Name: Dr. Paula Checchi
Title: Assistant Professor of Biology
Office Location: Donnelly DN228
Extension: (845) 575-3228
Email: Paula.Checchi@marist.edu
Degrees Held:

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)

 

 

Bio:

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)

2009 Adjunct Professor: Science Dept., Georgia Perimeter College, Dunwoody, GA [Summer 2009]

2007-2009 Assistant Professor: Biology, Chemistry and Physics Dept., Southern Polytechnic State University, Marietta, GA

2004;2006: Laboratory Instructor: Dept. of Biology, Emory University, Atlanta, GA

2003-2004: Teaching Assistant: Dept. of Biology, Emory University, Atlanta, GA

2001-2002: Capstone Scholar, Commonwealth College and Dept. of Biology, University of Massachusetts, Amherst, MA;
 

Interests:

trail running, rock climbing, hiking, art, cooking

Awards & Honors:

2011-2013 National Institutes of Health Contraception and Infertility Loan Repayment Program Award


2010-2012 Oncogenic Signals and Chromosome Biology Training Grant: University of Davis, CA
• NIH-1 T32 CA10849

Publications:

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.)


Checchi P.M. and Engebrecht, J. (2011) Heteromorphic Sex Chromosomes: Navigating Meiosis without a Homologous Partner. Molecular Repro and Dev. Molecular Repro and Dev. 78:623-632.


Checchi P.M. and Engebrecht, J. (2011) Caenorhabditis. elegans Histone Methyltransferase MET-2 Shields the Male X Chromosome from Checkpoint Machinery and Mediates Meiotic Sex Chromosome Inactivation. PLoS Genetics. 7: e1002267

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. and Kelly, W.G. (2006) emb-4 is a Conserved Gene Required for Efficient Germline-Specific Chromatin Remodeling during Caenorhabiditis elegans Embryogenesis. Genetics. 174, 1895-1906.

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.

Research Interests:

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.

Affiliations:

American Association for the Advancement of Science

NIH Loan Repayment Programs Ambassador Network

American Society for Cell Biology

Genetics Society of America

Presentations:

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.)


Paula M. Checchi and JoAnne Engebrecht. The SET domain histone methyltransferase MET-2 is required for meiotic sex chromosome inactivation and blocks recognition of unpaired sex chromosomes from meiotic checkpoints. Bay Area Worm Meeting 2011. (Oral Presentation).


Paula M. Checchi, Hirofumi Furuhashi, and William G. Kelly. Transcription is Essential for Germline-Specific Chromatin Remodeling During C. elegans Embryogenesis. 16th Biennial International C. elegans Conference, 2007. (Platform Presentation).


Paula M. Checchi, Christine E. Schaner and William G. Kelly. emb-4 Encodes a Highly Conserved Gene with a Role in Germline-Specific Chromatin Remodeling and Cell Fate Specification During C. elegans Embryogenesis. 15th Biennial International C. elegans Conference, 2005. (Platform Presentation).