Mismatch Repair of DNA Replication Errors Contributes to Microevolution in the Pathogenic Fungus Cryptococcus neoformans

ABSTRACT The ability to adapt to a changing environment provides a selective advantage to microorganisms. In the case of many pathogens, a large change in their environment occurs when they move from a natural setting to a setting within a human host and then during the course of disease development to various locations within that host. Two clinical isolates of the human fungal pathogen Cryptococcus neoformans were identified from a collection of environmental and clinical strains that exhibited a mutator phenotype, which is a phenotype which provides the ability to change rapidly due to the accumulation of DNA mutations at high frequency. Whole-genome analysis of these strains revealed mutations in MSH2 of the mismatch repair pathway, and complementation confirmed that these mutations are responsible for the mutator phenotype. Comparison of mutation frequencies in deletion strains of eight mismatch repair pathway genes in C. neoformans showed that the loss of three of them, MSH2, MLH1, and PMS1, results in an increase in mutation rates. Increased mutation rates enable rapid microevolution to occur in these strains, generating phenotypic variations in traits associated with the ability to grow in vivo, in addition to allowing rapid generation of resistance to antifungal agents. Mutation of PMS1 reduced virulence, whereas mutation of MSH2 or MLH1 had no effect on the level of virulence. These findings thus support the hypothesis that this pathogenic fungus can take advantage of a mutator phenotype in order to cause disease but that it can do so only in specific pathways that lead to a mutator trait without a significant tradeoff in fitness. IMPORTANCE Fungi account for a large number of infections that are extremely difficult to treat; superficial fungal infections affect approximately 1.7 billion (25%) of the general population worldwide, and systemic fungal diseases result in an unacceptably high mortality rate. How fungi adapt to their hosts is not fully understood. This research investigated the role of changes to DNA sequences in adaption to the host environment and the ability to cause disease in Cryptococcus neoformans, one of the world’s most common and most deadly fungal pathogens. The study results showed that microevolutionary rates are enhanced in either clinical isolates or in gene deletion strains with msh2 mutations. This gene has similar functions in regulating the rapid emergence of antifungal drug resistance in a distant fungal relative of C. neoformans, the pathogen Candida glabrata. Thus, microevolution resulting from enhanced mutation rates may be a common contributor to fungal pathogenesis. IMPORTANCE Fungi account for a large number of infections that are extremely difficult to treat; superficial fungal infections affect approximately 1.7 billion (25%) of the general population worldwide, and systemic fungal diseases result in an unacceptably high mortality rate. How fungi adapt to their hosts is not fully understood. This research investigated the role of changes to DNA sequences in adaption to the host environment and the ability to cause disease in Cryptococcus neoformans, one of the world’s most common and most deadly fungal pathogens. The study results showed that microevolutionary rates are enhanced in either clinical isolates or in gene deletion strains with msh2 mutations. This gene has similar functions in regulating the rapid emergence of antifungal drug resistance in a distant fungal relative of C. neoformans, the pathogen Candida glabrata. Thus, microevolution resulting from enhanced mutation rates may be a common contributor to fungal pathogenesis.

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Peroxisomal and Mitochondrial β-Oxidation Pathways Influence the Virulence of the Pathogenic Fungus Cryptococcus neoformans

Eukaryotic Cell ◽

10.1128/ec.00128-12 ◽

2012 ◽

Vol 11 (8) ◽

pp. 1042-1054 ◽

Cited By ~ 34

Author(s):

Matthias Kretschmer ◽

Joyce Wang ◽

James W. Kronstad

Keyword(s):

Carbon Source ◽

Cryptococcus Neoformans ◽

Virulence Factor ◽

Fungal Pathogens ◽

Pathogenic Fungus ◽

Subsequent Work ◽

Content Type ◽

Capsule Production ◽

Human Pathogenic Fungus ◽

Host Tissues

ABSTRACTAn understanding of the connections between metabolism and elaboration of virulence factors during host colonization by the human-pathogenic fungusCryptococcus neoformansis important for developing antifungal therapies. Lipids are abundant in host tissues, and fungal pathogens in the phylum basidiomycota possess both peroxisomal and mitochondrial β-oxidation pathways to utilize this potential carbon source. In addition, lipids are important signaling molecules in both fungi and mammals. In this report, we demonstrate that defects in the peroxisomal and mitochondrial β-oxidation pathways influence the growth ofC. neoformanson fatty acids as well as the virulence of the fungus in a mouse inhalation model of cryptococcosis. Disease attenuation may be due to the cumulative influence of altered carbon source acquisition or processing, interference with secretion, changes in cell wall integrity, and an observed defect in capsule production for the peroxisomal mutant. Altered capsule elaboration in the context of a β-oxidation defect was unexpected but is particularly important because this trait is a major virulence factor forC. neoformans. Additionally, analysis of mutants in the peroxisomal pathway revealed a growth-promoting activity forC. neoformans, and subsequent work identified oleic acid and biotin as candidates for such factors. Overall, this study reveals that β-oxidation influences virulence inC. neoformansby multiple mechanisms that likely include contributions to carbon source acquisition and virulence factor elaboration.

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Identification of ENA1 as a Virulence Gene of the Human Pathogenic Fungus Cryptococcus neoformans through Signature-Tagged Insertional Mutagenesis

Eukaryotic Cell ◽

10.1128/ec.00375-08 ◽

2009 ◽

Vol 8 (3) ◽

pp. 315-326 ◽

Cited By ~ 63

Author(s):

Alexander Idnurm ◽

Felicia J. Walton ◽

Anna Floyd ◽

Jennifer L. Reedy ◽

Joseph Heitman

Keyword(s):

Cryptococcus Neoformans ◽

Fungal Pathogens ◽

Insertional Mutagenesis ◽

Pathogenic Fungus ◽

Mammalian Host ◽

New Genes ◽

Strain Collection ◽

Mutant Strains ◽

Human Pathogenic Fungus

ABSTRACT A library of more than 4,500 signature-tagged insertion mutants of the human pathogenic fungus Cryptococcus neoformans was generated, and a subset was screened in a murine inhalation model to identify genes required for virulence. New genes that regulate aspects of C. neoformans virulence were also identified by screening the entire library for in vitro phenotypes related to the ability to cause disease, including melanin production, growth at high temperature, and growth under conditions of nutrient limitation. A screen of 10% of the strain collection in mice identified an avirulent mutant strain with an insertion in the ENA1 gene, which is predicted to encode a fungus-specific sodium or potassium P-type ATPase. The results of the deletion of the gene and complementation experiments confirmed its key role in mammalian virulence. ena1 mutant strains exhibited no change in sensitivity to high salt concentrations but were sensitive to alkaline pH conditions, providing evidence that the fungus may have to survive at elevated pH during infection of the mammalian host. The mutation of the well-characterized virulence factor calcineurin (CNA1) also rendered C. neoformans strains sensitive to elevated pH. ENA1 transcripts in wild-type and cna1 mutant strains were upregulated in response to high pH, and cna1 ena1 double mutant strains exhibited increased sensitivity to elevated pH, indicating that at least two pathways in the fungus mediate survival under alkaline conditions. Signature-tagged mutagenesis is an effective strategy for the discovery of new virulence genes in fungal pathogens of animals.

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Factors enforcing the species boundary between the human pathogens Cryptococcus neoformans and Cryptococcus deneoformans

PLoS Genetics ◽

10.1371/journal.pgen.1008871 ◽

2021 ◽

Vol 17 (1) ◽

pp. e1008871

Author(s):

Shelby J. Priest ◽

Marco A. Coelho ◽

Verónica Mixão ◽

Shelly Applen Clancey ◽

Yitong Xu ◽

...

Keyword(s):

Cryptococcus Neoformans ◽

Mismatch Repair ◽

Dna Sequences ◽

Meiotic Recombination ◽

Genetic Recombination ◽

Species Boundaries ◽

Repair System ◽

Hybrid Progeny ◽

Extant Species ◽

Species Boundary

Hybridization has resulted in the origin and variation in extant species, and hybrids continue to arise despite pre- and post-zygotic barriers that limit their formation and evolutionary success. One important system that maintains species boundaries in prokaryotes and eukaryotes is the mismatch repair pathway, which blocks recombination between divergent DNA sequences. Previous studies illuminated the role of the mismatch repair component Msh2 in blocking genetic recombination between divergent DNA during meiosis. Loss of Msh2 results in increased interspecific genetic recombination in bacterial and yeast models, and increased viability of progeny derived from yeast hybrid crosses. Hybrid isolates of two pathogenic fungal Cryptococcus species, Cryptococcus neoformans and Cryptococcus deneoformans, are isolated regularly from both clinical and environmental sources. In the present study, we sought to determine if loss of Msh2 would relax the species boundary between C. neoformans and C. deneoformans. We found that crosses between these two species in which both parents lack Msh2 produced hybrid progeny with increased viability and high levels of aneuploidy. Whole-genome sequencing revealed few instances of recombination among hybrid progeny and did not identify increased levels of recombination in progeny derived from parents lacking Msh2. Several hybrid progeny produced structures associated with sexual reproduction when incubated alone on nutrient-rich medium in light, a novel phenotype in Cryptococcus. These findings represent a unique, unexpected case where rendering the mismatch repair system defective did not result in increased meiotic recombination across a species boundary. This suggests that alternative pathways or other mismatch repair components limit meiotic recombination between homeologous DNA and enforce species boundaries in the basidiomycete Cryptococcus species.

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The Monothiol Glutaredoxin Grx4 Regulates Iron Homeostasis and Virulence inCryptococcus neoformans

mBio ◽

10.1128/mbio.02377-18 ◽

2018 ◽

Vol 9 (6) ◽

Cited By ~ 14

Author(s):

Rodgoun Attarian ◽

Guanggan Hu ◽

Eddy Sánchez-León ◽

Mélissa Caza ◽

Daniel Croll ◽

...

Keyword(s):

Cryptococcus Neoformans ◽

Fungal Pathogens ◽

Iron Homeostasis ◽

Pathogenic Fungus ◽

Nutrient Sensing ◽

Iron Availability ◽

Virulence Determinants ◽

Poor Growth ◽

Content Type

ABSTRACTThe acquisition of iron and the maintenance of iron homeostasis are important aspects of virulence for the pathogenic fungusCryptococcus neoformans. In this study, we characterized the role of the monothiol glutaredoxin Grx4 in iron homeostasis and virulence inC. neoformans. Monothiol glutaredoxins are important regulators of iron homeostasis because of their conserved roles in [2Fe-2S] cluster sensing and trafficking. We initially identified Grx4 as a binding partner of Cir1, a master regulator of iron-responsive genes and virulence factor elaboration inC. neoformans. We confirmed that Grx4 binds Cir1 and demonstrated that iron repletion promotes the relocalization of Grx4 from the nucleus to the cytoplasm. We also found that agrx4mutant lacking the GRX domain displayed iron-related phenotypes similar to those of acir1Δ mutant, including poor growth upon iron deprivation. Importantly, thegrx4mutant was avirulent in mice, a phenotype consistent with observed defects in the key virulence determinants, capsule and melanin, and poor growth at 37°C. A comparative transcriptome analysis of thegrx4mutant and the WT strain under low-iron and iron-replete conditions confirmed a central role for Grx4 in iron homeostasis. Dysregulation of iron-related metabolism was consistent withgrx4mutant phenotypes related to oxidative stress, mitochondrial function, and DNA repair. Overall, the phenotypes of thegrx4mutant lacking the GRX domain and the transcriptome sequencing (RNA-Seq) analysis of the mutant support the hypothesis that Grx4 functions as an iron sensor, in part through an interaction with Cir1, to extensively regulate iron homeostasis.IMPORTANCEFungal pathogens cause life-threatening diseases in humans, particularly in immunocompromised people, and there is a tremendous need for a greater understanding of pathogenesis to support new therapies. One prominent fungal pathogen,Cryptococcus neoformans, causes meningitis in people suffering from HIV/AIDS. In the present study, we focused on characterizing mechanisms by whichC. neoformanssenses iron availability because iron is both a signal and a key nutrient for proliferation of the pathogen in vertebrate hosts. Specifically, we characterized a monothiol glutaredoxin protein, Grx4, that functions as a sensor of iron availability and interacts with regulatory factors to control the ability ofC. neoformansto cause disease. Grx4 regulates key virulence factors, and a mutant is unable to cause disease in a mouse model of cryptococcosis. Overall, our study provides new insights into nutrient sensing and the role of iron in the pathogenesis of fungal diseases.

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Sterol-Response Pathways Mediate Alkaline Survival in Diverse Fungi

mBio ◽

10.1128/mbio.00719-20 ◽

2020 ◽

Vol 11 (3) ◽

Cited By ~ 1

Author(s):

Hannah E. Brown ◽

Calla L. Telzrow ◽

Joseph W. Saelens ◽

Larissa Fernandes ◽

J. Andrew Alspaugh

Keyword(s):

Cryptococcus Neoformans ◽

Fungal Pathogens ◽

Fungal Infections ◽

Membrane Integrity ◽

Extracellular Ph ◽

Alkaline Ph ◽

Content Type ◽

Alkaline Environment ◽

Ph Response ◽

The Impact

ABSTRACT The ability for cells to maintain homeostasis in the presence of extracellular stress is essential for their survival. Stress adaptations are especially important for microbial pathogens to respond to rapidly changing conditions, such as those encountered during the transition from the environment to the infected host. Many fungal pathogens have acquired the ability to quickly adapt to changes in extracellular pH to promote their survival in the various microenvironments encountered during a host infection. For example, the fungus-specific Rim/Pal alkaline response pathway has been well characterized in many fungal pathogens, including Cryptococcus neoformans. However, alternative mechanisms for sensing and responding to host pH have yet to be extensively studied. Recent observations from a genetic screen suggest that the C. neoformans sterol homeostasis pathway is required for growth at elevated pH. This work explores interactions among mechanisms of membrane homeostasis, alkaline pH tolerance, and Rim pathway activation. We find that the sterol homeostasis pathway is necessary for growth in an alkaline environment and that an elevated pH is sufficient to induce Sre1 activation. This pH-mediated activation of the Sre1 transcription factor is linked to the biosynthesis of ergosterol but is not dependent on Rim pathway signaling, suggesting that these two pathways are responding to alkaline pH independently. Furthermore, we discover that C. neoformans is more susceptible to membrane-targeting antifungals under alkaline conditions, highlighting the impact of microenvironmental pH on the treatment of invasive fungal infections. Together, these findings further connect membrane integrity and composition with the fungal pH response and pathogenesis. IMPORTANCE The work described here further elucidates how microorganisms sense and adapt to changes in their environment to establish infections in the human host. Specifically, we uncover a novel mechanism by which an opportunistic human fungal pathogen, Cryptococcus neoformans, responds to increases in extracellular pH in order to survive and thrive within the relatively alkaline environment of the human lung. This mechanism, which is intimately linked with fungal membrane sterol homeostasis, is independent of the previously well-studied alkaline response Rim pathway. Furthermore, this ergosterol-dependent alkaline pH response is present in Candida albicans, indicating that this mechanism spans diverse fungal species. These results are also relevant for novel antimicrobial drug development as we show that currently used ergosterol-targeting antifungals are more active in alkaline environments.

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Molecular Diagnosis of Invasive Fungal Infections: Species Identification and Quantitative Analysis by Broad-Spectrum PCR Assays.

Blood ◽

10.1182/blood.v106.11.5339.5339 ◽

2005 ◽

Vol 106 (11) ◽

pp. 5339-5339

Author(s):

Lenka Baskova ◽

Sandra Preuner ◽

Thomas Lion

Keyword(s):

Quantitative Analysis ◽

Dna Sequences ◽

Fungal Pathogens ◽

Fungal Infections ◽

Pathogenic Fungi ◽

Fungal Species ◽

Invasive Fungal Infections ◽

Fungal Genome ◽

Quantitative Detection ◽

Correct Identification

Abstract Invasive fungal infections (IFI) play an increasingly important role as life-threatening complications in immunocompromised patients. Early application of antimycotic agents is an essential prerequisite for successful therapy. However, standardized diagnostic techniques permitting rapid, sensitive and, no less importantly, economic screening for the clinically relevant fungi have been lacking. We have developed two different real-time PCR systems for quantitative analysis of pathogenic fungi. The Pan-AC assay* permits in a single reaction the detection of all important Aspergillus and Candida species, which are responsible for the great majority of IFI in immunosuppressed individuals. In view of the increasing incidence of invasive infections caused by hitherto uncommon fungal species, new diagnostic tests with very broad specificity are required. We have therefore developed an additional two-reaction Pan-fungus assay*, which facilitates quantitative detection of a wide spectrum of fungal species (n>50), including also the newly emerging pathogenic fungi. The assays display high sensitivity and show no cross-reactivity with non-fungal pathogens or human DNA sequences. We have established an additional rapid molecular assay based on PCR fragment length analysis of a variable region in the fungal genome permitting rapid identification of the fungal species present, in order to facilitate selection of the most appropriate antifungal treatment. Correct identification of specific fungal pathogens including different Aspergillus, Candida and Fusarium species detected by the above assays in patients with febrile neutropenia has been confirmed by sequence analysis. The new assays are readily applicable to routine clinical diagnosis and provide a rapid and economic approach to the screening and monitoring of invasive fungal infections.

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Factors enforcing the species boundary between the human pathogens Cryptococcus neoformans and Cryptococcus deneoformans

10.1101/2020.05.21.108084 ◽

2020 ◽

Cited By ~ 1

Author(s):

Shelby J. Priest ◽

Marco A. Coelho ◽

Verónica Mixão ◽

Shelly Clancey ◽

Yitong Xu ◽

...

Keyword(s):

Cryptococcus Neoformans ◽

Mismatch Repair ◽

Dna Sequences ◽

Meiotic Recombination ◽

Genetic Recombination ◽

Species Boundaries ◽

Repair System ◽

Hybrid Progeny ◽

Dna Mismatch ◽

Species Boundary

AbstractHybridization has resulted in the origin and variation in extant species, and hybrids continue to arise despite pre- and post-zygotic barriers that limit their formation and evolutionary success. One important system that maintains species boundaries in prokaryotes and eukaryotes is the mismatch repair pathway, which blocks recombination between divergent DNA sequences. Previous studies illuminated the role of the mismatch repair component Msh2 in blocking genetic recombination between divergent DNA during meiosis. Loss of Msh2 results in increased interspecific genetic recombination in bacterial and yeast models, and increased viability of progeny derived from yeast hybrid crosses. Hybrid isolates of two pathogenic fungal Cryptococcus species, Cryptococcus neoformans and Cryptococcus deneoformans, are isolated regularly from both clinical and environmental sources. In the present study, we sought to determine if loss of Msh2 would relax the species boundary between C. neoformans and C. deneoformans. We found that crosses between these two species in which both parents lack Msh2 produced hybrid progeny with increased viability and high levels of aneuploidy. Whole-genome sequencing revealed few instances of recombination among hybrid progeny and did not identify increased levels of recombination in progeny derived from parents lacking Msh2. Several hybrid progeny produced structures associated with sexual reproduction when incubated alone on nutrient-rich medium in light, a novel phenotype in Cryptococcus. These findings represent a unique, unexpected case where rendering the mismatch repair system defective did not result in increased meiotic recombination across a species boundary. This suggests that alternative pathways or other mismatch repair components limit meiotic recombination between homeologous DNA and enforce species boundaries in the basidiomycete Cryptococcus species.Author summarySeveral mechanisms enforce species boundaries by either preventing the formation of hybrids, known as pre-zygotic barriers, or preventing the viability and fecundity of hybrids, known as post-zygotic barriers. Despite these barriers, interspecific hybrids form at an appreciable frequency, such as hybrid isolates of the human fungal pathogenic species, Cryptococcus neoformans and Cryptococcus deneoformans, which are regularly isolated from both clinical and environmental sources. C. neoformans x C. deneoformans hybrids are typically highly aneuploid, sterile, and display phenotypes intermediate to those of either parent, although self-fertile isolates and transgressive phenotypes have been observed. One important mechanism known to enforce species boundaries or lead to incipient speciation is the DNA mismatch repair system, which blocks recombination between divergent DNA sequences during meiosis. The aim of this study was to determine if genetically deleting the DNA mismatch repair component Msh2 would relax the species boundary between C. neoformans and C. deneoformans. Progeny derived from C. neoformans x C. deneoformans crosses in which both parental strains lacked Msh2 had higher viability, and unlike previous studies in Saccharomyces, these Cryptococcus hybrid progeny had higher levels of aneuploidy and no observable increase in meiotic recombination at the whole-genome level.

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Identification of MLH2/hPMS1 dominant mutations that prevent DNA mismatch repair function

Communications Biology ◽

10.1038/s42003-020-01481-4 ◽

2020 ◽

Vol 3 (1) ◽

Author(s):

Gloria X. Reyes ◽

Boyu Zhao ◽

Tobias T. Schmidt ◽

Kerstin Gries ◽

Matthias Kloor ◽

...

Keyword(s):

Mismatch Repair ◽

Frameshift Mutation ◽

Human Cancer ◽

Mutation Rates ◽

Missense Mutations ◽

Mutator Phenotype ◽

Dna Mismatch ◽

Number Of Patients ◽

Exonuclease 1 ◽

Inactivating Mutations

AbstractInactivating mutations affecting key mismatch repair (MMR) components lead to microsatellite instability (MSI) and cancer. However, a number of patients with MSI-tumors do not present alterations in classical MMR genes. Here we discovered that specific missense mutations in the MutL homolog MLH2, which is dispensable for MMR, confer a dominant mutator phenotype in S. cerevisiae. MLH2 mutations elevated frameshift mutation rates, and caused accumulation of long-lasting nuclear MMR foci. Both aspects of this phenotype were suppressed by mutations predicted to prevent the binding of Mlh2 to DNA. Genetic analysis revealed that mlh2 dominant mutations interfere with both Exonuclease 1 (Exo1)-dependent and Exo1-independent MMR. Lastly, we demonstrate that a homolog mutation in human hPMS1 results in a dominant mutator phenotype. Our data support a model in which yeast Mlh1-Mlh2 or hMLH1-hPMS1 mutant complexes act as roadblocks on DNA preventing MMR, unraveling a novel mechanism that can account for MSI in human cancer.

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Identifying Mutator Phenotypes among Fluoroquinolone-Resistant Strains of Streptococcus pneumoniae Using Fluctuation Analysis

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.00336-07 ◽

2007 ◽

Vol 51 (9) ◽

pp. 3225-3229 ◽

Cited By ~ 25

Author(s):

Carolyn V. Gould ◽

Paul D. Sniegowski ◽

Mikhail Shchepetov ◽

Joshua P. Metlay ◽

Jeffrey N. Weiser

Keyword(s):

Cell Division ◽

Streptococcus Pneumoniae ◽

Mismatch Repair ◽

Mutation Rate ◽

In Vitro Selection ◽

Clinical Isolates ◽

Mutation Rates ◽

Fluctuation Analysis ◽

Missense Mutations ◽

Resistant Strains

ABSTRACT The occurrence of mutator phenotypes among laboratory-generated and clinical levofloxacin-resistant strains of Streptococcus pneumoniae was determined using fluctuation analysis. The in vitro selection for levofloxacin-resistant mutants of strain D39, each with point mutations in both gyrA and parC or parE, was not associated with a significant change in the mutation rate. Two of eight clinical isolates resistant to levofloxacin (MIC, >8 μg/ml) had estimated mutation rates of 1.2 × 10−7 and 9.4 × 10−8 mutations per cell division, indicating potential mutator phenotypes, compared to strain D39, which had an estimated mutation rate of 1.4 × 10−8 mutations per cell division. The levofloxacin-resistant isolates with the highest mutation rates showed evidence of dysfunctional mismatch repair and contained missense mutations in mut genes at otherwise highly conserved sites. The association of hypermutability in levofloxacin-resistant S. pneumoniae clinical isolates with mutations in DNA mismatch repair genes provides further evidence that mismatch repair mutants may have a selective advantage in the setting of antibiotic pressure, facilitating the development of further antibiotic resistance.

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Control of Winged Waterprimrose (Jussiaea decurrens) and Northern Jointvetch (Aeschynomene virginica) with Fungal Pathogens

Weed Science ◽

10.1017/s0043174500044477 ◽

1979 ◽

Vol 27 (5) ◽

pp. 497-501 ◽

Cited By ~ 46

Author(s):

C. D. Boyette ◽

G. E. Templeton ◽

R. J. Smith

Keyword(s):

Oryza Sativa ◽

Glycine Max ◽

Fungal Pathogens ◽

Liquid Culture ◽

Field Experiments ◽

Colletotrichum Gloeosporioides ◽

Pathogenic Fungus ◽

Field Tests ◽

Wide Range ◽

Growing Region

An indigenous, host-specific, pathogenic fungus that parasitizes winged waterprimrose [Jussiaea decurrens(Walt.) DC.] is endemic in the rice growing region of Arkansas. The fungus was isolated and identified asColletotrichum gloeosporioides(Penz.) Sacc. f.sp. jussiaeae(CGJ). It is highly specific for parasitism of winged waterprimrose and not parasitic on creeping waterprimrose (J. repensL. var.glabrescensKtze.), rice (Oryza sativaL.), soybeans [Glycine max(L.) Merr.], cotton (Gossypium hirsutumL.), or 4 other crops and 13 other weeds. The fungus was physiologically distinct from C.gloeosporioides(Penz.) Sacc. f. sp.aeschynomene(CGA), an endemic anthracnose pathogen of northern jointvetch[Aeschynomene virginica(L.) B.S.P.], as indicated by cross inoculations of both weeds. Culture in the laboratory and inoculation of winged waterprimrose in greenhouse, growth chamber and field experiments indicated that the pathogen was stable, specific, and virulent in a wide range of environments. The pathogen yielded large quantities of spores in liquid culture. It is suitable for control of winged waterprimrose. Winged waterprimrose and northern jointvetch were controlled in greenhouse and field tests by application of spore mixtures of CGJ and CGA at concentrations of 1 to 2 million spores/ml of each fungus in 94 L/ha of water; the fungi did not damage rice or nontarget crops.

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