Abstract

Downy mildew disease causes considerable yield loss in pearl millet. The disease has gained special attention due to the introduction of hybrid pearl millet. Sclerospora graminicola is an obligate biotroph. Though the pathogen behaves like a fungal pathogen but as far as its infection mechanism is concerned, the biology of the fungus, especially the cellulose-rich cell wall and motile zoospores, closely resemble golden-brown algae and diatoms. The pathogen is well adapted to the semi-arid climatic conditions. The disease gained epiphytotic status more than four decades ago, but even today this disease is devastating. Pathogen is soil, seed and air-borne. The disease could be controlled by seed treatment with fungicide Apron 35 SD and spray with Ridomil MZ. Reliable resistant gene candidates for downy mildew are not available. Further due to shift in virulence of the pathogen the host resistance breaks down. Reliable field screening procedures have been developed to identify the sources of resistance. Attempts have also been made to identify molecular markers for selection of promising genotypes in the downy mildew resistance breeding programme. Resistance gene analogues (RGAs) from pearl millet have been cloned and sequenced. The GenBank database search revealed the conserved Nucleotide-binding site (NBS). The accumulation of transcripts of RGA during infection in resistant pearl millet seedlings was shown. Extensive work has been done on the role of defense-responsive genes/proteins and induced resistance. It is essential to identify the potential biotic/abiotic elicitors and develop the formulations for effective control of downy mildew at Farmers’ field situations. The genome sequencing of host and pathogen and transgenic approach would help in developing an effective control strategy against downy mildew.

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