AEM Accepts, published online ahead of print on 6 November 2009

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Google Scholar Articles by Frenkel, O. Articles by Sherman, A. PubMed PubMed Citation Articles by Frenkel, O. Articles by Sherman, A. Agricola Articles by Frenkel, O. Articles by Sherman, A.

 Previous Article  |  Next Article 

Appl. Environ. Microbiol. doi:10.1128/AEM.01181-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Ecological divergence of the fungal pathogen Didymella rabiei on sympatric wild and domesticated chickpea

Omer Frenkel, Tobin L. Peever, Martin I. Chilvers, Hilal Özkilinc, Canan Can, Shahal Abbo^*, Dani Shtienberg, and Amir Sherman

Institute of Plant Sciences and Genetics in Agriculture, The Hebrew University of Jerusalem, Rehovot 76100, Israel; Department of Genomics, ARO, The Volcani Center, Bet-Dagan 50250, Israel; Department of Plant Pathology, Washington State University, Pullman, WA 99164-6430, USA; Department of Biology, University of Gaziantep, 27310, Turkey; Department of Plant Pathology and Weed Research, ARO, The Volcani Center, Bet-Dagan 50250, Israel

^* To whom correspondence should be addressed. Email: abbo{at}agri.huji.ac.il.

For millennia, chickpea (Cicer arietinum) has been grown in the Levant sympatrically with wild Cicer species. Chickpea is traditionally spring-sown while its wild relatives germinate in the autumn and develop in the winter. It has been hypothesized that the human-directed shift of domesticated chickpea to summer production was an attempt to escape the devastating Ascochyta disease caused by Didymella rabiei. We estimated genetic divergence between D. rabiei isolates sampled from wild C. judaicum and domesticated C. arietinum and the potential role of temperature adaptation in this divergence. Neutral genetic markers showed strong differentiation between pathogen samples from the two hosts. Isolates from domesticated chickpea demonstrated increased adaptation to higher temperatures when grown in vitro compared with isolates from the wild host. The distribution of temperature response among progeny from crosses of isolates from C. judaicum x isolates from C. arietinum was continuous, suggesting polygenic control of this trait. In vivo inoculations of host plants indicated that pathogenic fitness of the native isolates was higher than their hybrid progeny. The results indicate that there is a potential for adaptation to higher temperatures, however the chances for formation of hybrids which are capable of parasitizing both hosts over a broad temperature range are low. We hypothesize that this pathogenic fitness cost is due to breakdown of co-adapted gene complexes controlling pathogenic fitness on each host and may be responsible for maintenance of genetic differentiation between the pathogen demes.