Institutional Publications
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Item MicroRNA397 regulates tolerance to drought and fungal infection by regulating lignin deposition in chickpea root(John Wiley & Sons, 2023) Sharma, Nilesh Kumar; Yadav, Shalini; Gupta, Santosh Kumar; Irulappan, Vadivelmurugan; Francis, Aleena; Senthil-Kumar, Muthappa; Chattopadhyay, DebasisPlants deposit lignin in the secondary cell wall as a common response to drought and pathogen attacks. Cell wall localised multicopper oxidase family enzymes LACCASES (LACs) catalyse the formation of monolignol radicals and facilitate lignin formation. We show an upregulation of the expression of several LAC genes and a downregulation of microRNA397 (CamiR397) in response to natural drought in chickpea roots. CamiR397 was found to target LAC4 and LAC17L out of twenty annotated LACs in chickpea. CamiR397 and its target genes are expressed in the root. Overexpression of CamiR397 reduced expression of LAC4 and LAC17L and lignin deposition in chickpea root xylem causing reduction in xylem wall thickness. Downregulation of CamiR397 activity by expressing a short tandem target mimic (STTM397) construct increased root lignin deposition in chickpea. CamiR397-overexpressing and STTM397 chickpea lines showed sensitivity and tolerance, respectively, towards natural drought. Infection with a fungal pathogen Macrophomina phaseolina, responsible for dry root rot (DRR) disease in chickpea, induced local lignin deposition and LAC gene expression. CamiR397-overexpressing and STTM397 chickpea lines showed more sensitivity and tolerance, respectively, to DRR. Our results demonstrated the regulatory role of CamiR397 in root lignification during drought and DRR in an agriculturally important crop chickpea.Item Drought stress exacerbates fungal colonization and endodermal invasion and dampens defense responses to increase dry root rot in chickpea(American Phytopathological Society, 2022) Irulappan, Vadivelmurugan; Kandpal, Manu; Saini, Kumud; Rai, Avanish; Ranjan, Aashish; Sinharoy, Senjuti; Senthil-Kumar, MuthappaDrought plays a central role in increasing the incidence and severity of dry root rot (DRR) disease in chickpea. This is an economically devastating disease, compromising chickpea yields particularly severely in recent years due to erratic rainfall patterns. Macrophomina phaseolina (formerly Rhizoctonia bataticola) is the causal agent of DRR disease in the chickpea plant. The infection pattern in chickpea roots under well-watered conditions and drought stress are poorly understood at present. This study provides detailed disease symptomatology and the characteristics of DRR fungus at morphological and molecular levels. Using microscopy techniques, the infection pattern of DRR fungus in susceptible chickpea roots was investigated under well-watered and drought stress conditions. Our observations suggested that drought stress intensifies the progression of already ongoing infection by weakening the endodermal barrier and overall defense. Transcriptomic analysis suggested that the plant’s innate immune defense program is downregulated in infected roots when subjected to drought stress. Further, genes involved in hormonal regulation are differentially expressed under drought stress. These findings provide hints in terms of potential chickpea genes to target in crop improvement programs to develop climate change-resilient cultivars.Item A sick plot-based protocol for dry root rot disease assessment in field-grown chickpea plants(John Wiley & Sons, 2021) Irulappan, Vadivelmurugan; Mali, Komal Vitthalrao; Patil, Basavanagouda S.; Manjunatha, Hanumappa; Muhammad, Saifulla; Senthil-Kumar, MuthappaPremise: A comprehensive field-based screening protocol is lacking for dry root rot (DRR) disease in chickpea, which is caused by Macrophomina phaseolina (formerly referred to as Rhizoctonia bataticola). Here, we describe a protocol for establishing a sick plot for DRR to enable disease assessment of a large number of chickpea plants during the natural growing season. Methods and Results: We used a chickpea plot with >30% DRR incidence, and enriched the inoculum by cultivating highly susceptible chickpea plant genotypes and incorporating infected plant material into the soil. The chickpea plants were then subjected to infection in developed sick plots with various levels of soil moisture under natural field conditions. Conclusions: Our protocol provides a robust way to impose M. phaseolina infection on chickpea plants under natural field conditions and to investigate plant responses to the infection at morphological, physiological, and molecular levels. This method can also be used to screen for other soil‐borne diseases in a variety of plants.
