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

• Published in: Plant, cell and environment cell and environment, 2015-07, Vol.38 (7), p.1255-1274
• Main Authors: SUZUKI, KENSAKU, AOKI, NAOHIRO, MATSUMURA, HISAKAZU, OKAMURA, MASAKI, OHSUGI, RYU, SHIMONO, HIROYUKI
• Format: Article
• Language: English
• Subjects: abscisic acid (ABA); Abscisic Acid - metabolism; chilling‐induced pollen sterility; Cold Temperature; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; ethylene; Gene Expression Profiling; Gene Expression Regulation, Plant; Heat Shock Transcription Factors; Heat-Shock Proteins - genetics; Heat-Shock Proteins - metabolism; Lipid Peroxidation; low water temperature; malondialdehyde (MDA); Malondialdehyde - metabolism; Oligonucleotide Array Sequence Analysis; Oryza - genetics; Oryza - physiology; Oxidative Stress; Plant Growth Regulators - metabolism; Plant Infertility - genetics; Plant Proteins - genetics; Plant Proteins - metabolism; Pollen - genetics; Pollen - physiology; Stress, Physiological; Transcription Factors - genetics; Transcription Factors - metabolism; Water - physiology
• ISSN: 0140-7791; 1365-3040
• DOI: 10.1111/pce.12498

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. Chilling‐induced male sterility increased in the rice plants experienced low water temperature before panicle initiation. Gene expression analyses showed that the increase is linked with the loss of chilling‐induced expression of many stress‐responsive genes including OsFKBP65 and genes encoding the large heat shock protein OsHSP90.1, some heat shock factors, and many small heat shock proteins. The OsFKBP65‐modulated HSP accumulation, which is lost in low‐Tw spikelets, should be indispensable for chilling tolerance of rice spikelets. Commentary: Keeping a cool head: gene networks underlying chilling‐induced male sterility in rice