News and Congratulations
Tuberculosis is the world’s 9th leading cause of death. Antibiotic resistance in TB is solely the result of mistakes made during DNA replication or repair, rather than by swapping antibiotic resistance genes from other bacteria. Mistakes that inactivate drug targets or drug activating enzymes allow TB to resist antibiotics, however, the mechanisms that control this DNA mutagenesis are poorly defined not just in TB, but in many bacteria. In a recently published paper in Molecular Cell, TL1 trainee, Matthew Wipperman, elucidates a new mechanism that controls this DNA mutagenesis in TB and other mycobacteria through the common DNA repair enzyme RecA. RecA is a central player in DNA repair and mutagenesis and the authors found that phosphorylation of RecA controls its participation in DNA mutagenesis, while preserving its other functions. They also found that the membrane lipid cardiolipin also participates in controlling this mutagenesis function of RecA. Their findings may help researchers understand how to develop better drugs that target multi-drug resistant (MDR) TB, which is an escalating public health problem.
Wipperman, a postdoctoral researcher, at Memorial Sloan Kettering Cancer Center, is currently appointed as a TL1 trainee continuing his second year of CTSC support. His mentors are Michael Glickman, MD, Laboratory Head, Immunology (IMP) Program, MSKCC; Daniel Fitzgerald, MD, Professor, Medicine/Microbiology and Immunology, Director of the Center for Global Health, WCM; Vanni Bucci, PhD, Professor, Materials Science and Engineering, University of Massachusetts Dartmouth.
The CTSC TL1 Training Core Program supports early career development among pre- and early post-doctoral trainees by providing salary support, protected time, advanced degree training and practical skills necessary to conduct interdisciplinary Clinical and Translational Investigation in a team research environment.