Jean Gautier, PhD

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Overview

Academic Appointments

  • Professor of Genetics and Development (in the Institute for Cancer Genetics)

Administrative Titles

  • Leader, Cancer Genetics and Epigenetics Program, Herbert Irving Comprehensive Cancer Center
  • Associate Director of Research, Herbert Irving Comprehensive Cancer Center

The laboratory employs diverse experimental approaches to elucidate the role of genome instability in cancer. Cell-free extracts derived from the egg of the frog Xenopus laevis are used as a simple model system to study processes that govern genome stability, including DNA replication control, DNA repair, and the cellular response to DNA damage. In addition, cultured mammalian cells and mouse models are exploited to analyze biological responses to DNA damage. Several specific questions are currently being addressed in his lab. First, what repair pathways are involved in processing DNA lesions induced by cancer chemotherapeutic drugs? Specifically, Dr. Gautier’s lab examines double-strand break repair and DNA inter-strand crosslink repair. The second is, what conditions favor mis-repair of DNA and lead to chromosome rearrangements? The third is, what are the molecular origins of oncogene-induced genomic stress? 

Languages

  • French

Research

The main objective of our research is to better understand the molecular mechanisms responsible for the maintenance of genome stability. These controls are lost in cancer, which is characterized by genomic instability.

The laboratory employs diverse experimental approaches to elucidate the role of genome instability in cancer. Cell-free extracts derived from the egg of the frog Xenopus laevis are used as a simple model system to study processes that govern genome stability, including DNA replication control, DNA repair, and the cellular response to DNA damage. In addition, cultured mammalian cells and mouse models are exploited to analyze biological responses to DNA damage. Several specific questions are currently being addressed in his lab. First, what repair pathways are involved in processing DNA lesions induced by cancer chemotherapeutic drugs? Specifically, Dr. Gautier’s lab examines double-strand break repair and DNA inter-strand crosslink repair. The second is, what conditions favor mis-repair of DNA and lead to chromosome rearrangements? The third is, what are the molecular origins of oncogene-induced genomic stress? 

Grants

1. CANCER BIOLOGY TRAINING GRANT

4T32CA009503

Project Dates:  Sept 1 1984 to Jan 31 2018

2. DNA Repair and Genomic instability in cancer development and therapy

1R35CA197606

Project Dates:  Aug 1 2015 to July 31 2022

3. DNA double strand break repair, chromosome translocations and cancer

1PO1CA174653

Project Dates:  March 1 2014 to Feb 28 2019

4. Cancer Center Support Grant

5P30CA013696

Project Dates:  July 1 2014 to June 30 2019

Selected Publications

Williams H., Gottesman M. and Gautier J. (2012). Replication-independent repair of interstrand crosslinks. Molecular Cell, 47: 140-7.

Peterson, S., Li, Y., Wu-Baer, F., Chait, B., Baer, R., Yan, H., Gottesman, M. and Gautier J. (2013). Activation of DSB processing requires phosphorylation of CtIP by ATR. Molecular Cell, 49: 657-67.

Srinivasan, S., Dominguez-Sola, D., Wang, L.C., Hyrien, O. and Gautier, J. (2013) “Cdc45 is a critical effector of Myc-dependent DNA replication stress”. Cell Reports, 3:1629-39.

Sato, M., Rodriguez-Barrueco R., Yu J., Do C., Silva JM and Gautier J. (2015) “MYC is a critical target of FBXW7. Oncotarget 6: 3292-305.

Aparicio, T., Baer, R., Gottesman, M. and Gautier, J. (2016) “MRN, CtIP, and BRCA1 mediate repair of topoisomerase II–DNA adducts”. The Journal of Cell Biology. 212: 399-408.

Kato N., Kawasoe Y., Williams H., Coates E., Roy U., Shi Y., Beese L., Scharer O., Yan H., Gottesman M., Takahashi T. and Gautier J. (2017) Sensing and processing of DNA interstrand crosslinks by the mismatch repair pathway. Cell Reports. 21: 1375-1385.
Link to complete list of publications:: https://scholar.google.com/citations?user=OGR--C0AAAAJ&hl=en&oi=ao