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Comparative disease-responsive extracellular matrix proteome and phosphoproteome
of resistant chickpea under vascular wilt
Eman Elagamey1,2, Magdi A.E. Abdellatef 1,2, Niranjan Chakraborty1 Subhra Chakraborty1*
1
National Institute of Plant Genome Research, Aruna Asaf Ali Marg, New Delhi 110067,
India
2
Agricultural Research Center (ARC), Plant Pathology Research Institute, 9 Gamaa st.,
Giza 12619, Egypt
Patho-stress is the most significant factor that adversely affects plant growth, development
and productivity affecting agriculture and geographical distribution of crop plants worldwide.
Vascular wilt, caused by Fusarium oxysporum f. sp. ciceris, is the most important root disease
of chickpea. It is widespread in occurrence and causes significant economic losses every year
worldwide. ECM or cell wall in plant is a dynamic system that represent as a first line defence
to restrict entry of potential pathogen and mediating cell signalling to perceive and transmit
extra- and intercellular signals in many pathways the molecular interaction between microbial
pathogen and host occurs in the extracellular space, thus ECM plays an important role in cell
fate decision under various patho-stresses. In this study, we have developed a comprehensive
ECM proteome and phosphoproteome maps by 2-DE coupled with ESI-MS/MS for resistant
chickpea cultivar WR-315 during F. oxysporum f. sp. ciceris. vascular wilt to understand the
underlying mechanism that enables this variety to withstand disease conditions and to provide
new insight into the underlying mechanisms of patho-stress tolerance. The analysis of the wiltresponsive proteome and phosphopoteome revealed 1472 differentially expressed protein
spots of which a total of 211 were identified and 450 differentially expressed phosphoprotein
spots of which a total of 130 were identified respectively. The identified proteins were involved
in a variety of functions that might help in understanding the plant pathogen interaction and
enhancing our understanding on the physiological and molecular mechanisms underlying
patho-stress response.