Abstract

Verticillium wilt, caused by Verticillium dahliae, is a devastating disease for many important crops, including cotton. Kiwellins (KWLs), a group of cysteine-rich proteins synthesized in many plants, have been shown to be involved in response to various phytopathogens. To evaluate genes for their function in resistance to Verticillium wilt, we investigated KWL homologs in cotton. Thirty-five KWL genes (GhKWLs) were identified from the genome of upland cotton (Gossypium hirsutum). Among them, GhKWL1 was shown to be localized in nucleus and cytosol, and its gene expression is induced by the infection of V. dahliae. We revealed that GhKWL1 was a positive regulator of GhERF105. Silencing of GhKWL1 resulted in a decrease, whereas overexpression led to an increase in resistance of transgenic plants to Verticillium wilt. Interestingly, through binding to GhKWL1, the pathogenic effector protein VdISC1 produced by V. dahliae could impair the defense response mediated by GhKWL1. Therefore, our study suggests there is a GhKWL1-mediated defense response in cotton, which can be hijacked by V. dahliae through the interaction of VdISC1 with GhKWL1.

Highlights

  • Cotton, the leading fiber crop of the world, is widely planted in more than 80 countries [1]

  • GhKWL1 Is Induced by V. dahliae and the Protein Is Located in the Nucleus

  • The abundance of fungal DNA in the GhKWL1-overexpressing leaves was significantly lower than that of the control (Figure 2H). These results indicate that heterologous overexpression of GhKWL1 can increase the resistance of Arabidopsis to V. dahliae infection

Read more

Summary

Introduction

The leading fiber crop of the world, is widely planted in more than 80 countries [1]. Verticillium spp. produce a battery of proteins, including walldegrading enzymes, transcription factors, and membrane receptors, to facilitate host colonization, often by disturbing host immunity [6]. V. dahliae secretes more than 700 proteins, known as effectors [7], which either emphasize pathogenic virulence by overcoming plant defense responses or are directly/indirectly recognized by host surveillance systems, leading to effector-triggered immunity [8]. Some of these effectors interfere with host hormone signaling, by which the pathogens can use the host resources to their advantage [9,10]. In the process of colonization, V. dahliae produces VdISC1, an unconventionally secreted isochorismate mutase that converts isochorismate into 2,3-dihydro-2,3-dihydroxybenzoate (DDHB), to inhibit the biosynthesis

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call