Abstract
Despite the involvement of many members of the chitinase family in plant immunity, the precise functions of the majority of the members remain poorly understood. Herein, the gene ChiIV3 in Capsicum annuum encoding a chitinase protein containing a chitin binding domain and targeting to the plasma membrane was found to be induced by Phytophthora capsici inoculation (PCI) and applied chitin treatment. Besides its direct inhibitory effect on growth of Phytophthora capsici (P. capsici), ChiIV3 was also found by virus-induced gene silencing (VIGS) and transient overexpression (TOE) in pepper plants to act as a positive regulator of plant cell death and in triggering defense signaling and upregulation of PR (pathogenesis related) genes against PCI. A 5′ deletion assay revealed that pChiIV3−712 to −459 bp was found to be sufficient for ChiIV3’ response to PCI. Furthermore, a mutation assay indicated that W-box−466 to −461 bp in pChiIV3−712 to −459 bp was noted to be the PCI-responsible element. These results collectively suggest that ChiIV3 acts as a likely antifungal protein and as a receptor for unidentified chitin in planta to trigger cell death and defense signaling against PCI.
Highlights
During their life cycle, plants are frequently encountered by multiple types of pathogens and have been armed during their evolution with comprehensive defense mechanisms including two typical interconnecting layers of immunity, termed as pattern triggered immunity (PTI) and effector-triggered immunity (ETI), respectively [1,2]
Chitinases constitute a family of common antifungal proteins, which function against fungal pathogens through degrading chitin in both PTI and ETI [27,28]
Our data showed that ChiIV3 was transcriptionally regulated by exogenously applied chitin as well as Phytophthora capsici inoculation (PCI), which was further confirmed by the inducible expression of GUS driven by pChilV3 by P. capsici inoculation in pepper plants
Summary
Plants are frequently encountered by multiple types of pathogens and have been armed during their evolution with comprehensive defense mechanisms including two typical interconnecting layers of immunity, termed as pattern triggered immunity (PTI) and effector-triggered immunity (ETI), respectively [1,2]. The underlying mechanism of PTI and ETI has not yet been fully investigated. Other than their role as chief constituents in fungi, chitins are defined as a typical pathogen-associated molecular pattern (PAMP) that is highly conserved among different fungal pathogens. Chitinases, encoded by a gene family [6,7,8], play pivotal roles in plant immunity; for example, the overexpression of a specific chitinase in plants have been frequently found to augment resistance against fungal attacks [9,10]. The roles of some of these cis-elements have been investigated in the inducible expression of these genes [13,14]. The mechanisms underlying the inducible expression of chitinase genes have not been fully understood
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