Adaptive responses of plants to light stress: mechanisms of photoprotection and acclimation. A review

Abstract

Plants depend on solar energy for growth via oxygenic photosynthesis. However, when light levels exceed the optimal range for photosynthesis, it causes abiotic stress and harms plant physiology. In response to excessive light, plants activate a series of signaling pathways starting from the chloroplast and affecting the entire plant, leading to stress-specific physiological changes. These signals prompt various physiological and biochemical adjustments aimed at counteracting the negative impacts of high light intensity, including photodamage and photoinhibition. Mechanisms to protect against light stress involve scavenging of chloroplastic reactive oxygen species (ROS), adjustments in chloroplast and stomatal positioning, and increased anthocyanin production to safeguard the photosynthetic machinery. Given that this machinery is a primary target for stress-induced damage, plants have evolved acclimation strategies like dissipating thermal energy via non-photochemical quenching (NPQ), repairing Photosystem II (PSII), and regulating the transcription of photosynthetic proteins. Fluctuating light presents a less severe but consistent stress, which has not been extensively studied. Nevertheless, current research indicates that state transitions and cyclic electron flow play crucial roles in helping plants adapt to varying light conditions. This review encapsulates the latest understanding of plant physiological and biochemical responses to both high light and low light stress.

Keywords: biogenesis of PSII; climate change; light; photosystem II repair cycle; reactive oxygen species.

Figure 1

The influence of various light factors on plant growth stages and characteristics. This diagram illustrates how different aspects of light, including light quantity, light quality, and light duration, affect various stages of plant development and morphology. Light quantity (intensity) impacts the overall plant biomass. On the other hand, light quality (spectrum) affects plant morphology, including the development of specific physical traits. Light duration (photoperiod) regulates flowering and other photoperiod-sensitive processes in plants. The cycle demonstrates the interconnected nature of light factors and their cumulative effects on plant growth and development.

Figure 2

Molecular mechanisms of photoreceptor-mediated light signaling in plant cells. This diagram illustrates the signaling pathway used to send low and high light signals and responses in plants. Photoreceptors; Phot1 and Phot2, in the cell membrane; these molecules detect the intensity of light. Low light response protein Jac1 is activated by Phot1 and Phot2 in the cytoplasm, and they then transmit a signal to the nucleus. High light response Phot2 is in direct contact with the chloroplast protein CHUP1 and blue light’s CP FKF1 and degrades FKF1. Intracellular interaction with blue light affects cp-actin, which causes signal accumulation and subsequent reaction in the golgi bodies and chloroplasts. The extensive interconnected network ensures that plants can alter their growth and development depending on the light.

Figure 3

Anthocyanin biosynthesis pathway in plants. This diagram illustrates the enzymatic steps involved in the biosynthesis of anthocyanin. Highlighting the key enzymes and their respective positions in the pathway. PAL, phenylalanine ammonia-lyase; C4H, cinnamate 4-hydroxylase; 4CL, 4-coumarate CoA ligase; CHS, chalcone synthase; CHI, chalcone isomerase; F3H, flavanone 3-hydroxylase; F3′H, flavonoid 3 hydroxylase; F3′5′H, flavonoid 3,5 hydroxylase; FLS, flavonol synthase; DFR, dihydroflavonol 4-reductase; ANS, anthocyanidin synthase; UFGT, UDP-galactose flavonoid 3-O-galactosyltransferase; The pathway is divided into different branches, each leading to the synthesis of anthocyanin biosynthesis.

Figure 4

Reactive oxygen species (ROS) detoxification in the chloroplast. Singlet oxygen (1O₂) is generated when oxygen interacts with the triplet-excited state of chlorophyll in photosystem II (PSII). The excitation energy is transferred to carotenoids (Cars), resulting in the production of triplet molecular oxygen (3O₂) and excited triplet carotenoids (3Car*). The 3Car* then dissipates this energy as heat while reverting to its ground state. In photosystem I (PSI), oxygen photoreduction can produce superoxide (O₂), which is neutralized by superoxide dismutase (SOD) to form hydrogen peroxide (H₂O₂). This H₂O₂ is then reduced to water H₂O by ascorbate peroxidase (APX) using ascorbate (Asc), leading to elevated levels of mono-dehydroascorbate (MDA) and dehydroascorbate (DHA). MDA and DHA are reduced by monodehydroascorbate reductase (MDAR) and dehydroascorbate reductase (DHAR), respectively. These compounds are subsequently reduced by monodehydroascorbate reductase (MDAR) and dehydroascorbate reductase (DHAR), respectively. Additionally, during the ascorbate-glutathione recycling process, NADPH-dependent glutathione reductase (GR) facilitates the reduction of oxidized glutathione (GSSG) back to its reduced form, glutathione (GSH). This diagram illustrates how light absorption, electron transport, and antioxidant defense mechanisms are integrated within the chloroplast.

Figure 5

Schematic representation of the coordinated processes involved in the damage recognition, degradation, and repair of PSII, emphasizing the essential role of protein turnover for photosynthetic efficiency and stability under fluctuating light conditions. The interplay between assembly factors, chaperones, and proteases ensures the continuous function of PSII, maintaining optimal photosynthetic performance. PSII, Photosystem II; LHC-II, Light Harvesting Complex II proteins (green); OEC, Oxygen Evolving Complex (gray); Light-induced damage of D1 protein (red), cpSRP54, Chloroplast Signal Recognition Particle 54; cpSecY, Chloroplast SecY; STN, STN Kinase; LPA, Low PSII Accumulation; AtPD, Arabidopsis Thylakoid Protease.