PhD Candidate University of Arizona Tucson, Arizona
Body of Abstract: Photosynthesis is a fundamental process that converts light energy into chemical energy and, consequently, is crucial to life on earth. While this process benefits plant fitness, it can also be a source of reactive oxygen species (ROS) that can damage photosynthetic machinery, the chloroplast, and the cell if not mediated. Environmental stress can lead to excess ROS accumulation in the chloroplast, triggering retrograde signaling (chloroplast-to-nucleus) to regulate stress response and cellular degradation systems, making this organelle an environmental sensor. In plant cells, one ROS, singlet oxygen (1O2), is predominantly produced in the chloroplast, making 1O2 a chloroplast-specific stress signal. This raises two intriguing questions: How do plants sense when their chloroplasts have been damaged due to excess ROS accumulation caused by environmental stresses? -and- How are dysfunctional chloroplasts selectively degraded to maintain efficient photosynthesis and to prevent cytotoxic levels of ROS from accumulating?
To “shine a light” on these questions, we have employed a gain-of-function genetic screen to identify genes involved in 1O2-induced chloroplast quality control (CQC). The Arabidopsis ferrochelatase two mutant (fc2) conditionally accumulates 1O2 and has enhanced rates of selective chloroplast degradation and cell death, making this mutant a valuable system to study CQC. Here, fc2 mutants were further transformed/mutagenized using activation tagging to identify genes sufficient to suppress cell death in fc2 when overexpressed. This screen has yielded eight mutants of interest, all of which suppress the fc2 cell death phenotype and express a wide range of morphological and molecular phenotypes. One of these mutants appears to be generally stress-tolerant to heat, freezing, excess light, and carbon starvation, which may have implications beyond stresses that directly affect photosynthesis.