Jamie Rickmyre, Ph.D.

jamie-rickmyre

Ph.D. Student
Laura Lee Lab

Email:

jamie.rickmyre(at)vanderbilt.edu

Hometown:

South Daytona, FL

Education:

B.S. Biology
Stetson University, DeLand, FL 2002

Publications:

Merkle JA, Rickmyre JL, Garg A, Loggins EB, Jodoin JN, Lee E, Wu LP, Lee LA (2009). no poles encodes a predicted E3 ubiquitin ligase required for early embryonic development of Drosophila. Development 136(3): 449-59.

Rickmyre, JL, DasGupta, S, Ooi, DL-Y., Keel, J, Lee, E, Kirschner, MW, Waddell, S, Lee, LA (2007). The Drosophila homolog of a human microcephaly gene, MCPH1, is required for genomic stability in the early embryo. Journal of Cell Science 120(20): 3565-77.

Sefers, SE, Rickmyre, J, Blackman, A, Li, H, Edwards, K, and Tang, YW (2006). QIAamp MinElute virus kit effectively extracts viral nucleic acids from cerebrospinal fluids and nasopharyngeal swabs. J Clin Virol 35(2): 141-146.

Research:

My research focuses on the characterization of mcph1, the Drosophila homolog of the human microcephalin (MCPH1) gene. In humans, severe truncations of MCPH1 lead to primary microcephaly, a disorder in which the cerebral cortex fails to develop fully during gestation. Clinical phenotypes include mental retardation and a head size that is 4 or more standard deviations smaller than age- and sex-matched means. In Drosophila, homozygous mutations resulting in severe truncations of MCPH1 protein lead to maternal-effect lethality of early embryos; however, mcph1 mutations are viable at all other life stages.

Embryos from mcph1 females mitotically arrest after 1-8 cell cycles of the first 13 cycles during the early syncytial divisions of embryogenesis with barrel-shaped spindles lacking centrosomes. We have genetically determined this is due to activation of the centrosome inactivation pathway, a Chk2-mediated response to incomplete replication or DNA damage in the early Drosophila embryo. My current efforts are directed toward placing mcph1 within a molecular framework.