Studies on chickpea (Cicer arietinum L.) defence to blight pathogen Ascochyta rabiei
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Date
2019-07-30
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palampur
Abstract
Chickpea (Cicer arietinum L.), a self-pollinated diploid (2n=2x=16) with haploid genome size
of ∼740 Mbps, is an important food legume of subtropical and tropical regions and is
believed to be originated in the Mediterranean region. In cool and humid regions of the world,
chickpea blight caused by Ascochyta rabiei causes huge yield losses. Some accession of C.
arientinum and wild Cicer species possess resistance to the disease, however molecular
mechanism governing host resistance are poorly understood. With the aim to understand
regulation of expression of genes involved in defence to A. rabiei, the expression of six
defence genes [Phenylalanine ammonia lyase (PAL), Isoflavone reductase (IFR) Flavanone
3- hydroxylase (F3H), Pathogenesis related protein - 2b (PR-2b), Basic leucine zipper 24
(bzip24) and SNAKIN-2 (Antimicrobial peptides)] was elucidated in resistant and susceptible
genotype of chickpea after inoculation (2 h, 12 h, 24 h, 36 h, 72 h) with A. rabiei. Gene
expression was studied using quantitative Real-Time PCR and the expression was normalized
with two reference genes, Clathrin adaptor complexes (CAC) and ATP-binding cassette
transporter (ABCT). The sequences of the mRNAs were retrieved from National Center for
Biotechnology Information database followed by identification of coding sequences (CDS)
and design of primers. The genes (PAL, IFR, F3H) of the phenylpropanoid pathway that
govern phytoalexin production expressed within 2 h after landing of the spores on chickpea
surface and expression was considerably higher in resistant HC-1 then susceptible GPF2. The
genes for pathogenesis related protein (PR-2b), antimicrobial peptide (SNAKIN-2) and
transcription factor (bZIP24) had peaks at 24 h in the resistant genotype indicating maximum
expression in resistant genotype at the time of host penetration and subsequent pathogen
spread. The susceptible host (GPF2), on the other hand was slow in its response as is evident
from low or delayed overexpression as compared to resistant host. It appears that defence to
Ascochyta blight in chickpea is a precisely coordinated reaction of the host, where
phytoalexin accumulation appears to occur within hours of inoculation, whereas antimicrobial
peptides accumulate at the time of host invasion and pathogen spread