Phytophthora capsici causes a severe soil-borne disease in a wide variety of vegetables; to date, no effective strategies to control P. capsici have been developed. Liquiritin (LQ) is a natural flavonoid found in licorice (Glycyrrhiza spp.) root, and it is used in pharmaceuticals. However, the antifungal activity of LQ against P. capsici remains unknown. In the present study, we demonstrated that LQ inhibits P. capsici mycelial growth and sporangial development. In addition, the EC50 of LQ was 658.4 mg/L and LQ caused P. capsici sporangia to shrink and collapse. Next, LQ severely damaged the cell membrane integrity, leading to a 2.0-2.5-fold increase in relative electrical conductivity and malondialdehyde concentration, and a 65-70% decrease in sugar content. Additionally, the H2O2 content was increased about 2.0-2.5 fold, but the total antioxidant activity, catalase activity and laccase activity were attenuated by 40-45%, 30-35% and 70-75%. LQ also induced autophagy, apoptosis, and reduction of intracellular Ca2+ content. Furthermore, LQ inhibited P. capsici pathogenicity by reducing the expression of virulence genes PcCRN4 and Pc76RTF, and stimulating the plant defense (including the activated transcriptional expression of defense-related genes CaPR1, CaDEF1, and CaSAR82, and the increased antioxidant enzyme activity). Our results not only elucidate the antifungal mechanism of LQ but also suggest a promising alternative to commercial fungicides or a key compound in the development of new fungicides for the control of the Phytophthora disease.

Colocasia esculenta (L.) Schoot (Araceae), commonly known as taro, is grown worldwide as a starch-rich tuber, and has been cultivated extensively in southern China. In May 2016, leaf spot symptoms of Guangxi Lipu (varying from 30–40 × 12–15 cm in size) were frequently observed on lower taro leaves in many commercial fields (paddy field soil) located in Zhangzhou, Fujian province, China (percentage of symptomatic plants and fields were 10% and 80%, separately) and disease severity was positively influenced by suitable temperatures (25°C to 30°C ) and high humidity. Symptoms first appeared as necrotic lesions, which then elongated and became yellowish to light-brown and the necrotic lesions became thinner and many black pycnidia were found. Then, leaf spots later coalesced, becoming large and irregular, with yellow margins and some lesions eventually perforated. In most spots, black pycnidia were found in the thinner mesophyll tissues, varying from 20–70 µm in diameter. Conidia were hyaline, unicellular, el...

Ralstonia solanacearum can induce severe wilt disease in vital crops. Therefore, there is an urgent need to develop novel antifungal solutions. The natural compound 2,4-di-tert-butylphenol (2,4-DTBP) exhibits diverse physiological activities and affects soil function. However, its specific impact on the R. solanacearum remains unclear. Here, we investigated the antimicrobial potential of 2,4-DTBP. The results demonstrated that 2,4-DTBP effectively inhibited its growth and altered morphology. In addition, it substantially impeded biofilm formation, motility, and exopolysaccharide secretion. Transcriptomic analysis revealed that 2,4-DTBP inhibited energy production and membrane transport. Additionally, 2,4-DTBP hindered the growth by interfering with the membrane permeability, reactive oxygen species (ROS) production, and electrolyte leakage. Concomitantly, this led to a significant reduction in pathogenicity, as evidenced by the biomass of R. solanacearum in the invaded roots. Overall, our data strongly support the potential utility of 2,4-DTBP as a potent antibacterial agent capable of effectively preventing the onset of bacterial wilt caused by R. solanacearum.

As one of the most destructive bacterial phytopathogens, Ralstonia solanacearum causes substantial annual yield losses of many important crops. Deciphering the functional mechanisms of type III effectors, the crucial factors mediating R. solanacearum-plant interactions, will provide a valuable basis for protecting crop plants from R. solanacearum. Recently, the NEL (novel E3 ligase) effector RipAW was found to induce cell death on Nicotiana benthamiana in a E3 ligase activity-dependent manner. Here, we further deciphered the role of the E3 ligase activity in RipAW-triggered plant immunity. We found that RipAW^C177A, the E3 ligase mutant of RipAW, could not induce cell death but retained the ability of triggering plant immunity in N. benthamiana, indicating that the E3 ligase activity is not essential for RipAW-triggered immunity. By generating truncated mutants of RipAW, we further showed that the N-terminus, NEL domain and C-terminus are all required but not sufficient for RipAW-induced cell death. Furthermore, all truncated mutants of RipAW triggered ETI immune responses in N. benthamiana, confirming that the E3 ligase activity is not essential for RipAW-triggered plant immunity. Finally, we demonstrated that RipAW- and RipAW^C177A-triggered immunity in N. benthamiana requires SGT1 (suppressor of G2 allele of skp1), but not EDS1 (enhanced disease susceptibility), NRG1 (N requirement gene 1), NRC (NLR required for cell death) proteins or SA (salicylic acid) pathway. Our findings provide a typical case in which the effector-induced cell death can be uncoupled with immune responses, shedding new light on effector-triggered plant immunity. Our data also provide clues for further in-depth study of mechanism underlying RipAW-induced plant immunity.