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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
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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 |
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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. |
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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 |
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| 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 |
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