Table 1.
Growth and morphological characterization of NTG induced Trichoderma mutants.
Table 2.
Evaluation of antagonistic and diffusible volatile compounds inhibition ability of NTG induced Trichoderma mutants against chickpea pathogens.
Fig 1.
Carbendazim tolerance in N-methyl-n-nitro-N-nitrosoguanidine irradiated Trichoderma mutants.
Mutants N2-1, N2-2, N2-3 is compared with N2 mutant at carbendazim 250, 500, 750 and 1000 μg/ml in PDA plates, and observation are recorded when the control plates cover the whole plate.
Fig 2.
Carbendazim tolerance and dry mycelial productions in N-methyl-n-nitro-N-nitrosoguanidine irradiated Trichoderma mutants.
(a) The 1st round NTG induced N1, N2, N3 mutants carbendazim tolerance at 0–120 μg/ml carbendazim amended PDA; (b) 2st round NTG induced N2-1, N2-2, N2-3 mutants carbendazim tolerance at 0–1500 μg/ml carbendazim amended PDA; (c) dry mycelium production ability of N2-2, N2 and WT in 0–2000 μg/ml carbendazim amended potato dextrose broth.
Fig 3.
Integrated management of chickpea dry root rot disease under glasshouse condition.
(a) Overview of the experiments at 44 days after sowing; (b) complete dry rot infected plants in T1 (untreated) treatment; (c) partially dry rot infected plants in dry root rot in T7 (N2-2+0.5 RD carbendazim) treatment at 60 days after sowing in JG 62 cultivar.
Table 3.
Area under disease progress curve (AUDPC) and estimated apparent infection rate (r) in different treatments for chickpea dry root rot management under glasshouse conditions.
Fig 4.
Ribbon representations of Trichoderma N2, N2-2 and WT strain tub2 protein.
Deduced amino acids structural superimposition between N2 and N2-2 with WT of tub2 gene differ by 37 and 183 mutant residues. In both the images—yellow (mutant protein), cyan (WT protein) and magenta (mutant residues).