Diseases caused by the notorious Phytophthora spp. result in enormous economic losses to crops and forests. Increasing evidence suggests that small open reading frame-encoded polypeptides (SEPs) participate in environmental responses of animals, plants, and fungi. However, it remains largely unknown whether Phytophthora pathogens produce SEPs. Here, we systematically predicted and identified 96 SEP candidates in P. capsici. Among them, three may induce stable cell death in Nicotiana benthamiana. Phytophthora-specific and conserved SEP1 facilitated P. capsici infection. PcSEP1-induced cell death is BAK1 and SOBIR1 independent and is correlated with its virulence function. Finally, PcSEP1 may be targeted to the apoplast for carrying out its functions, for which the C terminus is indispensable. Together, our results demonstrated that SEP1 is a new virulence factor, and previously unknown SEPs may act as effector proteins in Phytophthora pathogens.

Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

由臭名昭著的疫霉属引起的疾病。给农作物和森林造成巨大的经济损失。越来越多的证据表明，小型开放阅读框编码的多肽（SEP）参与动物、植物和真菌的环境反应。然而，疫霉属病原体是否产生 SEP 仍知之甚少。在这里，我们系统地预测并鉴定了P. capsici 中的 96 个 SEP 候选者。其中，三种可能诱导本塞姆氏烟草稳定的细胞死亡。疫霉属特异性且保守的SEP1促进辣椒疫病菌感染。 PcSEP1 诱导的细胞死亡与 BAK1 和 SOBIR1 无关，并与其毒力功能相关。最后，PcSEP1 可能靶向质外体来执行其功能，其中 C 末端是不可或缺的。总之，我们的结果表明，SEP1 是一种新的毒力因子，以前未知的 SEP 可能充当疫霉菌病原体中的效应蛋白。

版权所有 © 2021 作者。这是一篇根据 CC BY-NC-ND 4.0 国际许可证分发的开放获取文章。