Date of Award


Degree Type


Degree Name

Doctor of Philosophy (PhD)


Botany and Plant Pathology

Committee Chair

Gurmukh S. Johal

Committee Co-Chair

Mitch Tuinstra

Committee Member 1

Anjali Iyer-Pascuzzi

Committee Member 2

Tesfaye Mengiste


Plants are under constant threat from various pathogens and have evolved a two-branched immune system to defend themselves. One aspect of plant defense involves the hypersensitive response (HR) which is characterized by localized cell death to prevent the spread of the pathogen. Lesion mimic mutants are a ubiquitous class of plant mutants that spontaneously develop lesions resembling HR. However, not all lesion mimic mutants have been found to encode genes involved in defense. les23 is a recessive lesion mimic mutant in maize that can be suppressed by the Mo20W allele of Slm1 (Suppressor of lesion mimics 1). Both QTLs have been mapped to chromosome 2, but the underlying genes have not been identified. Here, we demonstrate that the les23 mutant is indeed undergoing a defense response by analyzing transcriptome changes using RNA-seq. We also report the cloning of Les23 and Slm1 and found that they encode for a maize homolog of Arabidopsis RIN4 and an uncharacterized NLR resistance gene respectively. Transient expression of LES23 and SLM1 in Nicotiana benthamiana revealed that SLM1 is an autoactive NLR that requires LES23 to keep it quiescent. This model is similar to Arabidopsis RIN4/RPS2. Analyzing SLM1 found that it encodes a canonical NLR with all the typical domains and motifs. Despite Slm1 encoding for a NLR, it is unknown what effector(s) it recognizes. Sequencing Slm1 in the NAM founders found that it is not a highly conserved gene with several lines encoding for truncated, non-functional alleles. Thus, Slm1 may no longer be needed as a resistance gene against a certain pathogen. Finally, we describe the identification of a homeolog of Les23, Les23-like 1 (Ltl1) that is capable of suppressing SLM1-mediated cell death in N. benthamiana.