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Endophytic Bacillus amyloliquefaciens YTB1407 elicits resistance against two fungal pathogens in sweet potato (Ipomoea batatas (L.) Lam.)

The endophytic Bacillus amyloliquefaciens YTB1407 was previously reported to promote the growth of sweet potato (Ipomoea batatas cv. Yanshu 25). Here, we demonstrate in both in vitro and pot trial assays that pre-treatment with YTB1407 suspension could enhance resistance against root rot disease and...

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Bibliographic Details
Published in:Journal of plant physiology 2020-10, Vol.253, p.153260, Article 153260
Main Authors: Wang, Cui-Juan, Wang, Ying-Zi, Chu, Zhao-Hui, Wang, Pei-Song, Liu, Bao-You, Li, Bao-Yan, Yu, Xiao-Li, Luan, Bing-Hui
Format: Article
Language:English
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Summary:The endophytic Bacillus amyloliquefaciens YTB1407 was previously reported to promote the growth of sweet potato (Ipomoea batatas cv. Yanshu 25). Here, we demonstrate in both in vitro and pot trial assays that pre-treatment with YTB1407 suspension could enhance resistance against root rot disease and black rot disease, caused by Fusarium solani Mart. Sacc. f. sp. batatas McClure and Ceratocystis fimbriata Ell. & Halst on sweet potato, respectively. When seedlings were infected with fungal pathogens at 10 days post irrigation, pre-treatment with YTB1407 suspension decreased these pathogens and YTB1407 bacterial biomass in sweet potato roots. The pre-treatment activated the expression of salicylic acid (SA)-responsive PR-1 gene, raised SA content, and reduced hydrogen peroxide (H2O2) in the host to resist F. solani, while it enhanced the expression levels of SA-responsive NPR1 and PR1 genes and increased SA content to resist C. fimbriata. The disease resistance control effect initiated by pre-treatment with YTB1407 for root rot pathogen (F. solani) was better than for black rot pathogen (C. fimbriata). The results indicated that Bacillus amyloliquefaciens YTB1407 played a pivotal role in enhancing resistance to two fungi pathogens in sweet potato, through production of some antifungal metabolites to decrease infection in the early stage as well as induction of SA-dependent systemic resistance.
ISSN:0176-1617
1618-1328
DOI:10.1016/j.jplph.2020.153260