Research
What are the signal transduction pathways of chloroplast quality control?
To survive, all organisms must monitor their surroundings and adjust accordingly. This is particularly true for plants. As sessile organisms, they must employ a wide range of signaling mechanisms to thrive in an ever changing environment. During photosynthesis, chloroplasts constantly experience metabolic stress in the form of reactive oxygen species (ROS). The severity, timing, and location of these stresses fluctuates with the environment, therefore chloroplasts are able to sense these changes and signal out for acclimation. In response to changing environments, chloroplasts can send out “retrograde” signals that alter gene expression and/or cell physiology. Universal retrograde signals are typically used when all chloroplasts are experiencing similar levels of stress, or to coordinate chloroplast development.
But what if only a few chloroplasts are stressed or damaged?
Classic retrograde signals would not allow the nucleus to distinguish between damaged and healthy chloroplasts, while ignoring the problem would leave chloroplasts that are energetically inefficient, as well as dangerous ROS generators. A chloroplast quality control mechanism could be used to repair or remove defective/stressed chloroplasts from overall healthy cells.
Evidence for a chloroplast quality control mechanism was first revealed in Arabidopsis ferrochelatase 2 (fc2), which has impaired activity of the nuclear encoded ferrochelatase 2, a heme synthase. fc2 mutants cannot tolerate dark-to-light shifts due to a burst of singlet oxygen (1O2) attributable to the accumulation of the photosensitizing tetrapyrrole intermediate protoporphyrin-IX. The ROS burst leads to the ubiquitination of chloroplast envelope proteins, induction or chloroplast degradation, and eventually cell death.