Genetic architecture and inheritance dynamics governing Mungbean Yellow Mosaic Virus (MYMV) resistance in mungbean (Vigna radiata L. Wilczek)

Introduction

Mungbean [Vigna radiata (L.) Wilczek, [2𝑛 = 2𝑥 = 22], belonging to the family Fabaceae (subgenus Ceratotrophis), is one of the most critical self-pollinating pulse crops cultivated extensively across South and Southeast Asia. Rich in easily digestible protein (~24%) (Kumar et al. 2020) [6] , essential vitamins, and minerals, mungbean plays a vital role in dietary security and cropping systems owing to its short duration and atmospheric nitrogenfixing capabilities. In Maharashtra, mungbean represents the second most important pulse crop after pigeonpea. During the 2024-2025 cropping season, Maharashtra cultivated mungbean across 3.85 lakh hectares, producing 1.82 lakh tonnes with an average productivity of 460 kg/ha, which remains significantly lower than the national average productivity (1, 125 kg/ha across 35.27 lakh hectares) (IIPR). A major constraint limiting mungbean productivity is the susceptibility to biotic stresses, However, resistance breeding requires a thorough understanding of the genetic architecture and gene effects (𝑚, 𝑑, ℎ, 𝑖, 𝑗, 𝑙) governing viral resistance parameters. While classical studies often treated resistance as a simple monogenic trait, recent epidemiological evaluations suggest complex polygenic inheritance involving non-allelic interactions (Kumar et al. (2020) [6] . Generation Mean Analysis (GMA), developed by Cavalli (1952) [3] and Hayman (1958) [4] , is a powerful biometrical tool designed to resolve genetic variance into additive, dominance, and epistatic (additive × additive [𝑖], additive × dominance [𝑗], and dominance × dominance [𝑙]) components. Alam et al. (2014) [1] reported significant additive and dominance effects along with epistatic interactions for MYMV resistance and associated traits, demonstrating the contribution of both additive and nonadditive gene effects. Therefore, the primary objective of this investigation was to determine the precise mode of gene action and inheritance governing MYMV resistance parameters-specifically Disease Incidence (%), Percentage Disease Index (PDI), and Area Under Disease Progress Curve (AUDPC)-across five distinct cross combinations in mungbean.

Materials and Methods

Experimental Site and Agro-Climatic Conditions

The field trial was carried out at the experimental farm of the Seed Technology Research Unit (STRU), Dr. Panjabrao Deshmukh Krishi Vidyapeeth (PDKV), Akola, Maharashtra, India. The site represents the semi-arid tropical region of Central India. Hybridisation to generate 𝐹 1 , backcross (𝐵𝐶 1 , 𝐵𝐶 2 ), and selfed (𝐹 2 ) generations was completed during Kharif 2025. The evaluation of all developed generations along with parents and standard checks was conducted during the Summer 2026 season

Genetic Materials

The experimental material comprised six basic generations (𝑃 1 , 𝑃 2 , 𝐹 1 , 𝐹 2 , 𝐵𝐶 1 , 𝐵𝐶 2 ) derived from five crosses involving seven parents (3 females, 4 males) with contrasting reactions to MYMV, alongside three commercial checks and their Salient Features of Parental Genotypes and Standard Checks

Experimental Design and Layout

The 30 treatments (comprising parents, 𝐹 1 s, 𝐹 2 s, 𝐵𝐶 1 s, 𝐵𝐶 2 s, and 3 standard checks) were laid out in a Randomized Block Design (RBD) with three replications. Planting was performed by hand dibbling with a row-to-row spacing of 45 cm and plant-to-plant spacing of 15 cm. Fertilizer doses and cultural practices were maintained per state recommendations. Susceptible spreader rows (Kopergaon and SML 134) were planted around the experimental block to ensure uniform natural whitefly vector pressure and severe viral exposure.

Pathological Observations and Disease Scoring

MYMV disease screening was performed visually based on the 0-9 rating scale standardized by Mayee and Datar (1986) [7] Pathological data were recorded across five crop growth stages: 31, 40, 50, 61, and 73 Days After Sowing (DAS).

Three main epidemiological parameters were computed:

Area under Disease Progress Curve (AUDPC)

Calculated across the five time intervals using the formula (Shaner and Finney, 1977) [9] :

Statistical and Biometrical Analysis

Analysis of Variance (ANOVA) was executed across replications and treatments. Cavalli's (1952) [3] Joint Scaling Test was applied using a three-parameter model (𝑚, 𝑑, ℎ) evaluated via weighted least squares. Goodness-of-fit was tested using chi-square (𝜒 2 ) test with 3 degrees of freedom.

Where 𝜒 2 was statistically significant, Hayman's (1958) [4] six-parameter model was evaluated to resolve full additive, dominance, and non-allelic epistatic parameters: 𝑚 = Mean of all generations , 𝑑 = Additive gene effect , ℎ = Dominance gene effect, 𝑖 = Additive × Additive epistatic interaction effect , 𝑗 = Additive × Dominance epistatic interaction effect , 𝑙 = Dominance × Dominance epistatic interaction effect .

Results and Discussion

Analysis of Variance (ANOVA)

The ANOVA for MYMV resistance traits demonstrated highly significant differences (𝑝<0.01) among treatments across all parameters. Mean Sum of Squares (MSS) for treatments was 362.20 for Disease Incidence, 333.32 for PDI, and 1, 448, 632.98 for AUDPC values, against low error variances (9.66, 21.15, and 56.69 respectively). This confirms the existence of high genetic variability across the basic generations and crosses under evaluation.

References

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