Tiffany Oliver, Ph.D.

Emory University School of Medicine
Department of Human Genetics

Research Mentor: Stephanie Sherman, Ph.D., Professor

Teaching Mentor: Lisa Hibbard, Ph.D., Department of Chemistry, Spelman College



Education

B.S., Biology, Tennessee State University, Nashville, TN, 2003
Ph.D., Genetics and Molecular Biology, Emory University, Atlanta, GA, 2008
2nd year FIRST Postdoctoral Fellow, 2008 - present


Research Statement

Nondisjunction is defined as the failure of chromosomes to segregate during meiosis; this results in the production of aneuploid gametes.  Aneuploidy is the leading cause of pregnancy loss, intellectual disabilities and birth defects.  As a result it is important that we understand mechanisms underlying chromosome nondisjunction.  We are interested in determining if certain genomic features are associated with an increased risk for nondisjunction when they are present are the site of recombination.

Trisomy 21, caused by nondisjunction of human chromosome 21, is one the few autosomal trisomies that survives gestation.  As a result we use it as a model to determine if certain genomic features are associated with an increased risk for nondisjunction when they are present are the site of recombination.

Among maternal cases of trisomy 21 recombination has been found to be increased within the most telomeric 2.5Mb of 21q within cases that exhibit meiosis I errors and the most centromeric 3.2 Mb of 21q within cases that exhibit meiosis II errors. 

We have refined where recombination is increased to a 500Kb region on 21q in normal, maternal MI and maternal MII cases.  Within these regions we plan to examine the distribution of features that have previously been found to be associated with recombination; these include CpG content, PolyA/PolyT fraction, CG content and presence of ref seq genes.  We will then compare the distribution of these recombination-related features in regions of 21q where recombination is increased in MI and MII cases to that of where recombination is increased in normally segregating chromosomes.  This is expected to help us understand mechanisms underling abnormal chromosome segregation.

 

Publications

Oliver, T.R., Bhise, A., Feingold, E., Tinker,S., Masse, N., Sherman, S.L., (2009) Investigation of Factors Associated with Paternal Nondisjunction of Chromosome 21. Am J Med Genet A. 149A(8):1685-90.

Oliver, T.R., Feingold, E., Yu, K., Cheung, V., Tinker, S., Yadav-Shah, M., Masse, N., Sherman, S.L.  (2008) New insights into human nondisjunction of chromosome 21 in oocytes. PLoS Genet. 4(3):e1000033. PMCID: PMC2265487

 

Emory University School of Medicine
Department of Human Genetics
Whitehead Biomedical Research Bldg.,
Suite 335
615 Michael Street

Atlanta, GA 30322
Tel: 404.727.9396

Email: toliver@genetics.emory.edu


Emory University School of Medicine
Department of Physiology
Atlanta, GA 30322-3110
(404) 727-7410 Office ~ (404) 727-2648 FAX

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