Scientific article

Singlet oxygen-triggered chloroplast-to-nucleus retrograde signalling pathways: an emerging perspective

Published inPlant, Cell and Environment, vol. 41, no. 8, p. 1727-1738
Publication date2018

Singlet oxygen (¹O₂) is a prime cause of photo-damage of the photosynthetic apparatus. The chlorophyll molecules in the photosystem II reaction center and in the light-harvesting antenna complex are major sources of ¹O₂ generation. It has been thought that the generation of ¹O₂ mainly takes place in the appressed regions of the thylakoid membranes, namely, the grana core, where most of the active photosystem II complexes are localized. Apart from being a toxic molecule, new evidence suggests that ¹O₂ significantly contributes to chloroplast-to-nucleus retrograde signalling that primes acclimation and cell death responses. Interestingly, recent studies reveal that chloroplasts operate two distinct ¹O₂-triggered retrograde signalling pathways in which β-carotene and a nuclear-encoded chloroplast protein EXECUTER1 play essential roles as signalling mediators. The coexistence of these mediators raises several questions: their crosstalk, source(s) of ¹O₂, downstream signalling components, and the perception and reaction mechanism of these mediators towards ¹O₂. In this review, we mainly discuss the molecular genetic basis of the mode of action of these two putative ¹O₂ sensors and their corresponding retrograde signalling pathways. In addition, we also propose the possible existence of an alternative source of ¹O₂, which is spatially and functionally separated from the grana core.

  • Acclimation
  • Photoinhibition
  • Programmed cell death
  • Retrograde signalling
  • Singlet
  • Oxygen
  • β-carotene
Citation (ISO format)
DOGRA, Vivek, ROCHAIX, Jean-David, KIM, Chanhong. Singlet oxygen-triggered chloroplast-to-nucleus retrograde signalling pathways: an emerging perspective. In: Plant, Cell and Environment, 2018, vol. 41, n° 8, p. 1727–1738. doi: 10.1111/pce.13332
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Article (Published version)
ISSN of the journal1365-3040

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