Cooling water before panicle initiation increases chilling‐induced male sterility and disables chilling‐induced expression of genes encoding OsFKBP 65 and heat shock proteins in rice spikelets

• Published in: Plant, cell and environment Vol. 38; no. 7; pp. 1255 - 1274
• Main Authors: SUZUKI, KENSAKU, AOKI, NAOHIRO, MATSUMURA, HISAKAZU, OKAMURA, MASAKI, OHSUGI, RYU, SHIMONO, HIROYUKI
• Format: Journal Article
• Language: English
• Published: 01.07.2015
• ISSN: 0140-7791; 1365-3040
• DOI: 10.1111/pce.12498

Abstract In rice ( O ryza sativa   L .), chilling‐induced male sterility increased when plants experienced low water temperature ( T w , 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‐ T w plants, whereas it was 71% in normal‐ T w plants ( T w 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 OsFKBP 65 and genes encoding the large heat shock protein OsHSP 90.1, heat‐stress transcription factors and many small heat shock proteins) were strongly up‐regulated by chilling in normal‐ T w spikelets, but were unaffected or even down‐regulated by chilling in low‐ T w spikelets. OsAPX 2 and genes encoding some other antioxidant enzymes were also significantly down‐regulated by low T w in chilled spikelets. The levels of lipid peroxidation products (malondialdehyde equivalents) were significantly increased in low‐ T w spikelets by chilling. Ascorbate peroxidase activity in chilled spikelets was significantly lower in low‐ T w plants than in normal‐ T w plants. Our data suggest that an OsFKBP 65 ‐related chilling response, which protects proteins from oxidative damage, is indispensable for chilling tolerance but is lost in low‐ T w 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 OsHSP 90.1, 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