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Male infertility: It's all about the package
Date:5/13/2014

these males had severe fertility defects, ranging from low sperm counts to decreased sperm motility. The defective sperm failed to fertilize eggs when in vitro fertilization (IVF) was performed.

Mills has been interested in Chd5 since the time that her team first discovered it in 2007 as a potent tumor suppressor, one that can stop cells from becoming cancerous. "We know this ability has something to do with chromatin remodeling -- that when defective, causes normal cells to transform into tumors," says Mills. "But the most dramatic chromatin reorganization occurs when specialized cells carrying our genetic blueprint develop into sperm cells. It makes sense that Chd5 would be functioning there, too."

This, indeed, is what Mills and her team found. When Chd5 is missing, chromatin remodeling is disrupted. Histones are not efficiently replaced with protamines to repackage DNA, resulting in a more uneven, less condensed genome.

This change in DNA packaging has dramatic effects on the DNA itself. In the absence of Chd5, the double helix becomes damaged, breaking at multiple points throughout the genome. "So in addition to infertility, loss of Chd5 may put future generations the rare embryos that do get fertilized with defective sperm at risk for disease," says Mills. "Chd5 may protect a person from medical conditions related to DNA damage and spontaneous mutations, like cancer and autism."

The team is actively studying the role of Chd5 in human fertility. They analyzed Chd5 levels using data from testes biopsies obtained from men with fertility defects. "We found that men with more severe defects had the lowest levels of Chd5," says Mills. "While it is only a correlation at this point, we are eager to understand fully how Chd5 affects sperm development in humans."


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Contact: Jaclyn Jansen
jjansen@cshl.edu
516-367-8455
Cold Spring Harbor Laboratory
Source:Eurekalert  

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