Antioxidant controls spinal cord d...(proteins and examined how the mutations ...)

Date:9/18/2009

proteins and examined how the mutations affect the cells. Mutations that prevent the two proteins from binding resulted in no motor neurons. Similarly, mutations that disrupt the enzyme abilities of GDE2 and Prdx1 also resulted in no motor neurons. In fact, only when GDE2 and Prdx1 can bind each other and work as enzymes do motor neurons develop.

"So we thought maybe the antioxidant enzyme activity of Prdx1 is doing something to regulate GDE2 function," says Sockanathan. Her team then looked into what already was known about Prdx1's enzyme activity. They found that bacteria and yeast versions of Prdx1 are able to help alter certain chemical bonds in proteins that form between specific amino acids that contain so-called sulfhydryl or "-SH" groups.

That led them to reexamine the GDE2 protein for sulfhydryl groups. As it turns out, they found 4 in GDE2: Three are close together and one is clear on the other end of the protein. They first performed some biochemistry experiments to determine whether these sulfhydryl groups can form disulfide bondsthey can. Then, two at a time, the researchers engineered mutations to replace each -SH-containing amino acid in GDE2 and asked if the mutated protein could still bind to Prx1. They found one combination of mutations that did not behave the same as the unmutated control, leading them to conclude that Prx1 must break the chemical bond between those two specific amino acids.

"We think that Prx1 breaks this bond in GDE2, activating it to promote motor neuron differentiation," says Sockanathan. "This suggests a new general control mechanism that regulates when cells divide and when they differentiate. We're excited to see how widespread it might be."

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Contact: Audrey Huang audrey@jhmi.edu 410-614-5105 Johns Hopkins Medical Institutions Source:Eurekalert

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