Ergosterol‐targeting fusion antifungal peptide significantly increases the Verticillium wilt resistance of cotton

Abstract

Increasing the targeting ability of antifungal proteins towards specific components of fungal cells has the potential to improve their antifungal activity and reduce harmful effects to nontarget cells. To obtain effective disease resistance genes against cotton Verticillium wilt, we constructed several fusion genes, in which binding domains targeting chitin, sphingolipid or ergosterol in the fungal cell wall or cell membrane were individually fused to the antifungal peptide BbAFP1 from entomopathogenic fungus Beauveria bassiana. Transient expression of fusion genes in cotton cotyledons indicated that the BbAFP1::ErBD fusion peptide with an ergosterol binding domain exhibited better disease resistance against V. dahliae than wild-type BbAFP1 and other fusion genes. BbAFP1::ErBD and BbAFP1 transgenic cotton were obtained and verified by Southern and Western blotting. Compared with BbAFP1-expressing cotton, BbAFP1::ErBD-expressing cotton showed higher disease resistance against V. dahliae, with smaller lesion areas (0.07 cm 2 vs. 0.16 cm 2 ) on the leaves and a lower disease index (23.9 vs. 34.5). Overexpression of BbAFP1:: ErBD by transgenic tobacco also showed enhanced disease resistance against V. dahliae compared with that of the wild-type gene. These results indicated that construction of fusion antifungal peptides that target fungal cells is a powerful strategy to obtain new anti-disease genes, and the obtained fusion gene BbAFP1::ErBD has the potential to defend against plant fungal diseases.

GhENODL6 Isoforms from the Phytocyanin Gene Family Regulated Verticillium Wilt Resistance in Cotton

“…The yield damage of cotton caused by VW is approximately 10–35% each year [ 2 ]. For example, about 300 million hectares of cotton are subject to VW in China, and the economic loss is more than 12 billion Chinese Yuan per year [ 3 , 4 ]. Using genetic resistance is regarded as the most effective method in controlling VW in G. hirsutum, which accounts for over 90% of the yield in production; however, screening efforts globally examining thousands of cotton germplasm show few accessions displaying resistance [ 3 , 5 ].…”

Sphingolipid synthesis inhibitor fumonisin B1 causes verticillium wilt in cotton

“…Extensive efforts have been made to breed cotton varieties resistant to verticillium wilt; cotton genes involved in this resistance are reviewed in Song et al (2020). The tomato immune receptor Ve1 (Song et al, 2018), antifungal proteins (Wang et al, 2016; Wang et al, 2020b), and peptides (Tong et al, 2021) also play important roles in improving verticillium wilt resistance in cotton. Transcriptome analysis of FB1‐ and V. dahliae ‐treated cotton roots revealed that IQ67‐domain (IQD) protein‐encoding genes were significantly downregulated following either FB1 or V. dahliae treatment (Figure S9).…”

RVE2, a new regulatory factor in jasmonic acid pathway, orchestrates resistance to Verticillium wilt

“…It is generally believed that the hyphopodia of V. dahliae forms penetration peg infect the xylem vessels by root tips in cotton plants. However, under laboratory conditions, V. dahliae was able to infect plant leaves (Duan et al ., 2016; Gao et al ., 2016; Munis et al ., 2010; Tong et al ., 2021; Yang et al ., 2015). It is worth noting that leaf‐inoculation method circumvents the first line of defence mechanism against the infection by V. dahliae in root system.…”