The M35 Metalloprotease Effector FocM35_1 Is Required for Full Virulence of Fusarium oxysporum f. sp. cubense Tropical Race 4.
Xiaoxia ZhangHuoqing HuangBangting WuJianghui XieAltus ViljoenWei WangDiane MostertYanling XieGang FuDandan XiangShuxia LyuSiwen LiuChunyu LiPublished in: Pathogens (Basel, Switzerland) (2021)
Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4) causes Fusarium wilt of banana, the most devastating disease on a banana plant. The genome of Foc TR4 encodes many candidate effector proteins. However, little is known about the functions of these effector proteins on their contributions to disease development and Foc TR4 virulence. Here, we discovered a secreted metalloprotease, FocM35_1, which is an essential virulence effector of Foc TR4. FocM35_1 was highly upregulated during the early stages of Foc TR4 infection progress in bananas. The FocM35_1 knockout mutant compromised the virulence of Foc TR4. FocM35_1 could interact with the banana chitinase MaChiA, and it decreased banana chitinase activity. FocM35_1 induced cell death in Nicotiana benthamiana while suppressing the INF1-induced hypersensitive response (HR), and its predicted enzymatic site was required for lesion formation and the suppression to INF1-induced HR on N. benthamiana leaves. Importantly, treatment of banana leaves with recombinant FocM35_1 accelerates Foc TR4 infection. Collectively, our study provides evidence that metalloprotease effector FocM35 seems to contribute to pathogen virulence by inhibiting the host immunity.
Keyphrases
- pseudomonas aeruginosa
- escherichia coli
- staphylococcus aureus
- antimicrobial resistance
- regulatory t cells
- biofilm formation
- dendritic cells
- cell death
- high glucose
- diabetic rats
- type iii
- signaling pathway
- climate change
- drug induced
- immune response
- gene expression
- oxidative stress
- cystic fibrosis
- endothelial cells
- dna methylation
- genome wide
- nitric oxide
- combination therapy
- pi k akt