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Resistance to Magnaporthe grisea in transgenic rice with suppressed expression of genes encoding allene oxide cyclase and phytodienoic acid reductase.

机译:转基因水稻对稻瘟病菌的抗性,抑制了编码烯丙氧化物环化酶和植物二烯酸还原酶的基因的表达。

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摘要

Linolenic acid (18:3) and its derivative jasmonic acid (JA) are important molecules in disease resistance in many dicotyledonous plants. We have previously used 18:3- and JA-deficient rice (F78Ri) to investigate the roles of fatty acids and their derivatives in resistance to the blast fungus Magnaporthe grisea [A. Yara, T. Yaeno, J.-L. Montillet, M. Hasegawa, S. Seo, K. Kusumi, K. Iba, Enhancement of disease resistance to Magnaporthe grisea in rice by accumulation of hydroxy linoleic acid, Biochem. Biophys. Res. Commun. 370 (2008) 344-347; A. Yara, T. Yaeno, M. Hasegawa, H. Seto, J.-L. Montillet, K. Kusumi, S. Seo, K. Iba, Disease resistance against Magnaporthe grisea is enhanced in transgenic rice with suppression of omega-3 fatty acid desaturases, Plant Cell Physiol. 48 (2007) 1263-1274]. However, because F78Ri plants are suppressed in the first step of the JA biosynthetic pathway, we could not confirm the specific contribution of JA to disease resistance. In this paper, we generated two JA-deficientrice lines (AOCRi and OPRRi) with suppressed expression of the genes encoding allene oxide cyclase (AOC) and 12-oxo-phytodienoic acid reductase (OPR), which catalyze late steps in the JA biosynthetic pathway. The levels of disease resistance in the AOCRi and OPRRi lines were equal to that in wild-type plants. Our data suggest that resistance to M. grisea is not dependent on JA synthesis.
机译:亚麻酸(18:3)及其衍生的茉莉酸(JA)是许多双子叶植物抗病性的重要分子。我们以前曾使用18:3-和JA缺失水稻(F78Ri)来研究脂肪酸及其衍生物在对稻瘟病Magnaporthe grisea的抗性中的作用[A.亚拉(Yara),T。矢野(T. Yaeno),J.-L。 Montillet,M。Hasegawa,S。Seo,K。Kusumi,K。Iba,通过羟基亚油酸的积累增强水稻对稻瘟病的抗病性,Biochem。生物物理学。 Res。公社370(2008)344-347; A. Yara,T。Yaeno,M。Hasegawa,H。Seto,J.-L。 Montillet,K. Kusumi,S. Seo,K. Iba,在转基因水稻中,通过抑制omega-3脂肪酸去饱和酶,植物细胞生理学,提高了对稻瘟病的抗病性。 48(2007)1263-1274]。但是,由于F78Ri植物在JA生物合成途径的第一步受到抑制,因此我们无法确定JA对抗病性的特定作用。在本文中,我们生成了两个JA缺陷株(AOCRi和OPRRi),它们抑制了编码烯丙氧化物环化酶(AOC)和12-氧-植物二烯酸还原酶(OPR)的基因的表达,从而催化了JA生物合成途径的后期步骤。 。 AOCRi和OPRRi品系的抗病性水平与野生型植物相同。我们的数据表明,对稻瘟病菌的抗性不依赖于JA合成。

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