"When Pds5 is removed and sister chromatids become synapsed as a result, the segregation and recombination of homologs essential for genetic diversity fails," Yu said. "This finding is highly important, because failure to generate a crossover between homologs leads to chromosome missegregation and can cause human chromosomal birth defects such as Down syndrome, which affects about one in 800 newborns in the United States."

Yu said the landmark study has significantly extended previous observations of the role of Pds5 in the formation of meiotic chromosome structure.

"Now, we are investigating the other factors that interact with Pds5 during meiosis to regulate chromosome segregation and homolog synapsis," he said. "Long term, we hope to achieve a comprehensive understanding of the molecular mechanisms behind chromosomal birth defects and see our research contribute to the creation of targeted interventions during meiosis."

Currently, Yu's research at Florida State University is supported by a two-year, $150,000 Basil O'Connor Starter Scholar award from the March of Dimes Foundation, and by a three-year, $375,000 Bankhead Coley grant from the Florida Biomedical Research Program.

The Sept. 7, 2009, Journal of Cell Biology <jcb.rupress/cgi/content/full/186/5/713> paper ("Pds5 is required for homologue pairing and inhibits synapsis of sister chromatids during yeast meiosis") was co-authored by Hui Jin, a research technician in biology at Florida State, and Vincent Guacci, a postdoctoral assistant in the Department of Embryology at the Carnegie Institution of Washington.

Source: Florida State University