Transcriptional profiling of chickpea genes differentially regulated by salicylic acid, methyl jasmonate and aminocyclopropane carboxylic acid to reveal pathways of defence-related gene regulation.

Using microarray technology and a set of chickpea (Cicer arietinum L.) unigenes and grasspea (Lathyrus sativus L.) expressed sequence tags, chickpea responses to treatments with the defence signalling compounds salicylic acid (SA), methyl jasmonate (MeJA) and aminocyclopropane carboxylic acid (ACC) were studied in three chickpea genotypes with ranging levels of resistance to ascochyta blight [Ascochyta rabiei (Pass.) L.]. The experimental system minimised environmental effects and was conducted in reference design, where samples from untreated controls acted as references against post-treatment samples. Microarray observations were also validated by quantitative reverse transcription-polymerase chain reaction. The time-course expression patterns of 715 experimental microarray features resulted in differential expression of 425 transcripts. The A. rabiei resistant chickpea genotypes showed a more substantial range of defence-related gene induction by all treatments, indicating that they may possess stronger abilities to resist pathogens. Further, the involvement of SA, MeJA and ACC signalling was identified for the regulation of some important A. rabiei responsive transcripts, as well as cross-talk between these pathways. In the current study we also found evidence to suggest the involvement of A. rabiei-specific signalling mechanisms for the induction of several transcripts that were previously implicated in A. rabiei resistance. This study characterised the regulatory mechanisms of many chickpea transcripts that may be important in defence against various pathogens, as well as other cellular functions. These results provide novel insights to the molecular control of chickpea cellular processes, which may assist the understanding of chickpea defence mechanisms and allow enhanced development of disease resistant cultivars.