Jamie Rickmyre, Ph.D.


Ph.D. Student
Laura Lee Lab




South Daytona, FL


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


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.


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.