Dr. Croteau received her Ph.D. from Johns Hopkins University School of Medicine and currently works closely with Dr. Vilhelm Bohr to manage the group on DNA repair, premature aging disorders and mitochondria function.
We work on four major areas of research:
First, we are trying to understand the biological implications of losing one of the five human RecQ helicases. Presently we are focusing our attention on RECQL4 and RECQL5. RECQL4 plays important roles in DNA metabolism but they are not well understood. I am characterizing RECQL4 patient mutations in order to glean information about genotype:phenotype correlations. RECQL5 is another one of the lesser studied RecQ helicases and we are exploring how and when RECQL5 is recruited to DNA damage.
Second, I am interested in understanding how DNA repair impacts mitochondrial function. In these studies, we are employing DNA repair deficient cells and mouse models to quantify mitochondrial alterations and identify small molecule modulators that can ameliorate mitochondrial dysfunction.
Third, we are investigating how DNA repair deficiencies impact the ability of mice to recover from an acute stressor such as stroke. While a DNA repair deficiency may not predispose mice to strokes, their DNA repair capacity makes a significant impact on how well mice recover from stroke.
Fourth, we are investigating how a DNA repair deficiency impacts the progression of Alzheimer’s disease in the mouse model, 3xTg AD. We find that genes and pathways that are specific to mitochondrial dysfunction and cell death are specifically up-regulated in the DNA repair lacking 3xTg mouse model, and these pathways were not up-regulated in either single mutant mouse model.