Plant Light Stress

Abstract

Photosynthesis forms the basis for primary production and fuels the formation of biomass with valuable chemical composition in plants. Although photosynthesis requires sunlight, the very nature of sunlight also has negative effects on photosynthesis. Visible light and ultraviolet light, the inherent parts of sunlight, may cause damage to the photosynthetic machinery and other cellular components. Plants have therefore evolved various protective and response mechanisms, which monitor the intensity, wavelength, duration and direction of light and mitigate the negative effects of light stress. Currently, the underlying molecular mechanisms and functional overlaps among light receptor and chloroplast signalling, and the consequent light‐dependent adjustments in plant performance are emerging. The ability to delicately sense, signal and respond to the ambient light environment forms a key contributor to plant growth and productivity.

Key Concepts

  • Photosynthesis causes a potential risk of photodamage.
  • Excess light and ultraviolet radiation from sunlight lead to increased production of ROS, which may cause photooxidative damage.
  • Plants have evolved protective and response mechanisms against photodamage.
  • ROS act as signalling molecules that mediate vital functions in inducing resistance to light stress and other abiotic and biotic stresses.
  • Chloroplast retrograde signals play key roles in eliciting cross‐tolerance to biotic stress factors.

Keywords: light stress; photodamage; photosynthesis; reactive oxygen species; ultraviolet radiation; signalling

Figure 1. Summary of light‐sensing mechanisms and responses in plants. Excess light and UV radiation cause alterations in chloroplast chemistry and activate wavelength‐specific photoreceptors in the nucleus and cytoplasm. Light sensing triggers immediate adjustments in chloroplasts and initiates further signals to the nucleus. Together with the photoreceptor signalling, chloroplast retrograde signals regulate nuclear gene expression, cell metabolism and plant development.
Figure 2. Light stress as a modulator of whole cell physiology. Signalling mechanisms that control plant responses to excess light, UV radiation and pathogens deploy partially overlapping mechanisms. Tight interactions within signalling networks enable extensive cross‐talk between different stress signalling pathways and development of cross‐tolerance to a range of environmental factors.
Figure 3. Regulation of photomorphogenesis by chloroplast and light receptor signalling. In dark, CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) suppresses photomorphogenesis by targeting the transcription factor ELONGATED HYPOCOTYL 5 (HY5) for proteasomal degradation. In excess light, photomorphogenesis is downregulated by signals that initiate from chloroplasts and are mediated by the PHD TYPE TRANSCRIPTION FACTOR WITH TRANSMEMBRANE DOMAINS (PTM), which activates a transcription factor ABSCISIC ACID INSENSITIVE 4 (ABI4). This results in the accumulation of COP1 and the subsequent degradation of HY5. In moderate growth light, phytochrome B (PHYB) induces COP1 degradation hence activating photomorphogenesis through HY5. Under UVB radiation, UV RESISTANCE LOCUS 8 (UVR8) becomes activated and inhibits the association between COP1 and the ubiquitin ligase complex, which allows the activation of photomorphogenesis genes by HY5.
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Further Reading

Feng P, Guo H, Chi W, et al. (2016) Chloroplast retrograde signal regulates flowering. Proceedings of the National Academy of Sciences 113: 10708–10713.

Foyer CH, Rasool B, Davey JW and Hancock RD (2016) Cross‐tolerance to biotic and abiotic stresses in plants: a focus on resistance to aphid infestation. Journal of Experimental Botany 67: 2025–2037.

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Kleine T and Leister D (2016) Retrograde signaling: organelles go networking. Biochimica et Biophysica Acta 1857: 1313–1325.

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Pascual, Jesús, Rahikainen, Moona, and Kangasjärvi, Saijaliisa(Apr 2017) Plant Light Stress. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0001319.pub3]