Putting the brakes on chloroplast stress signaling

• Published in: Molecular plant Vol. 15; no. 3; pp. 388 - 390
• Main Authors: Tano, David W., Woodson, Jesse D.
• Format: Journal Article
• Language: English
• Published: England Elsevier Inc 07.03.2022; Elsevier
• Subjects: BASIC BIOLOGICAL SCIENCES; chloroplast; Chloroplasts; photosynthesis; post-translational modification; reactive oxygen species; Signal Transduction; signaling; singlet oxygen
• ISSN: 1674-2052; 1752-9867
• DOI: 10.1016/j.molp.2022.02.009

As sessile organisms, plants must be able to sense their surroundings and adjust. One way plants do this is by using their energy-producing organelles (chloroplasts and mitochondria). During environmental stress, these organelles experience metabolic changes that induce signals for acclimation. While many metabolites have been proposed as signaling factors, reactive oxygen species (ROS) are known to play prominent roles. In the chloroplast, the ROS singlet oxygen (1O2) is naturally produced during impaired photosynthesis and can lead to retrograde signaling to the nucleus (to control the expression of hundreds of genes), chloroplast degradation, and cell death. The mechanisms controlling these pathways have mostly remained obscure. Recently, Dogra et al. (2022) reported a new role for EXECUTER2 (EX2) in these chloroplast 1O2 signaling pathways, demonstrating that EX2 acts as a buffer to prevent premature activation of 1O2 signaling. Furthermore, these exciting findings reveal an unexpected complexity to chloroplast stress signaling, and identify a decoy mechanism to prevent early activation of cell death.