|Name:||Dr. Paula Checchi|
|Title:||Assistant Professor of Biology|
|Office Location:||Donnelly DN228|
EMORY UNIVERSITY- Graduate School of Arts and Sciences, Atlanta, GA. Department of Biology Ph.D. Biochemistry, Cell and Developmental Biology. (2007)
UNIVERSITY OF MASSACHUSETTS, AMHERST. B.S. Biology; Minor: Studio Art. (2002)
2009-2013 UNIVERSITY OF CALIFORNIA, DAVIS. Department of Molecular and Cellular Biology Postdoctoral Researcher
2009-2010 Faculty Member: University of Phoenix, Axia College (Online Classroom)
trail running, rock climbing, hiking, art, cooking
|Awards & Honors:||
2011-2013 National Institutes of Health Contraception and Infertility Loan Repayment Program Award
Checchi P.M., Lawrence, K.L., *Van, M., Larson, B.J. and Engebrecht, J. Pseudosynapsis and decreased stringency of meiotic repair pathway choice on the hemizygous sex chromosome of Caenorhabditis elegans males. Genetics. (In press.) (*denotes undergraduate researcher.)
Furuhashi, H., Phippen, T., Rechtsteiner, A., Li, T., Kimura, H., Strome, S., Checchi, P.M., and Kelly, W.G. (2010) Trans-generational epigenetic regulation of C. elegans primordial germ cells Epigenetics & Chromatin. 3:15.
Checchi, P.M., Nettles, J.H., Zhou, J., Snyder, J.P., and Joshi, H.C. (2003) Microtubule-interacting Drugs for Cancer Treatment. Trends Pharmacol. Sci. 24, 361-365.
The overall goal of my research is to decipher the molecular mechanisms underlying cellular surveillance pathways that respond to double stranded breaks and chromosome asynapsis during meiotic progression. Meiosis results in the generation of non-identical haploid gametes and maintenance of chromosome number during sexual reproduction. Precise meiotic chromosome segregation is essential for life, and understanding how these steps are regulated is of paramount importance for human health. Errors in this process contribute to numerous developmental disorders including Down Syndrome, miscarriage, infertility and predisposition to cancers. Cellular surveillance pathways known as checkpoints monitor the steps of meiosis, and if homologous chromosomes fail to pair and recombine, checkpoint machinery responds by eliciting signals to induce cell death. However, in many species including humans, males possess a single X chromosome that is transcriptionally silenced, accumulates repressive chromatin marks, and is not recognized as partnerless by meiotic checkpoints.
Throughout my postdoctoral work, I have investigated the fundamental differences in meiotic checkpoint activation between males and females. Checkpoints function during meiosis to detect errors and to subsequently activate a signaling cascade, the goal of which is to prevent the formation of aneuploid gametes that manifest as infertility and a number of developmental disorders. As in humans, the lone X in Caenorhabditis elegans males lacks a complementary partner to pair with during meiosis. Although the partnerless X is subject to programmed double strand breaks (DSBs; an essential step for proper meiotic chromosome segregation), this fails to activate checkpoints as would happen with unpaired autosomes. My data reveal that the male X chromosome possesses a number of specialized properties that modulate break repair and checkpoint activation. Specifically, I discovered a role for conserved chromatin-remodeling proteins that block checkpoints and mediate meiotic silencing. My current and future studies will dissect the cellular and molecular pathways that underlie checkpoint control and the response to errors in chromosome segregation and repair of DNA damage.
American Association for the Advancement of Science
NIH Loan Repayment Programs Ambassador Network
American Society for Cell Biology
Genetics Society of America
Paula M. Checchi, Mike Van and JoAnne Engebrecht. Sex chromosome-specific meiotic double-stranded break repair in the C. elegans male germ line. Bay Area Meiosis Meeting. 2012. (Oral Presentation.)