The influence of host genotype X environment Interactions on the response of Cassava Anthracnose disease in diverse agro-ecologies in Nigeria

Nine cassava ( Manihot esculenta ) genotypes were grown for three years (1992-1993, 1993-1994 and 1994-1995) in three agro-ecological zones in Nigeria to study their reaction to cassava anthracnose disease (CAD), caused by Colletotrichum gloeosporioides , investigate genotype x environment (G x E) interaction patterns for their reaction to anthracnose, and to identify genotypes with stability of resistance to the disease. Mean squares for environments, genotypes and G x E interactions were highly significant (P<0.0001) for anthracnose infection. Significant G x E interactions, accounting for 19% of the treatment sums of squares, indicated that genotypes responded differentially to anthracnose infection across environments. The additive main effects and multiplicative interaction (AMMI) statistical model selected AMMI3 as the best predictor for anthracnose because it had the smallest root mean square prediction difference (0.41), and explained 99% of the G x E interaction for cassava anthracnose disease. Anthracnose severity was low in all three years. Highest disease severity was recorded in 1992-93 (2.1) and the least in 1994-95 (1.69). Clone U/41044 was the most resistant and TME1 the most susceptible to CAD. Clone 30555 showed the most stable reaction and TME1 the least stability to CAD. The most disease was recorded in Ibadan and Owerri, making them good sites for screening cassava for anthracnose resistance.Neuf génotypes de manioc ( Manihot esculenta ) étaient cultivés pour trois années (1992–1993, 1993–1994 et 1994–19995) dans trois zones agro écologiques au Nigeria en vue d&apos;étudier leur réaction à la maladie d&apos;anthracnose du manioc (CAD), causée par les Colletotrichum gloeosporioides , examiner les modèles d&apos;interaction génotype x environnement (G x E) pour leur réaction à l&apos;anthracnose, et identifier les génotypes ayant une stabilité de résistance à la maladie. Les carrées des moyennes pour les interactions environnements, génotypes et G x E étaient significativement élevées (P