New Delhi, India
Indian Agricultural Research Institute (IARI)
Mandya, Karnataka, India
Univ. Agric. Sci. Regional Research Station
Udaipur, Rajasthan, India
Rajasthan College of Agriculture
Bangkok, Thailand
CIMMYT-ARMP
Inheritance of resistance to sorghum downy mildew (Peronosclerospora sorghi) and Rajasthan downy mildew (P. heteropogoni) in maize in India --Yen, TTO, Rathore, RS, Setty, TA, Kumar, R, Singh, NN, Vasal, SK, Prasanna, BM Among various diseases affecting production and productivity of maize in tropical Asia, Downy Mildew (Peronosclerospora sp.) is considered as one of the most destructive diseases. In India, important species causing downy mildew (DM) disease in maize are sorghum DM [Peronosclerospora sorghi (Weston & Uppal) Shaw], Philippine DM [P. philippinensis (Weston) Shaw] and Brown Stripe DM (Sclerophthora rayssiae var. zeae Payak & Renfro). Sorghum DM (SDM) causes considerable yield losses in several maize growing states, particularly Karnataka, Tamil Nadu and Rajasthan. A survey conducted in Karnataka revealed that the incidence of disease ranged from 10 to 90% and yield loss from 30-40% (Krishnappa et al., 1995).

In Rajasthan, the disease cycle of P. sorghi remained unknown until 1973 when Heteropogon contortus (speargrass), a wild grass growing in the vicinity of maize fields, was found to be a collateral host of this pathogen. Although the fungus resides on this perennial grass in the form of oospores, the conidial stage is the sole cause of primary infection of maize in that region. While some workers considered that the DM caused primarily through Heteropogon contortus should be redesignated as P. heteropogoni, others considered this a different isolate of P. sorghi, in view of the striking similarities in disease symptoms and very minor differences in pathogen morphology (Payak, 1975; Frederiksen and Renfro, 1977). The DM disease, caused by P. heteropogoni, has been recently designated as Rajasthan downy mildew (RDM) (White, 1999).

A detailed study was carried out to analyze the genetic variability and inheritance of resistance to two important DM diseases of maize in India - sorghum downy mildew (SDM) caused by P. sorghi and Rajasthan downy mildew (RDM) caused by P. heteropogoni. Experiments carried out under artificial infection during Kharif (Monsoon) season in 1999 and 2000 at two different DM 'hot spot' locations in India - Mandya in Karnataka and Udaipur in Rajasthan - aided in characterization of the responses of a set of public sector maize inbreds to the SDM and RDM pathogens, respectively.

Responses of maize inbred lines to SDM and RDM infection in India: A total of 41 inbred lines were evaluated after artificial infection by SDM and RDM at Mandya and Udaipur, respectively. Since a specific set of maize inbred lines was evaluated by both SDM and RDM infection at two different locations, the study provides an insight into the possible differences in the interaction of the genotypes with SDM and RDM. Analysis of the results obtained in two seasons (1999 and 2000) revealed five inbreds - AMB103 (Nei9008), AMB109 (AMATLCOHS115-1-2-3-3-1-2-B-B), AMB110 (AMATLCOHS233-1-1-1-1-2-2-BBB), AMB112 (P345C3S3B-46) and AMB119 (IPB9204-1-3-1-2-4-B) that are highly resistant to both SDM and RDM infection. The 'AMB' lines were those provided by the CIMMYT-Asian Regional Maize Program, Thailand. Among these lines, AMB103 and AMB112 were resistant to SDM (P. sorghi) in Thailand and Philippine DM (P. philippinensis) in the Philippines, and are currently being utilized for molecular marker mapping and marker-assisted selection under the Asian Maize Biotechnology Network (AMBIONET) program in these countries (Des Hautea, personal communication; Apichart Vanvichit, personal communication). Such inbred lines with broad-spectrum resistance to DM infection in tropical Asian countries would be highly useful for a variety of basic and applied research on downy mildew resistance breeding.

Significantly, among the 41 inbreds analyzed in the present investigation, no inbred could be found that was resistant to SDM disease at Mandya, and susceptible to RDM infection at Udaipur. A large number of inbreds resistant to RDM infection showed differential responses to SDM infection. Elite Indian maize inbreds such as CM119 and CM133 were highly susceptible to both SDM and RDM, highlighting the necessity of utilizing DM resistant germplasm for deriving elite Indian inbred lines, particularly for hybrid maize breeding. The CIMMYT inbred lines (CML20 and CML281) also showed severe susceptibility to both the SDM and RDM pathogens.

Inheritance of resistance/susceptibility to downy mildew infection in maize: Two sets of data were used to analyze the inheritance of resistance/susceptibility to SDM at Mandya and RDM at Udaipur: (a) responses of various experimental crosses generated among the materials under study; and (b) F2 and BC progenies of selected experimental crosses. Several cross combinations were generated using resistant (R), moderately resistant (MR), moderately susceptible (MS) and susceptible (S) inbreds identified in this study. F1 plants from three cross combinations - NAI116 x CM105; MAI110 x NAI139; and MAI113 x MAI110 - were selfed to generate the F2 population. Also, NAI116 x CM105 (a cross between resistant and susceptible lines) was backcrossed to both parents to generate backcross (BC) progenies. F1, F2 and BC progenies were evaluated for their responses to DM infection at both Mandya and Udaipur during Kharif 2000.

Inheritance of SDM resistance in maize: A total of 38 experimental crosses were evaluated for SDM resistance/susceptibility. Progeny of the R x R crosses showed only a resistant response, while the R x S crosses revealed only a moderately resistant response. The S x R crosses, in contrast, showed susceptibility in general (62.91%), with one cross combination recording moderate resistance and another recording moderate susceptibility. Both S x MR and MR x S crosses showed moderate susceptibility. Analysis of various categories of crosses indicated the complex and polygenic nature of inheritance of SDM resistance in maize. Orthogonal contrast also revealed distinct results depending on whether the resistant line was the male or female parent; DM incidence was greater in the second group than the first, highlighting the significance of the cytoplasmic constitution of the female parent in determining the inheritance of SDM resistance.

F2 progenies from the cross NAI116 x CM105 (R x S) showed a large number of resistant plants (190 out of 291 plants), while F2 progeny from the S x S crosses behaved differently. In the F2 progeny of MAI110 x NAI139 (S x S), only 16 plants were resistant among a total of 194 plants. In contrast, the F2 progeny of MAI113 x MAI110 recorded a significantly higher frequency of resistant plants (120 out of 245 plants). Recovery of resistant plants in F2 of S x S crosses suggests the possibility that resistance/susceptibility might be under the control of both dominant and recessive genes and susceptible lines might also contribute alleles contributing to resistance of the F1. While the F1 progeny of the cross NAI116 x CM105 had a moderately resistant phenotype, the BC1 progenies, designated as BC(P1) and BC(P2), revealed distinctly different responses. The BC(P1) progeny (backcross with highly resistant parent) showed a very high frequency of resistant plants, with only 8 SDM infected plants out of a total of 142. In contrast, the BC(P2) progeny (backcross with highly susceptible parent) revealed a very high frequency of DM susceptible plants. These observations not only suggest that resistance to SDM disease is under polygenic control, but also a 'threshold effect': accumulation of alleles governing resistance to SDM in BC(P1) led to distinctly different response in comparison with F1, while accumulation of alleles responsible for susceptibility in BC(P2) tilted the response towards high susceptibility. Also, susceptibility for SDM appears to be partially dominant over resistance, and both dominant and recessive alleles might be contributing to the susceptible/resistant responses.

Inheritance of RDM resistance in maize: A total of 32 experimental crosses, generated using various inbreds characterized for their RDM resistance/susceptibility during Kharif (Monsoon) 1999, were evaluated at Udaipur under artificial infection during Kharif 2000. Almost all of the R x R progeny showed a highly resistant response, except CM124 x MAI105 which showed moderate resistance. Both R x MR as well as MR x MR progeny revealed only resistant responses. The R x S progeny displayed resistance in all cases, except for MAI101 x CM119, which had moderate resistance. In contrast, the progeny of S x R crosses showed a different pattern, with two crosses resulting in resistance, two in moderate resistance, and two in moderate susceptibility. All three S x MR crosses resulted in a moderately susceptible phenotype. Similarly, progeny of the S x S crosses were always susceptible. It is interesting again to note that both R x S and S x R crosses of the inbred lines did not show either completely resistant or susceptible phenotypes in F1, suggesting a polygenic nature of inheritance of RDM resistance. Orthogonal contrast also revealed that the effect of the second group where the resistant line was used as the male parent is greater than the first where the resistant line was used as the female parent, indicating that DM incidence was greater in the second group than the first. This observation highlights the possible role of the cytoplasmic constitution, in combination with the nuclear genes, in determining the magnitude of RDM resistance. F2 progenies of R x S crosses clearly revealed the distinct differences in the number of infected plants. While the F2 progeny from the NAI116 x CM105 cross showed an extremely low incidence of susceptible plants, MAI110 x NAI139 included a relatively higher frequency of susceptible plants. The F2 progeny from the MR x R cross was largely resistant, similar to those for R x S crosses. The backcross of NAI116 x CM105 to the highly resistant parent (NAI116) had no susceptible plants in the progeny. A comparison of this response with that of the parent NAI116 x CM105 indicated an increase in the resistance capacity of the BC progeny (0% DM incidence in BC progeny vs. 3% in F1).

This study highlights the distinct modes of inherited resistance to SDM and RDM diseases in India. While susceptibility to SDM infection was found to be partially dominant over resistance, resistance to RDM infection appeared to be partially dominant over susceptibility. Analysis of F1, F2, BC(P1) and BC(P2) progenies clearly revealed the differences in modes of inheritance of SDM and RDM resistance. The data also suggested that both dominant and recessive alleles contribute to the response to SDM and RDM infection. Inheritance of resistance to RDM infection was found to be less complex than that of SDM resistance. Further studies are being carried out to clearly discern the significance of additive, dominance, epistatic effects and their interactions in the inheritance of resistance to SDM infection in India.
 
 


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