抄録
Rice seedlings, when kept at 42 ℃ for 24 h before being kept at 5 ℃ for 7 d, did not develop chilling injury. Chilling resistance was enhanced in parallel with the period of heat-treatment. The level of APX activity was higher in seedlings exposed to 42 ℃. The levels of apxa mRNA increased within 1 h after seedlings were exposed to 42 ℃. Elevated apxa mRNA levels could also be detected after 6, 9, 12 and 24 h of heat stress. The promoter of apxa had a minimal heat shock factor (HSF) binding motif, 5'-nGAAnnTTCn-3', located 81-bp upstream to the TATA box. Heat shock induction of apxa could be possible cause of reduced chilling injury in rice seedlings. Transgenic rice plants were generated via Agrobacterium tumefaciens-mediated transformation. The level of APX activity was higher in high-expression transgenic lines than the low-expression transgenic line and non-transformed control plants. Relative to the low-expression line and non-transformed control plants, high-expression lines showed significantly less injury from the chilling stress.
