Cooling water before panicle initiation increases chilling-induced male sterility and disables chilling-induced expression of genes encoding OsFKBP65 and heat shock proteins in rice spikelets.
In rice (Oryza sativa L.), chilling-induced male sterility increased when plants experienced low water temperature (Tw , 18 °C for 14 d) before panicle initiation. The number of mature pollen grains after chilling at the booting stage (12 °C for 5 d) was only 45% of total pollen grains in low-Tw plants, whereas it was 71% in normal-Tw plants (Tw not controlled; approximately 23 °C under air temperature of 26 °C/21 °C, day/night). Microarray and quantitative PCR analyses showed that many stress-responsive genes (including OsFKBP65 and genes encoding the large heat shock protein OsHSP90.1, heat-stress transcription factors and many small heat shock proteins) were strongly up-regulated by chilling in normal-Tw spikelets, but were unaffected or even down-regulated by chilling in low-Tw spikelets. OsAPX2 and genes encoding some other antioxidant enzymes were also significantly down-regulated by low Tw in chilled spikelets. The levels of lipid peroxidation products (malondialdehyde equivalents) were significantly increased in low-Tw spikelets by chilling. Ascorbate peroxidase activity in chilled spikelets was significantly lower in low-Tw plants than in normal-Tw plants. Our data suggest that an OsFKBP65-related chilling response, which protects proteins from oxidative damage, is indispensable for chilling tolerance but is lost in low-Tw spikelets.