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Cell Wall Invertase Promotes Fruit Set under Heat Stress by Suppressing ROS-Independent Cell Death

文献类型： 外文期刊

作者： Liu, Yong-Hua 1 ; Offler, Christina E. 1 ; Ruan, Yong-Ling 1 ;

作者机构： 1.Univ Newcastle, Sch Environm & Life Sci, Callaghan, NSW 2308, Australia

2.Univ Newcastle, Australia China Res Ctr Crop Sci, Callaghan, NSW 2308, Australia

3.Zhejiang Acad Agr Sci, Inst Vegetable Sci, Hangzhou 310021, Zhejiang, Peoples R China

4.Hainan Univ, Coll Hort & Landscape Architecture, Haikou 570228, Hainan, Peoples R China

期刊名称：PLANT PHYSIOLOGY （ 影响因子：8.34； 五年影响因子：8.972 ）

ISSN：

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收录情况： SCI

摘要： Reduced cell wall invertase (CWIN) activity has been shown to be associated with poor seed and fruit set under abiotic stress. Here, we examined whether genetically increasing native CWIN activity would sustain fruit set under long-term moderate heat stress (LMHS), an important factor limiting crop production, by using transgenic tomato (Solanum lycopersicum) with its CWIN inhibitor gene silenced and focusing on ovaries and fruits at 2 d before and after pollination, respectively. We found that the increase of CWIN activity suppressed LMHS-induced programmed cell death in fruits. Surprisingly, measurement of the contents of H2O2 and malondialdehyde and the activities of a cohort of antioxidant enzymes revealed that the CWIN-mediated inhibition on programmed cell death is exerted in a reactive oxygen species-independent manner. Elevation of CWIN activity sustained Suc import into fruits and increased activities of hexokinase and fructokinase in the ovaries in response to LMHS. Compared to the wild type, the CWIN-elevated transgenic plants exhibited higher transcript levels of heat shock protein genes Hsp90 and Hsp100 in ovaries and HspII17.6 in fruits under LMHS, which corresponded to a lower transcript level of a negative auxin responsive factor IAA9 but a higher expression of the auxin biosynthesis gene ToFZY6 in fruits at 2 d after pollination. Collectively, the data indicate that CWIN enhances fruit set under LMHS through suppression of programmed cell death in a reactive oxygen species-independent manner that could involve enhanced Suc import and catabolism, HSP expression, and auxin response and biosynthesis.

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