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Indiana University Bloomington

Department of Biology

Faculty & Research

Faculty Profile

Brian Calvi

Photo of Brian Calvi
Research Images
Research photo by Brian Calvi

Associate Professor of Biology

IU Affiliations
Medical and Molecular Genetics, IU School of Medicine
Medical Sciences

Contact Information
By telephone: 812-855-5450
JH 361B

Calvi Lab website

Genome, Cell & Developmental Biology
Research Areas
  • Chromatin, Chromosomes, and Genome Integrity
  • Developmental Mechanisms and Regulation in Eukaryotic Systems
  • Eukaryotic Cell Biology, Cytoskeleton and Signaling

Ph.D., Harvard University, 1993
Postdoctoral Fellow, Carnegie Insitution of Washington, 1993-1998


American Cancer Society Research Scholar

Research Description

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.

Specific subtopics:

  • Variant polyploid cell cycles in development and cancer.
  • Cell cycle regulation of DNA replication and genome stability.
  • Cell cycle and chromatin regulation of apoptosis.
Select Publications
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  [article]
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.  [article]
Chen, S., Stout, J. R., Dharmaiah, S., Yde,S., Calvi,B.R. and Walczak, C.E. (2016) The Kinesin-14 HSET Contributes to Genomic Integrity in Polyploid Cell Division (Mol. Biol. Cell, in press.  [article]
Zhang B, Rotelli M, Dixon M, Calvi BR. (2015). The function of Drosophila p53 isoforms in apoptosis. Cell Death Differ. doi: 10.1038/cdd.2015.40
Liu J, Zimmer K, Rusch DB, Paranjape N, Podicheti R, Tang H, Calvi BR. (2015). DNA sequence templates adjacent nucleosome and ORC sites at gene amplification origins in Drosophila. Nucleic Acids Res. gkv766
Zhang, B., Mehrotra, S., Ng, W. L., and Calvi, B.R. (2014) Low levels of p53 protein and chromatin silencing of p53 target genes repress apoptosis in Drosophila endocycling cells. PLoS Genetics, Sept.

Hassel, C., Zhang, B., Dixon, M., and Calvi, B.R. (2014) Induction of endocycles represses apoptosis independent of differentiation and predisposes cells to genome instability. Development 141:112-123.

Calvi BR. (2014) HBO1:JADE1 at the cell cycle chromatin crossroads. Cell Cycle 2014; 13:15, 2322–2322. (News and Views).

Calvi, B.R. (2013) Making Big Cells: One size does not fit all. Proceedings of the National Academy of Sciences, 110 (24) 9621-9622 (invited commentary).

McConnell, K., Dixon, M., and Calvi, B.R. (2012) The histone acetyltransferases CBP and Chameau integrate developmental and DNA replication programs in Drosophila ovarian follicle cells. Development, 139: 3880-3890. PMD 22951641. (featured by an "In this issue" article)
Liu, J., McConnell, K., Dixon, M. and Calvi, B.R. (2011) Analysis of model replication origins in Drosophila reveals new aspects of the chromatin landscape and its relationship to origin activity and the pre-RC. Mol. Biol. Cell. 23(1): 200-212 PMID:22049023.
Maqbool SB, Mehrotra S, Kolpakas A, Durden C, Zhang B, Zhong H, Calvi BR. (2010) Dampened activity of E2F1-DP and Myb-MuvB transcription factors in Drosophila endocycling cells. J Cell Sci. 123: 4095-4106. PMID: 21045111
Mehrotra, S., S. B. Maqbool, A. Kolpakas, K. Murnen and B.R. Calvi. (2008) Endocycling cells do not apoptose in response to DNA re-replication genotoxic stress. Genes & Development 22:3158-3171. [cover article]
Clark et al. (2007). Evolution of genes and genomes on the Drosophila phylogeny. Nature, 450:203-218.
Calvi, BR, Byrnes, BA, and Kolpakas, AJ. (2007) Conservation of epigenetic regulation, ORC binding, and developmental timing of DNA replication origins in the genus Drosophila. Genetics 177:1291-1301.
White, A.E., Leslie, M.E., Calvi, B.R., Marzluff, W.F., and Duronio,R.J. (2007) Cyclin E/CDK2 regulation of the Drosophila melanogaster histone locus body. Molecular Biology of the Cell 18(7), 2491-2502.
Review: B.R. Calvi. (2006) Developmental Gene Amplification. In: DNA Replication and Human Disease. Cold Spring Harbor Laboratory Press. Melvin DePamphilis (ed.), pp 233-255.
May, N.R., Thomer, M., Murnen, K.F., and Calvi, B.R. 2005 The origin binding protein Double parked, and its inhibitor Geminin, increase in response to replication stress. Journ. Cell Sci. 118:4207-4217.
Bandura JL, Beall E., Bell M, Silver H, Botchan, M, and Calvi, BR (2005) humpty dumpty is required for developmental DNA amplification and cell proliferation in Drosophila. Current Biology 15: 755-759.
Thomer, M., May, N.R., Aggarwal, B.D., Kwok, G., and Calvi, B.R. (2004). Drosophila double-parked is sufficient for re-replication during development and is regulated by Cyclin E / CDK2. Development 131(19): 4807-4818.
Aggarwal, B.D. and Calvi, B.R. (2004). Chromatin regulates origin activity in Drosophila follicle cells. Nature 430: 372-376.
Schwed GM, May NR, Pechersky Y, Calvi BR. (2002). Drosophila MCM6 is required for chorion gene amplification and genomic replication. Mol. Biol. of the Cell 13(2): 607-620.

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