Wood Laboratory
Areas of Research
- DNA Repair Research
- DNA Polymerases Research
- Genome Stability Research
- Genetic Predisposition to Cancers Research
Wood Lab Group Photo
Welcome to the Wood Laboratory at MD Anderson Cancer Center. We are a research lab in the Department of Epigenetics and Molecular Carcinogenesis at Science Park, a basic science research campus of MD Anderson located near Austin, Texas. Research in our group explores the mechanisms of genome stability and the consequences for cancer, including the biochemical mechanism of repair of cross-links between DNA strands and the DNA polymerases that help cells tolerate DNA damage.
It is important to understand the mechanisms of DNA repair in detail, because this process is a front-line defense against the mutations that cause cancer. Mammalian cells have numerous strategies for repair of DNA damage and devote many hundreds of genes and proteins to DNA repair. Moreover, the aim of many cancer therapies is to disable tumor DNA by using DNA-damaging radiation and drugs. Our research employs a broad range of investigations, ranging from fundamental biochemical studies and proteomics through cellular biology, to genetically engineered mouse models having impaired pathways of repair and mutagenesis.
Postdoctoral Position Available
We have a funded postdoctoral position open to carry out research on the biochemistry of DNA repair and DNA polymerases. Please contact us by sending your CV and references.
Recent Events
New Publications
Lange SS, Bhetawal S, Reh S, Powell KL, Kusewitt D, Wood RD. DNA polymerase ζ deficiency causes impaired wound healing and stress-induced skin pigmentation. Life Science Alliance. 2018 June 29; 1(3):e201800048. PMID: 30046772
Tomida J, Takata Ki, Bhetawal S, Person MD, Chao HP, Tang DG, Wood RD. FAM35A associates with REV7 and modulates DNA damage responses of normal and BRCA1-defective cells. EMBO J. 2018;37(12):e99543. PMID: 29789392
Wood RD, Fifty years since DNA Repair was linked to cancer. Nature. 2018; 557(7707):648-649. PMID: 29844546
Malaby AW, Martin SK, Wood RD, Doublié S. Expression and Structural Analyses of Human DNA Polymerase θ (POLQ). In: Eichman B, editor. DNA Repair Enzymes: Structure, Biophysics, and Mechanism. Methods in Enzymology. 592. 1st Edition ed. Burlington: Academic Press; 2017. p. 103-21. PMID: 28668117
Events
The lab is happy to welcome postdoc Denisse Carvajal, Ph.D., from St. Louis University. She is characterizing the activity of full-length PolQ.
Rick Wood, Ph.D., has been elected to the American Academy of Arts and Sciences! Congratulations, Rick!
Rick chaired the Gordon Research Conference: DNA Damage, Mutation, and Cancer. March 24-25, 2018 in Ventura, CA. Sara Martin, Kei-ichi Takata and Junya Tomida also attended. Sara co-chaired the associated Gordon Research Seminar. In 2019, Sara gave a platform presentation "Translesion DNA Polymerase Zeta Suppresses an Innate Immune Response" at the 2019 Nucleic Acids Gordon Research Seminar.
Sara is now a CPRIT Scholar. She was also honored at the GSBS Evening of Discovery at the Houston Country Club.
Congratulations and farewell to Kei-ichi Takata, who recently started a new position leading a laboratory at the Institute for Basic Science, Center for Genomic Integrity, Ulsan National Institute of Science and Technology in Ulsan, S. Korea.
Congratulations to Junya Tomida, who started his own lab as an Assistant Professor at the University of North Carolina at Charlotte. We look forward to collaborating with you.
We are pleased to have research support including: a new NIH P01 grant; a DoD Development Award; an NIH R03 award; a CPRIT award; and a SPORE developmental research program grant.
In the image below, a double-fluorescent Cre reporter system was used to monitor Cre recombinase activity in skin. In this system, the transgene mT/mG expresses red fluorescence in cell membranes before Cre-mediated recombination and green fluorescence after Cre-mediated recombination. We can use this system in conditional knock-out strains to monitor cell-specific expression of Cre activity and infer where our gene of interest is no longer expressed.
