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Reduced cell wall degradation plays a role in cow dung-mediated management of wilt complex disease of chickpea
Chickpea, a major pulse crop, is highly prone to a devastating wilt disease commonly caused by the complex interaction of soilborne fungal pathogens of the genus Fusarium , Rhizoctonia and Sclerotinia . These pathogens collectively cause both superficial and sunken lesions resulting in symptoms like...
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Published in: | Biology and fertility of soils 2013-10, Vol.49 (7), p.881-891 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Chickpea, a major pulse crop, is highly prone to a devastating wilt disease commonly caused by the complex interaction of soilborne fungal pathogens of the genus
Fusarium
,
Rhizoctonia
and
Sclerotinia
. These pathogens collectively cause both superficial and sunken lesions resulting in symptoms like wilting and yellowing causing plant losses at seedling stage and become a major limiting factor for its growth and yield. Earlier studies demonstrated the role of composted mixture in protection against soilborne pathogens. However, there is paucity of substantial evidence for the mechanism of protection. The present study predicts the probable mechanism of cow dung-mediated reduction of wilt in
Cicer arietinum
. Cow dung-coated seeds sown in presence of mixture of fungi (FCD) could reduce the activities of cell wall-degrading enzymes produced by plant roots in response to pathogens, which were otherwise higher in mixture of wilt complex fungi/pathogens (FUN) treatment. Reduction in transcript accumulation of related genes followed by histological studies showed intercellular fungal colonization in FUN treatment, whereas it was undetected in FCD. Results indicate that cow dung treatment of chickpea seeds reduces activities of the cell wall-degrading enzymes in a transcriptionally regulated manner, which in turn function as biocontrol measure for disease. |
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ISSN: | 0178-2762 1432-0789 |
DOI: | 10.1007/s00374-013-0782-x |