Ecological Genetic Divergence of the Fungal Pathogen Didymella rabiei on Sympatric Wild and Domesticated Cicer spp. (Chickpea)

Frenkel O., Peever T. L., Chilvers M. I., ÖZKILINÇ H., Can C., Abbo S., ...More

APPLIED AND ENVIRONMENTAL MICROBIOLOGY, vol.76, no.1, pp.30-39, 2010 (SCI-Expanded) identifier identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 76 Issue: 1
  • Publication Date: 2010
  • Doi Number: 10.1128/aem.01181-09
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.30-39
  • Çanakkale Onsekiz Mart University Affiliated: No


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 Cicer 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 responses among progeny from crosses of isolates from C. judaicum with 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 that of 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 coadapted gene complexes controlling pathogenic fitness on each host and may be responsible for maintenance of genetic differentiation between the pathogen demes.