Photosynthesis and Heat Stress

Study Notes

Heat stress and oxidative stress can prevent the healing of damaged PSII by inhibiting PSII protein production, leading to a reduction in plant photosynthesis efficacy.
Chlorophyll, the principal photosynthetic component, can absorb light energy and facilitate electron transport in the early and most critical phases of photosynthesis.
Under heat stress, the amount of chlorophyll in leaves declines, resulting in leaf senescence or chlorosis.
Thermal treatment raises the efficiency of chlorophyllase and Chl-degrading peroxidase, leading to a significant drop in Chl levels.

Plant responses to heat stress accumulate ROS, including singlet oxygen, superoxide radical, hydrogen peroxide, and hydroxyl radical, causing oxidative damage.
The activation sites of PSI and PSII in chloroplasts are primary locations of ROS formation, although ROS is produced in other organelles such as peroxisomes and mitochondria.
The maximum efficacy of PSII and the acquired ROS have a linear relation.
Heat stress has been proposed as a primary source of ER stress.

ROS are produced by enzymatic and nonenzymatic processes in plants under normal and stressful situations and are linked to several stages of plant development and growth.
Heat stress triggers the release of ROS scavengers, which eliminate excessive ROS.
ROS scavengers in plants include Ascorbate peroxidase (APX), Catalase (CAT), CSD1, CSD2, and CCS1.
Heat stress induces the release of cell wall binding protein Expansin 1 (AsEXP1) in hair grass, involved in cell wall remodeling.

Epigenetic modifications occur at the DNA level in response to heat stress.
Epigenetic modifications, including DNA methylation, histone modifications, histone variations, short RNAs, and long noncoding RNAs, may upregulate to defend plants from destruction.
These modifications are related to heat stress response (HSR) gene expression.
The activation of methyltransferases has been examined extensively in response to heat stress.

Plants that thrive at high temperatures retain permeability and stability, necessitating membrane fluidity variability.
Thylakoids and cell membranes are usually one of the first to be altered by high thermal effects.
Heat stress causes the decomposition of the structural proteins of the cellular membrane, leading to membrane permeability and disruption of cellular functions.