Putting the brakes on chloroplast stress signaling

Journal Article · 16 February 2022 · Molecular Plant

DOI: https://doi.org/10.1016/j.molp.2022.02.009 · OSTI ID:1880343

Tano, David W.  ^[1]; Woodson, Jesse D.  ^[2]

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1. Univ. of Arizona, Tucson, AZ (United States); The University of Arizona
2. Univ. of Arizona, Tucson, AZ (United States)

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.

• Research Organization: Univ. of Arizona, Tucson, AZ (United States)
• Sponsoring Organization: USDOE
• Grant/Contract Number: SC0019573
• OSTI ID: 1880343
• Journal Information: Molecular Plant, Journal Name: Molecular Plant Journal Issue: 3 Vol. 15; ISSN 1674-2052
• Publisher: ElsevierCopyright Statement
• Country of Publication: United States
• Language: English