Abstract
BackgroundColletotrichum truncatum is a haploid, hemibiotrophic, ascomycete fungal pathogen that causes anthracnose disease on many economically important leguminous crops. This pathogen exploits sequential biotrophic- and necrotrophic- infection strategies to colonize the host. Transition from biotrophy to a destructive necrotrophic phase called the biotrophy-necrotrophy switch is critical in symptom development. C. truncatum likely secretes an arsenal of proteins that are implicated in maintaining a compatible interaction with its host. Some of them might be transition specific.ResultsA directional cDNA library was constructed from mRNA isolated from infected Lens culinaris leaflet tissues displaying the biotrophy-necrotrophy switch of C. truncatum and 5000 expressed sequence tags (ESTs) with an average read of > 600 bp from the 5-prime end were generated. Nearly 39% of the ESTs were predicted to encode proteins of fungal origin and among these, 162 ESTs were predicted to contain N-terminal signal peptides (SPs) in their deduced open reading frames (ORFs). The 162 sequences could be assembled into 122 tentative unigenes comprising 32 contigs and 90 singletons. Sequence analyses of unigenes revealed four potential groups: hydrolases, cell envelope associated proteins (CEAPs), candidate effectors and other proteins. Eleven candidate effector genes were identified based on features common to characterized fungal effectors, i.e. they encode small, soluble (lack of transmembrane domain), cysteine-rich proteins with a putative SP. For a selected subset of CEAPs and candidate effectors, semiquantitative RT-PCR showed that these transcripts were either expressed constitutively in both in vitro and in planta or induced during plant infection. Using potato virus X (PVX) based transient expression assays, we showed that one of the candidate effectors, i. e. contig 8 that encodes a cerato-platanin (CP) domain containing protein, unlike CP proteins from other fungal pathogens was unable to elicit a hypersensitive response (HR).ConclusionsThe current study catalogues proteins putatively secreted at the in planta biotrophy-necrotrophy transition of C. truncatum. Some of these proteins may have a role in establishing compatible interaction with the host plant.
Highlights
Colletotrichum truncatum is a haploid, hemibiotrophic, ascomycete fungal pathogen that causes anthracnose disease on many economically important leguminous crops
This corresponded to 48-56 hours after inoculation and we referred to this period of infection as the biotrophy-necrotrophy switch
The abundance of plant origin transcripts had declined with fungal proliferation in infected host tissues as shown by RT-PCR analysis of L. culinaris 60S ribosomal gene in the same infection time-course used for assessing the fungal biomass (Figure 2A)
Summary
Colletotrichum truncatum is a haploid, hemibiotrophic, ascomycete fungal pathogen that causes anthracnose disease on many economically important leguminous crops This pathogen exploits sequential biotrophic- and necrotrophic- infection strategies to colonize the host. Colletotrichum truncatum (Schwein.) Andrus W.D. Moore causes anthracnose disease of many leguminous species, including lentil (L. culinaris Medik.), soybean (Glycine max (L) Merr.), fababean (Vicia faba L.), and pea (Pisum sativum L.) [1]. Moore causes anthracnose disease of many leguminous species, including lentil (L. culinaris Medik.), soybean (Glycine max (L) Merr.), fababean (Vicia faba L.), and pea (Pisum sativum L.) [1] This fungal pathogen employs a bi-phasic hemibiotrophic infection strategy to colonize lentil plants. C. truncatum probably secretes a range of proteins to establish a compatible interaction with its host, including some that may exclusively be involved in switching the pathogen to the necrotrophic phase
Sign-in/Register to view highlights & summary 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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
