- Ph.D., Harvard University, 1993
- Postdoctoral Fellow, Carnegie Institution of Washington, 1993-1998
Jordan Hall 361
Calvi Lab website
It is critical to discover the mechanisms of normal cell cycle regulation if we are to fully understand what goes awry in cancer cells. Genomic DNA must be fully and accurately replicated and then segregated into two daughter cells when cells divide. DNA replication that is uncoordinated from cell division causes “replication stress” and DNA damage, which is sensed and corrected by cell cycle checkpoints. Defects in both DNA replication and cell cycle checkpoints lead to high rates of DNA mutation (genome instability) and cause cancer. There have been major advances in understanding the molecular mechanisms that regulate DNA replication, the responses to replication stress, and how defects in these processes lead to cancer. Yet, there are many variations on the canonical cell cycle and checkpoint themes during development that remain little understood. Defining these themes and variations is necessary to fully understand how cell division and development are normally coordinated, and how errors in these molecular mechanisms in different tissue types cause cancer.
The research in my laboratory focuses on defining the molecular mechanisms that regulate DNA replication and cell cycle checkpoints during development. We have primarily used Drosophila melanogaster (fruit fly) as a model system. We have also worked with human cells in culture, both in my lab and as collaborations, to determine whether the mechanisms we have defined in flies are operative in humans. We have discovered new aspects of DNA replication and cell cycle checkpoint regulation in development.
Zhang, C, Montooth, K.L., and Calvi, B.R. (2017) Incompatibility between mitochondrial and nuclear genomes during oogenesis results in ovarian failure and embryonic lethality. Development, 144, 2490-2503 doi:10.1242/dev.151951
Qi, S., and Calvi, B.R. (2016) Different cell cycle modifications repress apoptosis at different steps independent of developmental signaling in Drosophila. Mol. Biol. Cell, 10.1091/mbc.E16-03-0139
Paranjape, N, and Calvi, BR. (2016) The histone variant H3.3 is enriched at Drosophila amplicon origins but does not bookmark them for pre-RC assembly or activation. Genes Genomes and Genetics (G3), 10.1534/g3.116.028068.
Chen, S., Stout, J. R., Dharmaiah, S., Yde, S., Calvi,B.R. and Walczak, C.E. (2016) Transient endoreplication down-regulates the kinesin-14 HSET and contributes to genomic instability. Mol. Biol. Cell, August 3, 2016 mbc.E16-03-0159