Molecular Characterization of the Maize Rp1-D Rust Resistance Haplotype and Its Mutants

Abstract

The Rp1-D gene for resistance to maize common rust (Puccinia sorghi) is a member of a complex locus (haplotype) composed of Rp1-D and approximately eight other gene homologs. The identity of Rp1-D was demonstrated by using two independent gene-tagging approaches with the transposons Mutator and Dissociation. PIC20, a disease resistance (R) gene analog probe previously mapped to the rp1 locus, detected insertion of Dissociation in an Rp1-D mutation and excision in three revertants. Independent libraries probed with the PIC20 or Mutator probes resulted in isolation of the same gene sequence. Rp1-D belongs to the nucleotide binding site, leucine-rich repeat class of R genes. However, unlike the rust resistance genes M and L6 from flax, the maize Rp1-D gene does not encode an N-terminal domain with similarity to the signal transduction domains of the Drosophila Toll protein and mammalian interleukin-1 receptor. Although the abundance of transcripts of genes from the rp1 complex changed with leaf age, there was no evidence of any change due to inoculation with avirulent or virulent rust biotypes. A set of 27 Rp1-D mutants displayed at least nine different deletions of Rp1-D gene family members that were consistent with unequal crossing-over events. One mutation (Rp1-D*-24) resulted in deletion of all but one gene family member. Other unique deletions were observed in the disease lesion mimic Rp1-D*-21 and the partially susceptible mutant Rp1-D*-5. Different rp1 specificities have distinct DNA fingerprints (haplotypes). Analysis of recombinants between rp1 specificities indicated that recombination had occurred within the rp1 gene complex. Similar analyses indicated that the rust R genes at the rp5 locus, 2 centimorgans distal to rp1, are not closely related to Rp1-D.

Identification of a Maize Locus That Modulates the Hypersensitive Defense Response, Using Mutant-Assisted Gene Identification and Characterization

“…The Rp1-D21 disease lesion phenotype has typical hallmarks of the hypersensitive response: Genetic and molecular studies have clearly demonstrated that the Rp1-D21 gene is a structurally aberrant allele of functional R genes at the complex Rp1 disease-resistance locus (Collins et al 1999;Sun et al 2001). However, the question remained whether lesions associated with the Rp1-D21 mutation truly represented cell death typical of the HR response induced in response to pathogen attack.…”

“…The Rp1-D21 gene is an autoactive allele from the maize Rp1 disease-resistance locus that initiates HR randomly all over the plant (Pryor 1993;Collins et al 1999;Sun et al 2001). Our objective for this study was to use the Rp1-D21 gene phenotype as a test case for the Mutant-Assisted Gene Identification and Characterization approach.…”

Rapidly evolving R genes in diverse grass species confer resistance to rice blast disease

“…In particular, the Rp1/Pi37 family includes R genes for maize rust resistance at the Rp1-D locus (22) as well as for rice blast resistance at the Pi37 locus (15); and the Rp3/Pc family includes maize R genes against rust resistance at the Rp3 locus (23) as well as sorghum R genes against root rot caused by Periconia circinata at the Pc-B locus (16). It is remarkable that the same R-gene families can confer resistance to blast and rust diseases.…”

“…The phylogenetic tree of the 12 selected rice blast strains constructed by using nucleotide sequences from six Avr genes (Avr-pita, Avr-pia, Avr-pik, Avr-pii, Avr-pwl2, and Avr-Ace-1) (15,22,23,26) by maximum likelihood and bootstrapped 1,000 times with a Kimura two-parameter model by using MEGA version 5.02 (SI Appendix, Fig. S2) (27).…”

Simple Sequence Repeat-Based Comparative Genomics Between Brassica rapa and Arabidopsis thaliana: The Genetic Origin of Clubroot Resistance

“…This could also lead to an increased complexity of the resistance mechanism. In maize, the rp1 complex for common rust resistance has evolved with a duplication and recombination of genes in the evolution of a family of resistance genes, leading to a diversification of resistance (Collins et al 1999). Another possibility is that the resistance genes for clubroot were originally clustered in that genomic region of the ancestral genome and distributed into two different genomic regions following chromosomal rearrangements in Brassica.…”