Mechanisms and quantitative trait loci for Striga hermonthica resistance in maize (Zea mays L.) inbred line

Idris Olawale Amusan, Purdue University

Abstract

Striga weeds constitute a significant bottleneck to profitable maize (Zea mays L) production and food security in sub-Saharan Africa. Annual yield loss from Striga infestation of African crops has been estimated at US $7 billion in the savannah region of Africa alone. Genetic resistance in host plant is central to the success of integrated control measures for minimizing the menace of Striga. However, breeding for Striga resistance in maize has proved elusive for decades. This is due to paucity of resistance sources with known mechanisms of resistance in cultivated maize, perhaps because maize did not co-evolve with Striga; as maize is not an African crop. Decades of effort on Striga research at the International Institute of Tropical Agriculture (IITA) Ibadan, has recently led to successful release and registration of Striga resistance maize inbred lines from diverse genetic background. The mechanisms and quantitative trait loci governing resistance to Striga in these germplasm have not been known. Discovering the underlying resistance mechanisms requires an in-vitro system, which can reveal the hidden interactions between parasite and host roots normally concealled in the soil. In this study, we developed a new in-vitro screening technique which we have dubbed the Sand Packed Titer Plate Assay (SPTPA). We used this assay to evaluate 20 Striga resistant maize inbred lines for reactions to Striga post germination infections. These 20 maize inbred lines consisted of 5 lines each from 4 different populations that were sources of resistance. We observed different levels of incompatible response to Striga infection among these maize inbred lines. Resistance manifested as significantly fewer attachments of pre-germinated Striga seeds on the roots of resistant lines, in addition to delayed parasitic development and higher mortality of attached parasites. Striga on the susceptible inbred usually penetrated the xylem and showed substantial internal haustorial development. Haustorial ingress on the resistant inbred was often stopped at the endodermis. Parasites able to reach resistant host xylem vessels showed diminished haustorial development relative to those invading susceptible roots. Putative resistant maize inbred lines differed significantly in their ability to cause arrested parasite growth, delayed parasitic development, and death of Striga seedlings that attached to their roots. Hierarchical cluster analysis separated the maize inbred lines into three groups, based on differences in Striga development on infested host roots. Further assessment of grouping of the lines using canonical analysis also separated the lines into three distinct groups. The first canonical variate which accounted for 93% of the variance clearly distinguished the three clusters. Cluster 1 exhibited the strongest level of incompatible response to Striga parasitism, causing arrested parasitic growth and death of parasite that attached to their roots. The same 20 Striga resistant maize inbred lines were genotyped with simple sequence repeat markers to assess the genetic diversity present within this diverse germplasm. A total of 352 allelic fragments were obtained, with average gene diversity value of 0.78, ranging from 0.44 to 0.94. Cluster and principal component analyses reflect mixed composition of genetic background during development of these inbred lines. Genotypic distance matrix showed some degree of resemblance to dendrogram topologies based on incompatible response to Striga infestation previously reported. However, no significant correlation was found between the two distance matrices. To identify genomic regions that confer resistance to Striga parasitism, an F2 mapping population from a cross between the susceptible (5057) and resistant (ZD05) maize inbred lines were evaluated for their responses to Striga infestation. Composite interval mapping located two putative quantitative trait loci (QTL) on chromosome 6 of maize linkage group that governs incompatible response to Striga parasitism. These QTL accounted for 55% of observed phenotypic variation for incompatible response to Striga infestation on host roots. Both additive and dominance genetic effects were important for resistance to Striga. However, there appear to be a preponderance of dominance genetic effects over additive genetic effect for the expression of these two major Striga resistance QTL.

Degree

Ph.D.

Advisors

Ejeta, Purdue University.

Subject Area

Agronomy|Plant Pathology

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