There are three natural openings in a mature sugarbeet fruit which serve as avenues of entry for microorganisms: 1) the basal pore which contains dried parenchyma and vascular tissue and is the point where the flower was connected to the stalk; 2) the apical pore where the style was inserted; and 3) the peripheral zone of dehiscence where the operculum separates from the fruit cavity wall during germination. The apical pore was first described in this study. Scanning electron microscopy of the naturally infected fruits showed, for the first time, hyphal penetration through both the basal pore and the peripheral zone. Examination of sugarbeet flowers artificially infected with Phoma betae also showed fungal penetration through the apical pore. Dense hyphal growth was associated with stigmal lobes and ungerminated pollen grains. Fungal growth apparently was stimulated by excretions from the stigma. Penetration of the fruit cavity wall and the operculum would render the fungus inaccessible to protectant fungicides and explains why the most successful seed treatments for P. betae have included volatile mercury fungicides or seed soak in thiram. Such treatment allows direct contact between the toxin and the pathogen. / North Dakota State University (NDSU) / Kiesling, Richard L.

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Cercospora leaf spot is an economically devastating disease of sugar beet caused by the fungus Cercospora beticola. It has been demonstrated recently that the C. beticola CTB cluster is larger than previously recognized and includes novel genes involved in cercosporin biosynthesis and a partial duplication of the CTB cluster. Several genes in the C. nicotianae CTB cluster are known to be regulated by ‘feedback’ transcriptional inhibition. Expression analysis was conducted in wild type (WT) and CTB mutant backgrounds to determine if feedback inhibition occurs in C. beticola. My research showed that the transcription factor CTB8 which regulates the CTB cluster expression in C. nicotianae also regulates gene expression in the C. beticola CTB cluster. Expression analysis has shown that feedback inhibition occurs within some of the expanded CTB cluster genes. The partial duplication of the CTB cluster was not found to be light activated or subject to feedback inhibition. / USDA Bolton Sugar Beet Pathology Lab

Field surveys were conducted in the Red River Valley (RRV) of North Dakota and Minnesota during 2016 and 2017 to determine the incidence, abundance, and distribution of plant-parasitic nematodes (PPNs) on sugarbeet. Seventy-two and 65 % of the fields surveyed were positive for PPNs in 2016 and 2017, respectively. The major genera of PPNs identified from sugarbeet production fields were Heterodera, Helicotylenchus, Tylenchorhynchus, Paratylenchus, Pratylenchus, Paratrichodorus, Hoplolaimus, and Xiphinema. Eight of PPNs were identified at the species level using species-specific PCR assays, and sequencing of the ribosomal rDNA gene. Stubby-root nematode, Paratrichodorus allius, is one of the important nematode pests for sugarbeet production worldwide. An experiment was conducted to determine the host status of sugarbeet and their rotational crops for P. allius under greenhouse conditions. The results from two experiments indicated sugarbeet and most rotational crops support the reproduction of P. allius. / Sugarbeet Research and Education Board (Minn.) / Sugarbeet Research and Education Board (N.D.) / American Crystal Sugar Company

A new disease of sugar beet, named Fusarium yellowing decline, was recently found in in the Red River Valley of MN and ND. This disease is caused by a novel pathogen named Fusarium secorum. Pathogens such as F. secorum secrete proteins during infection called ‘effectors’ that help establish disease. Since pathogenicity and disease development may depend on effector proteins produced by F. secorum during infection, effector protein identification furthers our understanding of the biology of this important pathogen. A list of 11 candidate effectors was generated previously. In this study, to characterize putative effectors, we developed a transformation system using polyethylene glycol–mediated transformation. Several mutant lines were created with an effector deleted from the genome using a split-marker knock-out strategy. To explore their role in pathogenicity, mutant strains have been inoculated to sugarbeet and compared to WT F. secorum.

Cercospora leaf spot (CLS), caused by the fungal pathogen Cercospora beticola, is the most important foliar disease of sugar beet worldwide. Control strategies for CLS rely heavily on fungicides including quinone outside inhibitor (QOI) fungicides. We collected 866 C. beticola isolates from sugar beet growing regions in France and Italy and assessed their sensitivity to the QOI fungicide pyraclostrobin. To gain an understanding of the molecular basis of QOI resistance, we cloned the full-length coding region of Cbcytb. All tested QOI-resistant isolates harbored a point mutation in Cbcytb at nucleotide position 428 that conferred an exchange from glycine to alanine at amino acid position 143 (G143A). A PCR assay was developed to discriminate QOI-sensitive and QOI-resistant isolates based on the G143A mutation. Our results indicate that QOI resistance has developed in some European C. beticola populations in Italy and monitoring the G143A mutation is an essential fungicide resistance management strategy.