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马铃薯 E3 泛素连接酶 StRFP1 通过降解糖转运蛋白 StSWEET10c 和 StSWEET11 正向调控晚疫病抗性。

Potato E3 ubiquitin ligase StRFP1 positively regulates late blight resistance by degrading sugar transporters StSWEET10c and StSWEET11.

机构信息

National Key Laboratory for Germplasm Innovation & Utilization of Horticultural Crops, Huazhong Agricultural University (HZAU), Wuhan, 430070, China.

Hubei Hongshan Laboratory (HZAU), Wuhan, 430070, China.

出版信息

New Phytol. 2024 Jul;243(2):688-704. doi: 10.1111/nph.19848. Epub 2024 May 20.

DOI:10.1111/nph.19848
PMID:38769723
Abstract

Potato (Solanum tuberosum) is the fourth largest food crop in the world. Late blight, caused by oomycete Phytophthora infestans, is the most devastating disease threatening potato production. Previous research has shown that StRFP1, a potato Arabidopsis Tóxicos en Levadura (ATL) family protein, positively regulates late blight resistance via its E3 ligase activity. However, the underlying mechanism is unknown. Here, we reveal that StRFP1 is associated with the plasma membrane (PM) and undergoes constitutive endocytic trafficking. Its PM localization is essential for inhibiting P. infestans colonization. Through in vivo and in vitro assays, we investigated that StRFP1 interacts with two sugar transporters StSWEET10c and StSWEET11 at the PM. Overexpression (OE) of StSWEET10c or StSWEET11 enhances P. infestans colonization. Both StSWEET10c and StSWEET11 exhibit sucrose transport ability in yeast, and OE of StSWEET10c leads to an increased sucrose content in the apoplastic fluid of potato leaves. StRFP1 ubiquitinates StSWEET10c and StSWEET11 to promote their degradation. We illustrate a novel mechanism by which a potato ATL protein enhances disease resistance by degrading susceptibility (S) factors, such as Sugars Will Eventually be Exported Transporters (SWEETs). This offers a potential strategy for improving disease resistance by utilizing host positive immune regulators to neutralize S factors.

摘要

马铃薯(Solanum tuberosum)是世界上第四大粮食作物。晚疫病是由卵菌 Phytophthora infestans引起的,是威胁马铃薯生产的最具破坏性的疾病。先前的研究表明,马铃薯拟南芥 Tóxicos en Levadura(ATL)家族蛋白 StRFP1 通过其 E3 连接酶活性正向调节晚疫病抗性。然而,其潜在机制尚不清楚。在这里,我们揭示 StRFP1 与质膜(PM)相关,并进行组成性内吞运输。其 PM 定位对于抑制 P. infestans 定殖至关重要。通过体内和体外测定,我们研究了 StRFP1 在质膜(PM)上与两种糖转运蛋白 StSWEET10c 和 StSWEET11 相互作用。StSWEET10c 或 StSWEET11 的过表达(OE)增强了 P. infestans 的定殖。StSWEET10c 和 StSWEET11 都具有在酵母中转运蔗糖的能力,OE StSWEET10c 导致马铃薯叶片质外体液中的蔗糖含量增加。StRFP1 泛素化 StSWEET10c 和 StSWEET11 以促进其降解。我们说明了一种新的机制,即马铃薯 ATL 蛋白通过降解感病(S)因子,如 Sugars Will Eventually be Exported Transporters(SWEETs),来增强抗病性。这为利用宿主正向免疫调节剂来中和 S 因子从而提高抗病性提供了一种潜在策略。

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