Cole Haynes — CBC/RBC Seminar
“Sensing and Adapting to Mitochondrial Dysfunction”
4:00 pm –
5:00 pm
Beadle Center
Room: N172
1901 Vine St
Lincoln NE 68503
Lincoln NE 68503
Additional Info: BEAD
Contact:
Hannah Kahler, 402-472-3173, hannah.kahler@unl.edu
Cole Haynes is an assistant member of the Cell Biology Program, Memorial Sloan Kettering Cancer Center.
Mitochondrial dysfunction occurs in a number of pathologies including Parkinson’s, cancer, bacterial infection as well as general aging. However, the cellular mechanisms in place to detect mitochondrial stress and activate protective responses are poorly understood. To be presented: a recently discovered transcription factor that “monitors” mitochondrial function and activates a mitochondrial unfolded protein response (UPRmt). These studies suggest an elegant strategy employed by cells to survive mitochondrial stress and ultimately regenerate healthy mitochondria. Interestingly, recent findings indicate that the UPRmt also interacts with innate immunity pathways suggesting this signaling pathway can detect and kill those pathogenic bacteria that target mitochondria to promote infection.
Mitochondrial dysfunction occurs in a number of pathologies including Parkinson’s, cancer, bacterial infection as well as general aging. However, the cellular mechanisms in place to detect mitochondrial stress and activate protective responses are poorly understood. To be presented: a recently discovered transcription factor that “monitors” mitochondrial function and activates a mitochondrial unfolded protein response (UPRmt). These studies suggest an elegant strategy employed by cells to survive mitochondrial stress and ultimately regenerate healthy mitochondria. Interestingly, recent findings indicate that the UPRmt also interacts with innate immunity pathways suggesting this signaling pathway can detect and kill those pathogenic bacteria that target mitochondria to promote infection.