Peng Liu

Toxicity of Fe²⁺ is one of the major constraints for lowland rice production in tropical and subtropical areas. The root tip is a primary site of iron (Fe²⁺) toxicity in rice. To explore the effects of iron toxicity on the morphological and biological characteristics on the border cells in rice (Oryza sativa L.), experiments were carried out using the border cells in two cultivars. The experimental results revealed the following properties of border cells shared by both rice cultivars: the first border cells appeared almost synchronously with the emergence of the primary root tip; the number of border cells reached maximum when the root was 25 mm long; the border cells were most viable when the root length was 20 mm; and the relative activity of pectin methylesterase (PME) was the highest when the root length was 2 mm. The two rice cultivars exhibited different trends in their response to Fe²⁺ toxicity: the number of root border cells in Fe²⁺-resistant Zhongyou 9288 increased when experiencing low levels of Fe²⁺ treatment, but then declined at higher Fe²⁺ levels. The number of root border cells in Fe²⁺-sensitive Shanyou No. 10, however, declined rapidly when the concentration of Fe²⁺ increased. The results also showed that Fe²⁺ toxicity hindered the development of root border cells of both rice cultivars, but the Fe²⁺ sensitive variety experienced thickened the root cap cell walls that led to programmed cell death.

A solution culture experiment was conducted to determine the effects of different potassium concentrations on the chlorophyll fluorescence and oxidation resistance of the Fe²⁺-tolerant rice (Oryza sativa L.) genotype Xieyou 9308 and the Fe²⁺-sensitive genotype IIyou 838 exposed to 250 mg/L of Fe²⁺. The minimal fluorescence, maximum fluorescence efficiency, maximum fluorescence, and non-photochemical quenching coefficient showed no significant changes. However, the photochemical quenching coefficient increased. Under 200 mg/L K⁺ concentration, the effects of Fe²⁺ stress decreased. Compared with the control group, chlorophyll content and peroxidase, superoxide dismutase, and catalase activities decreased, whereas MDA content increased under Fe²⁺ stress. Exogenous K⁺ alleviated Fe²⁺ toxicity in the test subjects compared with the control group. Overall, external K⁺ could alleviate the toxic effects of Fe²⁺ toxicity.

Root border cells are a population of rhizosphere cells surrounding the root tips but separated from them. The root tip is a major target of Fe²⁺ toxicity; thus, it was hypothesized that the border cells might protect or exacerbate Fe²⁺ toxicity. To explore the effects of excess Fe²⁺ on the border cells in rice (Oryza sativa L.), experiments were carried out using the border cells in vitro (Shanyou No. 10). The border cells were precultured under “hanging in the air” and detached from the root tips. The shape, numbers, and viability of border cells were examined during exposure to toxic levels of Fe²⁺. When the root was 1 mm long, there were 205 border cells on average. With the growth of the root, more border cells were observed. When the root grew to 25 mm long, the total number of border cells reached a maximum, while the maximum activity of border cells appeared when the root was 20 mm long. The pectin methyl esterase (PME) activity of the root cap peaked at a root length of 2 mm. Border cell development was related to PME activity in rice. Excessive Fe²⁺ was toxic to detached border cells. After treatment with 200 μM Fe²⁺ solution for 48 h, cell viability decreased by 72.70%. However, when treated with 400 μM Fe²⁺ solution, the number of viable cells was actually higher, suggesting the induction of a cellular self-protection response. The activity of PME first increased under high concentrations of Fe²⁺ and then decreased. These results indicate that toxic levels of Fe²⁺ modulate PME activity and border cell survival.