Two Lysin-Motif Receptor Kinases, Gh-LYK1 and Gh-LYK2, Contribute to Resistance against Verticillium wilt in Upland Cotton.
Two Lysin-Motif Receptor Kinases, Gh-LYK1 and Gh-LYK2, Contribute to Resistance against Verticillium wilt in Upland Cotton.
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两种赖氨酸基序受体激酶 Gh-LYK1 和 Gh-LYK2 有助于陆地棉抵抗黄萎病
DOI:
10.3389/fpls.2017.02133
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发表时间:
2017
影响因子:
5.6
通讯作者:
Zhou X
中科院分区:
文献类型:
--
作者:
Gu Z;Liu T;Ding B;Li F;Wang Q;Qian S;Ye F;Chen T;Yang Y;Wang J;Wang G;Zhang B;Zhou X
Lysin-motif (LysM) receptor kinases (LYKs) play essential roles in recognition of chitin and activation of defense responses against pathogenic fungi in the model plants Arabidopsis and rice. The function of LYKs in non-model plants, however, remains elusive. In the present work, we found that the transcription of two LYK-encoding genes from cotton, Gh-LYK1 and Gh-LYK2, was induced after Verticillium dahliae infection. Virus-induced gene silencing (VIGS) of Gh-LYK1 and Gh-LYK2 in cotton plants compromises resistance to V. dahliae. As putative pattern recognition receptors (PRRs), both Gh-LYK1 and Gh-LYK2 are membrane-localized, and all three LysM domains of Gh-LYK1 and Gh-LYK2 are required for their chitin-binding ability. However, since Gh-LYK2, but not Gh-LYK1, is a pseudo-kinase and, on the other hand, the ectodomain (ED) of Gh-LYK2 can induce reactive oxygen species (ROS) burst in planta, Gh-LYK2 and Gh-LYK1 may contribute differently to cotton defense. Taken together, our results establish that both Gh-LYK1 and Gh-LYK12 are required for defense against V. dahliae in cotton, possibly through different mechanisms.
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影响因子:
4.6
作者:
Fu W;Shen Y;Hao J;Wu J;Ke L;Wu C;Huang K;Luo B;Xu M;Cheng X;Zhou X;Sun J;Xing C;Sun Y
通讯作者:
Sun Y
影响因子:
7.4
作者:
Arrighi, Jean-Francois;Barre, Annick;Gough, Clare
通讯作者:
Gough, Clare
DOI:
10.1073/pnas.97.7.3718
发表时间:
2000-03-28
影响因子:
11.1
作者:
Cutler, SR;Ehrhardt, DW;Somerville, CR
通讯作者:
Somerville, CR
DOI:
10.1073/pnas.0508882103
发表时间:
2006-07-18
影响因子:
11.1
作者:
Kaku, Hanae;Nishizawa, Yoko;Shibuya, Naoto
通讯作者:
Shibuya, Naoto
影响因子:
1.8
作者:
DAAYF, F;NICOLE, M;GEIGER, JP
通讯作者:
GEIGER, JP