Transcript profiles in sugar beet genotypes uncover timing and strength of defense reactions to Cercospora beticola infection.

Cercospora leaf spot disease, caused by the fungus Cercospora beticola, is the most destructive foliar disease of sugar beet (Beta vulgaris) worldwide. Despite the great agronomical importance of this disease, little is known about its underlying molecular processes. Technical resources are scarce for analyzing this important crop species. We developed a sugar beet microarray with 44,000 oligonucleotides that represent 17,277 cDNAs. During the four stages of C. beticola-B. vulgaris interactions, we profiled the transcriptional responses of three genotypes: susceptible, polygenic partial resistance, and monogenic resistant. Similar genes were induced in all three genotypes during infection but with striking differences in timing. The monogenic resistant genotype displayed strong defense responses at 1 day postinoculation (dpi). The other genotypes displayed defense responses in a later phase (15 dpi) of the infection cycle. The partially resistant genotype displayed a strong defense response in the late phase of the infection cycle. Furthermore, the partially resistant genotype expressed pathogen-related transcripts that the susceptible genotype lacked. These results indicate that resistance was achieved by the ability to mount an early defense response, and partial resistance was determined by additional defense and signaling transcripts that allowed effective defense in the late phase of the infection cycle.

Accumulation of the hormone abscisic acid (ABA) at the infection site of the fungus Cercospora beticola supports the role of ABA as a repressor of plant defence in sugar beet.

Inducible plant defence responses in sugar beet (Beta vulgaris L.) leaves are repressed during the early phase of infection by the fungus Cercospora beticola. In this report, we show that the concentration of the plant hormone abscisic acid (ABA) increases in sugar beet leaves during C. beticola infection. After an initial burst of ABA induced by inoculation of the fungus, elevated ABA concentrations were detected during the fungal penetration and colonization phases 3-9 days after inoculation. Fifteen days after inoculation, with visible onset of the necrotic phase of infection, the strongly elevated ABA concentrations in infected leaves were at levels similar to drought-stressed plants. A synthetic promoter composed of four copies of the ABA-responsive element (ABRE) A2 and the coupling element CE3 of the ABA-inducible barley gene HVA1 was strongly induced by ABA and C. beticola infection in transgenic sugar beet leaves. Analysis of the spatial pattern of promoter activity revealed that the ABA-inducible promoter was locally activated at the fungal infection sites. Furthermore, expression of the basic leucine zipper transcription factor AREB1 was induced by drought stress and fungal infection in the sugar beet. Application of ABA reduced the promoter activity of the phenylalanine ammonia lyase (BvPAL) gene, and this effect was observed with the -34 to +248 BvPAL promoter region. This region is equivalent to the core promoter, which is necessary for the suppression of BvPAL expression by C. beticola, as recently shown. These data indicate that ABA accumulation and activation of the ABA-dependent signalling cascade are the primary cause of suppression of BvPAL expression during infection of sugar beet leaves.