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同时过表达 PvPGIP2 和 TAXI-III 而非 PvPGIP2 和 PMEI 增强了对禾谷镰刀菌的抗性。

Pyramiding PvPGIP2 and TAXI-III But Not PvPGIP2 and PMEI Enhances Resistance Against Fusarium graminearum.

机构信息

1 Dipartimento di Scienze Agrarie e Forestali (DAFNE) Università della Tuscia, Via S. Camillo de Lellis snc, 01100 Viterbo;

2 Dipartimento di Biologia e Biotecnologie "Charles Darwin", Sapienza Università di Roma, Piazzale Aldo Moro, 5, 00185 Roma, Italy; and.

出版信息

Mol Plant Microbe Interact. 2016 Aug;29(8):629-39. doi: 10.1094/MPMI-05-16-0089-R. Epub 2016 Jul 27.

DOI:10.1094/MPMI-05-16-0089-R
PMID:27366923
Abstract

Plant protein inhibitors counteract the activity of cell wall-degrading enzymes (CWDEs) secreted by pathogens to breach the plant cell-wall barrier. Transgenic plants expressing a single protein inhibitor restrict pathogen infections. However, since pathogens secrete a number of CWDEs at the onset of infection, we combined more inhibitors in a single wheat genotype to reinforce further the cell-wall barrier. We combined polygalacturonase (PG) inhibiting protein (PGIP) and pectin methyl esterase inhibitor (PMEI), both controlling the activity of PG, one of the first CWDEs secreted during infection. We also pyramided PGIP and TAXI-III, a xylanase inhibitor that controls the activity of xylanases, key factors for the degradation of xylan, a main component of cereal cell wall. We demonstrated that the pyramiding of PGIP and PMEI did not contribute to any further improvement of disease resistance. However, the presence of both pectinase inhibitors ensured a broader spectrum of disease resistance. Conversely, the PGIP and TAXI-III combination contributed to further improvement of Fusarium head blight (FHB) resistance, probably because these inhibitors target the activity of different types of CWDEs, i.e., PGs and xylanases. Worth mentioning, the reduction of FHB symptoms is accompanied by a reduction of deoxynivalenol accumulation with a foreseen great benefit to human and animal health.

摘要

植物蛋白抑制剂可抵抗病原菌分泌的细胞壁降解酶(CWDEs)的活性,从而破坏植物细胞壁屏障。表达单一蛋白抑制剂的转基因植物可限制病原菌感染。然而,由于病原菌在感染初期会分泌多种 CWDEs,因此我们将更多抑制剂组合在单个小麦基因型中,以进一步加强细胞壁屏障。我们将聚半乳糖醛酸酶(PG)抑制蛋白(PGIP)和果胶甲酯酶抑制剂(PMEI)组合在一起,这两种抑制剂都能控制 PG 的活性,PG 是感染过程中最初分泌的 CWDEs 之一。我们还将 PGIP 和 TAXI-III(木聚糖酶抑制剂)进行了基因叠加,TAXI-III 能控制木聚糖酶的活性,木聚糖酶是木聚糖降解的关键因素,而木聚糖是谷物细胞壁的主要成分。我们证明,PGIP 和 PMEI 的叠加并没有进一步提高抗病性。然而,两种果胶酶抑制剂的存在确保了更广泛的抗病谱。相反,PGIP 和 TAXI-III 的组合有助于进一步提高赤霉病抗性,这可能是因为这些抑制剂针对不同类型的 CWDEs(即 PGs 和木聚糖酶)的活性。值得一提的是,赤霉病症状的减轻伴随着脱氧雪腐镰刀菌烯醇积累的减少,这对人类和动物健康具有巨大的预期益处。

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