4.7 Article

The E3 ubiquitin ligase RING1 interacts with COP9 Signalosome Subunit 4 to positively regulate resistance to root-knot nematodes in Solanum lycopersicum L.

期刊

PLANT SCIENCE
卷 322, 期 -, 页码 -

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.plantsci.2022.111344

关键词

COP9 Signalosome Subunit 4 (CSN4); E3 ubiquitin ligase; Jasmonic acid; Solanum lycopersicum; RING1; Root-knot nematodes

资金

  1. National Key Research and Development Program of China [2018YFD1000800]
  2. National Natural Science Foundation of China [32020103013, 31922078, 31872089, 31950410555]
  3. Fundamental Research Funds for the Central Uni-versities [226-2022-00122]
  4. Ministry of Science and Technology of the People 's Republic of China [QNJ2021026001, QNJ20200226001]
  5. Henan Engineering Technology Research Center for Horticultural Crop safety and Disease Control and Henan International Joint Laboratory of Stress Resistance Regulation and Safe Production of Protected Vegetables
  6. Starry Night Science Fund of Zhejiang University Shanghai Institute for Advanced Study [SN-ZJU-SIAS-0011]

向作者/读者索取更多资源

The tomato E3 ubiquitin ligase RING1 interacts with COP9 Signalosome Subunit 4 (CSN4) and positively regulates JA-dependent basal defense against root-knot nematodes (RKNs).
Globally, root-knot nematodes (RKNs) cause massive production losses in all major crops. E3 ubiquitin ligases are involved in plant growth, development and immune response. But their roles in plant defense against RKNs are largely unclear. Here, we show that tomato E3 ubiquitin ligase RING1 interacts with COP9 Signalosome Subunit 4 (CSN4) which is essential for jasmonic acid (JA)-dependent basal defense against RKNs. Tissue-specific expression analysis showed that RING1 expression was the highest in tomato roots and the expression was significantly increased with RKN (Meloidogyne incognita) infection. Compared with the wild-type plants, the number of egg masses in roots significantly increased in the ring1 mutants, while RING1 overexpression conferred resistance against RKNs. Furthermore, RKN infection increased the accumulation of CSN4 protein in the roots of wild-type plants, which was largely compromised in the ring1 mutants but was enhanced in the RING1 overexpressing plants. The RKN-induced transcripts of JA biosynthetic and signaling genes as well as the accumulation of JA and JA-isoleucine were compromised in ring1 mutants but were increased in RING1 overexpressing plants. These results suggest that RING1 positively regulates JA-dependent basal defense against RKNs by interacting with CSN4 proteins.

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