State Key Laboratory of Crop Genetics and Germplasm Enhancement, Nanjing Agricultural University, Nanjing, 210095, China; MOA Key Laboratory of Plant Nutrition and Fertilization in Lower-Middle Reaches of the Yangtze River, Nanjing Agricultural University, Nanjing, 210095, China; Laboratory Center of Life Sciences, College of Life Sciences, Nanjing Agricultural University, Nanjing, 210095, China.
Plant Cell Environ. 2015 Jan;38(1):129-43. doi: 10.1111/pce.12380. Epub 2014 Jul 4.
Despite substantial evidence showing the ammonium-altered redox homeostasis in plants, the involvement and molecular mechanism of heme-heme oxygenase 1 (heme-HO1), a novel antioxidant system, in the regulation of ammonium tolerance remain elusive. To fill in these gaps, the biological function of rice HO1 (OsSE5) was investigated. Results showed that NH4 Cl up-regulated rice OsSE5 expression. Oxidative stress and subsequent growth inhibition induced by excess NH4 Cl was partly mitigated by pretreatment with carbon monoxide (CO, a by-product of HO1 activity) or intensified by zinc protoporphyrin (ZnPP, a potent inhibitor of HO1 activity). Pretreatment with HO1 inducer hemin, not only up-regulated OsSE5 expression and HO activity, but also rescued the down-regulation of antioxidant transcripts, total and related isozymatic activities, thus significantly counteracting the excess NH4 Cl-triggered reactive oxygen species overproduction, lipid peroxidation and growth inhibition. OsSE5 RNAi transgenic rice plants revealed NH4 Cl-hypersensitive phenotype with impaired antioxidant defence, both of which could be rescued by CO but not hemin. Transgenic Arabidopsis plants over-expressing OsSE5 also exhibited enhanced tolerance to NH4 Cl, which might be attributed to the up-regulation of several antioxidant transcripts. Altogether, these results illustrated the involvement of heme-HO1 system in ammonium tolerance by enhancing antioxidant defence, which may improve plant tolerance to excess ammonium fertilizer.
尽管有大量证据表明铵会改变植物的氧化还原稳态，但血红素-血红素加氧酶 1（heme-HO1）作为一种新的抗氧化系统，其在调节铵耐性中的参与和分子机制仍不清楚。为了填补这些空白，研究了水稻 HO1（OsSE5）的生物学功能。结果表明，NH4Cl 上调了水稻 OsSE5 的表达。过量 NH4Cl 诱导的氧化应激和随后的生长抑制部分被一氧化碳（HO1 活性的副产物）预处理减轻，或被锌原卟啉（HO1 活性的强效抑制剂）增强。HO1 诱导剂血红素预处理不仅上调了 OsSE5 的表达和 HO 活性，还挽救了抗氧化转录物、总酶和相关同工酶活性的下调，从而显著抑制了过量 NH4Cl 引发的活性氧过度产生、脂质过氧化和生长抑制。OsSE5 RNAi 转基因水稻表现出对 NH4Cl 的超敏表型，抗氧化防御受损，这两者都可以被 CO 挽救，但不能被血红素挽救。过表达 OsSE5 的转基因拟南芥也表现出对 NH4Cl 的耐受性增强，这可能归因于几种抗氧化转录物的上调。总之，这些结果表明血红素-HO1 系统通过增强抗氧化防御参与了铵耐性，这可能提高植物对过量铵肥的耐受性。
