Ophiostoma novo-ulmi

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1. Classification

Higher order taxa

Eukaryota; Opisthokonta; Fungi; Dikarya; Ascomycota; saccharomyceta; Pezizomycotina; leotiomyceta; sordariomyceta; Sordariomycetes; Sordariomycetidae; Ophiostomatales; Ophiostomataceae; Ophiostoma

Species

NCBI: [1]

Ophiostoma novo-ulmi subsp. americana

	Ophiostoma novo-ulmi subsp. novo-ulmi [1].

Ophiostoma Novo-Ulmi fruiting bodies that form in galleries made by the bark beetle. Photo: Joseph OBrien, USDA Forest Service, Bugwood.org http://www.invasive.org/browse/detail.cfm?imgnum=5252020.

2. Introduction

Ophiostoma novo-ulmi is classified as an ascomycete fungus that spreads its spores by projecting them from elongated sacs (asci) into the air. Morphologically it consists of white/grey hyphae and a perithecial neck (250-640 µm in width), which encloses the asci. Also O. novo-ulmi can withstand temperatures of up to 33°C and the fungi’s optimal growth temperature is around 20-22°C [2]. In the 1960s O. novo-ulmi was found to cause Dutch Elm Disease (DED), which devastated the elm tree population throughout North America [3]. The pathogenicity of O. novo-ulmi can be attributed to the Pat1 gene, as well as metabolic products like diaporthic acid and phenolic acids, which are toxic to elm tree species [4] [5] [6. Through thorough research, the mechanisms and cellular components of O. novo-ulmi’s pathogenicity seem to be very well understood, but there is more research needed on the other processes unrelated to the pathogenicity. O. novo-ulmi can be further classified into two subspecies, americana and novo-ulmi, which have the ability to hybridize. This hybridization can create enhanced toxic mechanisms and host resistance that has the ability to hinder the establishment of new elm tree populations. This ultimately limits scientists’ ability to develop preventative mechanisms for population recovery [7]. There is little known about the specific differences between the subspecies, therefore this is an area open to further research. Dutch Elm Disease is spread by adult bark beetles, which carry the O. novo-ulmi spores. The spores eventually enter the secondary xylem of elm trees, which clogs the internal vessels of the tree and eventually causes death [8] [7]. Due to the aggressiveness of DED throughout Europe and North America, establishing proper control mechanisms has been a challenging feat [9]. Different solutions have been developed to protect elms from DED. For instance, as further described in the article, chemical treatments to eradicate the disease as well as genetic manipulation in order to target the root cause of pathogenicity were created [9] [10] [11]. Treating the trees with salicylic acid and genetically modifying them to resist the toxins of the fungus have been shown to be effective measures of combating the pathogen [10] [11]. Nevertheless, future research needs to be conducted to fully halt the spread of this disease.

3. Genome structure

Genomic Overview

The ascomycete fungus, O. novo-ulmi , is composed of a genome of 2617 nucleotides and has double stranded RNA [12]. The primary strand of the dsRNA contains an open reading frame (ORF) that has the potential to encode for 718 different types of proteins and the complementary strand contains two smaller ORFs that have the potential to encode for 178-182 proteins [12]. The large ORF on the primary strand contains 12 UGA codons that code for tryptophan, which terminates the translation of proteins on cytoplasmic ribosomes in the ascomycete mitochondria [12]. Two important nucleotide sequences of the O. novo-ulmi genome include the RNA-7 segment (1057 nucleotides) and the RNA-10 segment (317-330 nucleotides) [12]]. RNA-7 may be regarded as satellite DNA due to its distinct un-relatedness to any other sequence in the genome [12]. Also RNA-7 has the ability to exist as a single stranded form or as a double stranded form, while RNA-10 exists as a mosaic of sequences acquired from RNA-7 [12]. The loss of the RNA-7 and/or RNA-10 segments in the genome have been attributed to the reversion of diseased elm trees to uninfected phenotypes, thus suggesting that one or both of these segments contribute to the pathogenicity of ‘’O. novo-ulmi’’ [12].

RNA-dependent RNA polymerases

An important feature of the O. novo-ulmi genome resides in the fact that amino acid motifs are characteristic of RNA-dependent RNA polymerases (RdRps) [12]. RNA- dependent RNA polymerases are enzymes that have the ability to catalyze the replication of RNA from an RNA template. There are many conserved amino acid motifs in the O. novo-ulmi genome, which could explain O. novo-ulmi's strong pathogenic relationship to elm tree species [12]. From an important evolutionary standpoint it has been determined that the RdRps of mitochondrial dsRNAs for ascomycete fungi and basidiomycete fungi resemble that of ‘’O. novo-ulmi’’ [12]. Through multiple sequence alignments the fungal mitochondrial dsRNA-encoded RdRp-like proteins have been found to form a cluster. This explains how O. novo-ulmi is ancestrally related to the RdRps of positive-stranded RNA bacteriophages of the Leviviridae family (Enterobacteria, caulobacter, pseudomonas, and acinetobacter serve as natural hosts for these bacteriophages) [12]. Therefore, O. novo-ulmi could have gained pathogenicity through horizontal gene transfer with members of the Leviviridae family due to the link between the acquisition of disease and genomic elements like bacteriophages. However, the RdRps of other fungal RNA viruses and related plant and animal RNA viruses have also been found to be distinct from that of O. novo-ulmi [12]. Thus, further research needs to be conducted for a solid conclusion.

Transposable Elements

Transposable elements (TEs) have been found to account for about 14% of the O. novo-ulmi genome [13]. TEs are repetitive sequences that have the ability to move from one chromosomal location to another creating genomic rearrangements and variability in gene expression. Three main types of transposable elements (OPHIO1, OPHIO2, OPHIO3) have been found in the genome of O. novo-ulmi [13]. All three transposons have different distribution patterns in the O. novo-ulmi genome, which could allow intraspecific hybrids to serve as genetic bridges for transposable elements [13]. Of the three, OPHIO3 has the ability to elicit gene silencing due to repeat-induced point mutations [13].

Pat1 Gene

The pathogenesis of O. novo-ulmi can be attributed to a genetic cross between the AST27 gene, a Eurasian (EAN) isolate with a low level of pathogenicity and a H327 gene, which has a high level of pathogenicity [5].The cross between these two genes has led to the conclusion that one specific gene, Pat1, has led to the pathogenicity of the O. novo-ulmi species. The Pat 1 gene is located on a 3.5 Mb chromosome and is controlled by two alleles, Pat1-h and Pat1-m, which confers high to moderate levels of pathogenicity [5]. In addition to the Pat1 gene it has also been discovered that minor genes are involved in the aggressiveness of pathogenicity, however their roles are still unknown [5].

4. Cell structure

Morphology

Colonies of O. novo-ulmi are usually grey to white colored when cultured in agar [2]. The colonies generally show mycelium that are separated into fibrous ropes [2]. The base of the fungus is spherical with numerous ostiolar (pore) hyphae [2]]. Hyphae are septated, meaning that they are divided into two separate strands [2]. Mycelium conidia, which are non-motile spores (ascospores) are also produced in abundance by ‘’O. novo-ulmi’’ [2]. Mycelial conidia aggregate into mucilaginous droplets, budding in a yeast-like fashion [2]. After prolonged cultivation, conidia often fuse to create a yeast-like mass, which leads to a waxy appearance of the colony [2].

Surface Proteins

O. novo-ulmi's pathogenicity is thought to be attributed to cerato-ulmin, a hydrophobic protein that resides on the cell surface of the fungus [6. Macromolecules like cerato-ulmin that are exposed to the cell surface are important for biological activities (spread disease) of the O. novo-ulmi fungus [6. Cerato-ulmin has been defined as a class II Hydrophobin, which is characterized as being small (75-167 amino acids), possessing an amino acid terminal sequence, localized hydrophobic regions, and eight conserved cysteine residues [6. The cerato-ulmin surface protein is important due to its ability to cause wilting and involvement in disease transmission [6. The secretion of cerato-ulmin into the xylem of elm tree species leads to an obstruction in the xylem tube, which elicits tree death [6.

5. Metabolic processes

Metabolic products of O. novo-ulmi include phenolic acids, 2-4-dihydroxyl-6-acetonylbenzoic acid, 6-(1-hydroxacetonyl) and 6-pyruval analogs [4]. These metabolic products have been found and produced on elm tissue mediums, however they are rapidly metabolized by the fungus once the carbon source of the elm tree is exhausted [4]. Of the metabolites, phenolic acids, which produce high molecular weight glycoproteins can cause wilting, but not leaf necrosis [4]. Low molecular weight glycoproteins produced by phenolic acids have shown no evidence of toxicity to elm tree species. Another metabolic product of O. novo-ulmi , diaporthic acid has been found to cause severe wilting like that of phenolic acids as well as leaf necrosis [4]. Another metabolic product found in some strains of O. novo-ulmi , 4-hydroxyphenylacetic acid has been found to be toxic to elm tree species as well as other plant species [4].

6. Ecology

Habitat; symbiosis; contributions to the environment.

7. Pathology

How does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.

7. Key microorganisms

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8. Current Research

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9. References

It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.