WIPK–NtLTP4 pathway confers resistance to Ralstonia solanacearum in tobacco

Key message WIPK–NtLTP4 module improves the resistance to R. solanacearum via upregulating the expression of defense-related genes, increasing the antioxidant enzyme activity, and promoting stomatal closure in tobacco. Lipid transfer proteins (LTPs) are a class of small lipid binding proteins that p...

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Veröffentlicht in:Plant cell reports 2022, Vol.41 (1), p.249-261
Hauptverfasser: Xu, Yang, Shang, Kaijie, Wang, Chenchen, Yu, Zipeng, Zhao, Xuechen, Song, Yunzhi, Meng, Fanxiao, Zhu, Changxiang
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Sprache:eng
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Zusammenfassung:Key message WIPK–NtLTP4 module improves the resistance to R. solanacearum via upregulating the expression of defense-related genes, increasing the antioxidant enzyme activity, and promoting stomatal closure in tobacco. Lipid transfer proteins (LTPs) are a class of small lipid binding proteins that play important roles in biotic and abiotic stresses. The previous study revealed that NtLTP4 positively regulates salt and drought stresses in Nicotiana tabacum . However, the role of NtLTP4 in biotic stress, especially regarding its function in disease resistance remains unclear. Here, the critical role of NtLTP4 in regulating resistance to Ralstonia solanacearum ( R. solanacearum ), a causal agent of bacterial wilt disease in tobacco, was reported. The NtLTP4-overexpressing lines markedly improved the resistance to R. solanacearum by upregulating the expression of defense-related genes, increasing the antioxidant enzyme activity, and promoting stomatal closure. Moreover, NtLTP4 interacted with wound-induced protein kinase (WIPK; a homolog of MAPK3 in tobacco) and acted in a genetically epistatic manner to WIPK in planta. WIPK could directly phosphorylate NtLTP4 to positively regulate its protein abundance. Taken together, these results broaden the knowledge about the functions of the WIPK–NtLTP4 module in disease resistance and may provide valuable information for improving tobacco plant tolerance to R. solanacearum .
ISSN:0721-7714
1432-203X
DOI:10.1007/s00299-021-02808-z