• Deutsch
    • English
  • English 
    • Deutsch
    • English
  • Login
Item View 
  •   Home
  • Zentren & Graduiertenschulen
  • GGNB - Göttinger Graduiertenzentrum für Neurowissenschaften, Biophysik und molekulare Biowissenschaften
  • Item View
  •   Home
  • Zentren & Graduiertenschulen
  • GGNB - Göttinger Graduiertenzentrum für Neurowissenschaften, Biophysik und molekulare Biowissenschaften
  • Item View
JavaScript is disabled for your browser. Some features of this site may not work without it.

Defense remodelling by ectomycorrhizal fungi in non-hosts

by Kishore Vishwanathan
Doctoral thesis
Date of Examination:2019-09-11
Date of issue:2020-08-04
Advisor:Prof. Dr. Andrea Polle
Referee:Prof. Dr. Andrea Polle
Referee:Prof. Dr. Ivo Feussner
Referee:Dr. Cara Haney
Referee:Prof. Dr. Volker Lipka
Referee:Prof. Dr. Gerhard Braus
Referee:PD Dr. Marcel Wiermer
crossref-logoPersistent Address: http://dx.doi.org/10.53846/goediss-8139

 

 

Files in this item

Name:PhD dissertation_Kishore VISHWANATHAN.pdf
Size:1.95Mb
Format:PDF
Description:Dissertation: "Defense remodelling by ectomycorrhizal fungi in non-hosts"
ViewOpen

The following license files are associated with this item:


Abstract

English

Root colonizing beneficial microorganisms promote growth of host plants and protect them against biotic threats. These microbes are considered as sustainable replacements for the hazardous chemical treatments in agriculture. Ectomycorrhizal fungi, a class of beneficial fungi colonizing trees of a certain genera, protects the host’s systemic tissue from herbivory by priming defense genes and metabolites. Whether host-symbiotic interaction is a requisite for induced systemic resistance (ISR) has not been determined so far. This thesis aimed to investigate host specificity in ISR by studying the altercations in a non-mycorrhizal host, Arabidopsis thaliana (Col-0), against cabbage looper (Trichoplusia ni) after root treatment with an ectomycorrhizal fungus (L. bicolor). To find out if mycorrhization is essential for ISR, Col-0 roots were treated with L. bicolor and the foliar tissue was challenged with T. ni larvae. Though there was no visible penetration of L. bicolor in Col-0 roots, ISR was triggered by negatively affecting T. ni weight gain. The expression of defense genes (VSP, PDF1.2 or PR1) or phytohormone accumulation (JA, JA-Ile, ABA, SA) in Col-0 leaves was not significantly influenced by L. bicolor. However, L. bicolor-triggered ISR was attributed by increasing the accumulation of the secondary metabolite, camalexin, in systemic leaves. Further characterization of the ISR signalling pathway using Arabidopsis mutants, showed that L. bicolor-induced ISR is dependent on the CYP79B2/B3 and CYP81F2 of the tryptophan pathway, jasmonic acid signalling via COI1 and salicylic acid signalling via SID2 and NPR3/4 and the iron homeostasis regulator, MYB72. Unlike other beneficial microbes that suppress basal plant defenses, L. bicolor induced oxidative burst and activated the mitogen-activated protein kinase signalling cascade in Col-0. Also, Col-0 root treatment with heat-killed L. bicolor induced ISR against the larvae. These observations indicated that cell wall component(s) of L. bicolor can trigger ISR. The fungal cell wall component, chitin, when treated on Col-0 roots, reduced T. ni growth by 38% and L. bicolor-triggered ISR was dependent on the chitin receptor, CERK1. Moreover, at the expense of triggering ISR against herbivory, chitin induced susceptibility in Col-0 against the hemibiotrophic pathogen, Pseudomonas syringae. Data from this thesis highlights that host adaptability or symbiotic association is not necessary for altering systemic defense responses. Screening other microbial patterns with hosts and non-hosts can provide us answers whether ISR is a broadly conserved mechanism in systemic plant immunity.
Keywords: Arabidopsis, ectomycorrhiza, Laccaria bicolor, Trichoplusia ni, Induced systemic resistance, chitin
 

Statistik

Publish here

Browse

All of eDissFaculties & ProgramsIssue DateAuthorAdvisor & RefereeAdvisorRefereeTitlesTypeThis FacultyIssue DateAuthorAdvisor & RefereeAdvisorRefereeTitlesType

Help & Info

Publishing on eDissPDF GuideTerms of ContractFAQ

Contact Us | Impressum | Cookie Consents | Data Protection Information | Accessibility
eDiss Office - SUB Göttingen (Central Library)
Platz der Göttinger Sieben 1
Mo - Fr 10:00 – 12:00 h


Tel.: +49 (0)551 39-27809 (general inquiries)
Tel.: +49 (0)551 39-28655 (open access/parallel publications)
ediss_AT_sub.uni-goettingen.de
[Please replace "_AT_" with the "@" sign when using our email adresses.]
Göttingen State and University Library | Göttingen University
Medicine Library (Doctoral candidates of medicine only)
Robert-Koch-Str. 40
Mon – Fri 8:00 – 24:00 h
Sat - Sun 8:00 – 22:00 h
Holidays 10:00 – 20:00 h
Tel.: +49 551 39-8395 (general inquiries)
Tel.: +49 (0)551 39-28655 (open access/parallel publications)
bbmed_AT_sub.uni-goettingen.de
[Please replace "_AT_" with the "@" sign when using our email adresses.]