INHERITANCE STUDY OF RESISTANCE TO MUNGBEAN YELLOW MOSAIC VIRUS DISEASE IN MUNGBEAN (Vigna radiata L. Wilczek)

Abstract

The objectives of this study were screening of 50 genotypes of mungbean [Vigna radiata (L.) Wilczek] against MYMV disease during two seasons of kharif  2015 and rabi 2015-16 under natural field condition at Research cum Instructional Farm, College of Agriculture, Indira Gandhi Krishi Vishwavidyalaya, Raipur, Chhattisgarh and to determine the inheritance of MYMV resistance in F1 and F2 generation and to identify the role of each resistance gene. During kharif season 2015 two genotypes i.e. AKM 1210 and Samrat were found to be highly resistant against MYMV disease, 12 genotypes were resistant, 15 genotypes were moderately resistant, eight genotypes were moderately susceptible, 11genotypes were susceptible and two genotypes were highly susceptible. Same set of 50 genotypes screened during rabi 2015-16 revealed that none of the entries were highly resistant, 11 genotypes to be resistant, nine genotypes were moderately resistant, 12 were moderately susceptible, 14 genotypes were susceptible and four genotypes showed highly susceptible reaction against MYMV disease indicating the role of weather conditions in expression of disease. Six crosses between resistant and susceptible genotypes were attempted. Goodness of fit test pertaining to MYMV resistance confirmed that all the F1 cross combinations viz., IGKM -08 x TM 96-2, Ling MS Thung M-1 x HUM -12, TM 2000-1 x PUSA 9072 and SGC -20 x Malviya Jyoti were resistance to MYMV clearly indicated the resistance nature was dominant over susceptibility, while the F1s of crosses DDGV 2 x IPM 409-4 and IGKM -0642 x PUSA 1471 were susceptible to MYMV, indicating that resistance is recessive. Thus the investigation revealed that MYMV resistance was digenically controlled in the five crosses with various types of interaction i.e., duplicate interaction (IGKM 0642 x PUSA 1471, F2 having two recessive genes in complementation for resistance), complementary interaction (IGKM-08 x TM 96-2 and TM 2000-1 x PUSA 9072, F2 having two complementary dominant genes for resistance) and inhibitory interaction (DGGV-2 x IPM 409-4, F2 having one recessive and one dominant gene in complementation and Ling MS Thung M-1 x HUM 12, F2 having two independent genes one dominant gene and other recessive gene for resistance) and monogenic controlled in cross SGC 20 x Malviya Jyoti, F2 having one independent dominant gene for resistance.