabled.

The researchers are able to overexpress every yeast gene to determine which genes can rescue the yeast cells from the TDP-43 toxicity. In addition to these genetic screens, Gitler and colleagues are pursuing drug screens with their TDP-43 model. We can screen hundreds of thousands of small molecules to see which can get into a yeast cell and prevent TDP-43 from being toxic, says Gitler. Then we can take the hits we find and test them in animal models. We have already made mutations identical to what have been found in patients and have introduced those in the yeast model.


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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
Source:Eurekalert

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