Abstract

Cotton is an important economic crop worldwide. Verticillium wilt (VW) caused by Verticillium dahliae (V. dahliae) is a serious disease in cotton, resulting in massive yield losses and decline of fiber quality. Breeding resistant cotton cultivars is an efficient but elaborate method to improve the resistance of cotton against V. dahliae infection. However, the functional mechanism of several excellent VW resistant cotton cultivars is poorly understood at present. In our current study, we carried out RNA-seq to discover the differentially expressed genes (DEGs) in the roots of susceptible cotton Gossypium hirsutum cultivar Junmian 1 (J1) and resistant cotton G. hirsutum cultivar Liaomian 38 (L38) upon Vd991 inoculation at two time points compared with the mock inoculated control plants. The potential function of DEGs uniquely expressed in J1 and L38 was also analyzed by GO enrichment and KEGG pathway associations. Most DEGs were assigned to resistance-related functions. In addition, resistance gene analogues (RGAs) were identified and analyzed for their role in the heightened resistance of the L38 cultivar against the devastating Vd991. In summary, we analyzed the regulatory network of genes in the resistant cotton cultivar L38 during V. dahliae infection, providing a novel and comprehensive insight into VW resistance in cotton.

Highlights

  • Plants are under constant attack from various pests including bacteria, fungi, oomycetes, nematodes, and insects

  • Our findings suggest that the expression of several resistance-related genes was induced in the resistant cotton cultivar Liaomian 38 (L38) in a manner different from the susceptible cultivar Junmian 1 (J1) during V. dahliae infection, providing an insight into the genomic networks at play that result in the Verticillium wilt (VW) resistance of the L38 cotton cultivar

  • To probe the resistance of the L38 cultivar to V. dahliae, seedlings of both L38 and VW susceptible J1 cultivars at four weeks were inoculated with Vd991

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Summary

Introduction

Plants are under constant attack from various pests including bacteria, fungi, oomycetes, nematodes, and insects. PTI is the first line of a plant’s active defense response upon microbial perception. It is initiated upon recognition of conserved microbial molecular signatures by plant cell-surface receptors, and induction of PTI is associated with activation of MAP kinase signaling leading to transcriptional induction of pathogen-responsive genes, production of reactive oxygen species (ROS), and deposition of callose to reinforce the cell wall at sites of infection, all of which contribute to restrict microbial growth [4]. The second line of defense response is regulated by intracellular R proteins of the host which are designed to recognize specific effectors secreted by the pathogen, and is designated as the ETI [1,3]. SA-dependent signaling is critical in establishing local and systemic bacterial resistance, ET-dependent signaling is crucial for the response to necrotrophic pathogens and mechanical wounding, while JA-dependent signaling is induced in response to mechanical wounding and herbivore predation [10]

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