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Maize and Cercospora zeina transcriptome analysis during gray leaf spot foliar disease

ABSTRACT: Gray leaf spot (GLS) disease of maize can be caused by either of two sibling fungal species Cercospora zeina or Cercospora zeae-maydis. These species differ in geographical distribution, for example to date only C. zeina is associated with GLS in African countries, such as South Africa. Maize inbred line B73, which is susceptible to GLS, was planted in the field, and subjected to natural infection with C. zeina. Samples were collected from lower leaves with substantial GLS lesions and younger upper leaves of the same plants with very few immature GLS lesions. The first aim of the experiment was to determine which maize genes are induced in response to C. zeina infection. The second aim was to identify C. zeina genes expressed in planta during a compatible interaction. The third aim was to determine whether the C. zeina cercosporin biosynthetic (CTB) genes are expressed in planta. C. zeina fails to produce cercosporin in vitro in contrast to C. zeae-maydis. Cercosporin is a phytotoxin that is thought to play a role in pathogenicity of several Cercospora spp., however its role in the pathogenicity strategy of C. zeina is currently under investigation.

OTHER RELATED OMICS DATASETS IN: PRJNA369690PRJNA355557

ORGANISM(S): Zea mays Cercospora zeina

PROVIDER: GSE94442 | GEO | 2017/06/14

SECONDARY ACCESSION(S): PRJNA369690

REPOSITORIES: GEO

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Project description:In fungi, sexual compatibility is controlled by mating type loci that prevent self-fertilization. In the plant pathogenic fungus Ustilago maydis, the b mating type locus encodes a pair of unrelated homeodomain proteins, termed bE and bW. After fusion of two compatible, haploid cells, the bE and bW proteins form a heterodimeric complex, but only if they are derived from different, compatible alleles. The active bE/bW complex is required and sufficient to initiate pathogenic development of U. maydis, which is prerequisite for sexual reproduction of the fungus. However, the role of the b heterodimer during later stages of pathogenic development was unclear. To analyze b function during in planta development, we generated a temperature-sensitive bE allele (bEts) encoding a protein with a single amino acid alteration at the border of the homeodomain. This mutation leads to a stop in pathogenic development at the restrictive temperature in planta, while bEts strains show normal development at permissive temperature. At restrictive temperature, hyphae develop enlarged, bulbous cells at their tips that contain multiple nuclei, indicating a severe defect in cell division. DNA array analysis of bEts mutant strains in planta revealed a b-dependent regulation of genes coding for secreted proteins that were shown to influence fungal virulence. Our data demonstrate that in U. maydis the b heterodimer is not only essential to establish the heterodikaryon after mating of two compatible sporidia and to initiate fungal pathogenicity, but also to sustain in planta proliferation and ensure sexual reproduction. Maize plants were infected with a mixture of either FB1 and FB2 (wild-type), or RAb1ts and RAb2ts (temperature-sensitive b heterodimer) and kept at 22Â°C (permissive conditions). Control samples of FB1/FB2 and RAb1ts and RAb2ts were taken 5 days post inoculation at 22 Â°C (1 replicate each), to see if strains expressing the bts heterodimer show wildtype-like biotrophic development. To measure the impact of the b heterodimer on pathogenic development, infected plants were shifted for 9 hours to resrictive conditions (31Â°C) 111 hours post infection. After the temperature shift FB1/FB2 (3 replicates) infections developed normal, whereas RAb1ts/RAb2ts (3 replicates) infections were not able to further proliferate in planta because of a none-functional b heterodimer.

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Maize and Cercospora zeina transcriptome analysis during gray leaf spot foliar disease

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