Fig 1.
Response in physiological parameters of rice genotypes treated to low temperature stress.
Plants under control (28° C) and stress (10° C) conditions show response in: A) Photosynthesis, B) Transpiration Rate, C) Water use efficiency (WUE), D) Intracellular CO2 concentration (Ci), E) Stomatal conductance, F) Fv'/Fm'. Data are expressed as the result of five replications (plants). The asterisks indicate significance at P ≤ 0.01 (analyzed by Student’s t-test) for comparison of stress treatment vs control, and between control plants for difference to Nipponbare, as standard tolerant genotype.
Fig 2.
ROS mediated damage evaluated in different rice genotypes treated to low temperatures.
Plants under control (28° C) and stress (10° C) conditions showed response in: A) Chlorophyll content, B) Hydrogen peroxide H2O2 and C) Lipid peroxidation MDA. Data was expressed as the mean of five replications. The asterisks indicate significance at P ≤ 0.01 (analyzed by Student’s t-test) for comparison of stress treatment vs control, and between control plants for difference to Nipponbare, taken as standard tolerant genotype.
Fig 3.
Non enzymatic antioxidants and enzymatic antioxidants were evaluated in different rice genotypes treated to low temperatures.
Plants under control (28° C) and stress (10° C) conditions showed response in: A) Anthocyanin content, B) total phenolic content, C) superoxide dismutase (SOD) activity, D) catalase CAT activity, E) Peroxidase activity, and F) 2,2-diphenyl-1-picrylhydrazyl-DPPH activity. Data are expressed as the result of five replications. The asterisks indicate significance at P ≤ 0.01 (analyzed by Student’s t-test) for comparison of stress treatment vs control, and between control plants for difference to Nipponbare, taken as standard tolerant genotype.
Fig 4.
Response of rice plants to temperature treatments, with control (28° C) and stress (10° C) conditions showing differential response in osmolyte content.
A) Proline, B) Glucose content and C) Sucrose content. Data are expressed as the mean of five replications. The asterisks indicate significance at P ≤ 0.01 (analyzed by Student’s t-test) for comparison of stress treatment vs control, and between control plants for difference to Nipponbare, taken as standard tolerant genotype.
Fig 5.
Relative expression of genes (S1 Table) conferring stress tolerance to low temperatures in rice.
Stress tolerance related genes are shown in a time-course of 03–48 h after stress initiation. Data are results from three biological replicates and are expressed as the relative quantification (RQ) ratio of fold change of stress treatment to control.
Fig 6.
Model displaying mechanisms of tolerance to low temperatures in rice.
The regulatory cascade indicates the perception and induction of damage in response to low temperatures, the response in gene expression changes to the stress treatment, as well as the induction of biochemical responses (S3 Table) leading to low temperature tolerance, with an increase in concentration due to the presence of ROS. Abbreviations shown indicate the changes in components affected. Pm: Plasma membrane; Cw: Cell wall; Ch: Chloroplast; N: Nucleus; Grey arrow: Calcium efflux Black arrows: Cold perception; X: Degradation of pectin caused by increased polygalacturonase induced by increased expression of OsBURP16; Red arrow: Induction; Blue arrow: Induction of cold tolerance; Between brackets: Increase in concentration due to ROS. Dotted: Association of Ctb1 and CAT for miRNA induction. Upward arrows: Increased concentration due to induction of ROS; X: Association of Ctb1 and CAT for miRNA induction. The regulatory cascade of perception and induction of damage in response to low temperatures, and response of genes to the stress treatment, as well as the induction of biochemical responses leading to tolerance to low temperatures, leading from an increased concentration of ROS.