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Apple scab caused by the fungus Venturia inaequalis (Cke.) Wint. is a destructive disease of apple. The pathogen is a facultative saprophyte that grows subcuticularly on the host. V. inaequalis must obtain nutrients through an active means. The fungus grows as a stroma of thick-walled cells between the cuticle and the outer wall of the host epidermis. Initial infections can lead to production of conidia on infected tissues within 9 to 17 days. The asexual spores can cause numerous secondary infections. Several waves of secondary infection can occur during a single growing season. Complete crop loss can result and severe infection can reduce blossom bud formation and crop potential for the following year, which may promote biennial bearing. Scab management is an essential component of orchard management in climates that are conducive to infection. Fungicides that are currently available for control of apple scab can be categorized as either protectant or eradicant in nature.

A chalcone synthase (CHS)-like gene, SbCHS8, with high expressed sequence tag abundance in a pathogen-induced cDNA library, was identified previously in sorghum (Sorghum bicolor). Genomic Southern analysis revealed that SbCHS8 represents a single-copy gene. SbCHS8 expression was induced in sorghum mesocotyls following inoculation with Cochliobolus heterotrophus and Colletotrichum sublineolum, corresponding to nonhost and host defense responses, respectively. However, the induction was delayed by approximately 24 h when compared to the expression of at least one of the other SbCHS genes. In addition, SbCHS8 expression was not induced by light and did not occur in a tissue-specific manner. SbCHS8, together with SbCHS2, was overexpressed in transgenic Arabidopsis (Arabidopsis thaliana) tt4 (transparent testa) mutants defective in CHS activities. SbCHS2 rescued the ability of these mutants to accumulate flavonoids in seed coats and seedlings. In contrast, SbCHS8 failed to complement the mutation, suggesting that the encoded enzyme does not function as a CHS. To elucidate their biochemical functions, recombinant proteins were assayed with different phenylpropanoid-Coenzyme A esters. Flavanones and stilbenes were detected in the reaction products of SbCHS2 and SbCHS8, respectively. Taken together, our data demonstrated that SbCHS2 encodes a typical CHS that synthesizes naringenin chalcone, which is necessary for the formation of different flavonoid metabolites. On the other hand, SbCHS8, now retermed SbSTS1, encodes an enzyme with stilbene synthase activity, suggesting that sorghum accumulates stilbene-derived defense metabolites in addition to the well-characterized 3-deoxyanthocyanidin phytoalexins. © 2005 American Society of Plant Biologists., preprint

Although fungal adhesion to plants has been recognized for over a century, this aspect of fungal-plant interaction has not been well characterized (Nicholson and Epstein 1991). The importance of adhesion has rarely been critically tested, no fungal adhesive compound that mediates attachment to plants has been fully characterized, and few data are available that describe the molecular bases of fungal-substratum binding. The detailed description of fungal-plant attachment is further complicated by the fact that adhesion occurs at multiple stages of fungal morphogenesis; adhesion can be associated with zoospores and their cysts, conidia, germlings, appressoria, and infection cushions (Nicholson 1984). In some species of rust and anthracnose fungi, several different types of cells (i.e., spores, germlings and appressoria) attach to the host surface before penetration (Chap. 2, this Vol.; Chap. 5, Vol. V, Part B).

A sorghum cDNA clone has been isolated that encodes a protein containing six imperfect leucine-rich repeats (LRRs) of approximately 22 amino acids in length. The putative protein, designated SLRR, also contains a signal peptide, and six potential N-glycosylation sites. Comparisons of SLRR and its LRR consensus sequences found significant homology to the extracellular binding domains of receptor-protein kinases RLK5 and TMK1 of Arabidopsis, and some plant disease resistance genes. Results from RNA gel blot analyses showed that SLRR mRNA accumulates rapidly in mesocotyls and juvenile leaves by 6 h postinoculation with the fungus Colletotricum graminicola. Further experiments suggest that the gene encoding SLRR is neither systemically induced by fungal inoculation, nor transcriptionally activated in a host-fungal-pathogen-specific manner. The presence of LRRs strongly suggests that the SLRR protein is involved in protein-ligand binding and therefore may be a component of a signal transduction pathway.

The fungus Cochliobolus carbonum causes leaf spot disease of maize. Highly virulent isolates of the pathogen produce a host-selective, peptide toxin that is active against susceptible genotypes of maize. Prior to infection, spores must germinate and differentiate appressoria, structures specialized for leaf penetration. Analysis of spore germination fluids by plasma desorption mass spectrometry, which allowed detection of as little as 0.5 ng toxin, revealed that spores induced to form appressoria in vitro synthesized and released the toxin at a time coincident with maturation of appressoria. Spores incubated under conditions that did not induce appressorium formation failed to produce toxin. These observations indicate that synthesis of the host-selective toxin, which is essential for successful pathogenesis of maize by C. carbonum, is regulated by infection-related morphogenesis.

Adhesion is a well established phenomenon that occurs during the normal growth of organisms within their environments. This review will present recent literature which is pertinent to our understanding how adhesion occurs across a broad spectrum of organisms, to our current knowledge of the chemistry of adhesives, and in particular to the significance of adhesion to the fungal infection process. The pathogens Colletotrichum graminicola and Erysiphe graminis will provide examples of adhesion and its relevance to the infection process as they represent both necrotrophic and biotrophic pathogens with very different requirements for their survival and success as pathogens.

Made available in DSpace on 2022-04-28T18:55:37Z (GMT). No. of bitstreams: 0 Previous issue date: 1993-01-01 Colletotrichum graminicola is the causal agent of anthracnose on a variety of graminaceous monocotyledonous plants, including corn and sorghum. When conidia of C. graminicola are produced in acervuli on infected plant tissues or in culture, they are surrounded by a mucilage. The mucilage, which is composed of high molecular weight glycoproteins, various enzymes, and a self-inhibitor of conidium germination, functions to protect condidia from untimely germination, from desiccation, and from toxic phenolic metabolites produced by the host plant in response to infection. The present investigation demonstrates that the mucilage contains four cutinases whose molecular weights are similar to those of other fungal cutinases. Like other cutinases these enzymes are of the serine-esterase class of hydrolases as shown by inhibition of enzyme activity with diisopropyl fluorophosphate (DIPF). In the presence of high concentrations of DIPF, conidia produced apparently normal, mature appressoria yet were unable to cause disease of corn leaves. The function of the mucilage cutinases is discussed with regard to their importance to the infection process. © 1993 Academic Press, Inc. Department of Botany and Plant Pathology Purdue University, West Lafayette, IN 47907-1155 Department of Plant Pathology ESALQ/Sao Paulo State University, Piracicaba, SP Fäkultat fürBiologie Phytopatologie Universitat Konstanz, Universitatsstrasse 10, YV 7750 Konstanz Department of Plant Pathology ESALQ/Sao Paulo State University, Piracicaba, SP

Historically, mechanisms of fungal infection have attracted plant pathologists, and our understanding of infection processes has been increased significantly for many disease interactions. Fungi generally undergo a series of distinct morphological changes before attempting host penetration. To date, most studies on infection processes deal with penetration and post-penetration stages of fungal development. However, several observations suggest that phenomena associated with initial stages of fungal contact on host surfaces play a critical role in host recognition, fungal differentiation, and success of infection [1, 13, 20, 26, 37, 38, 44, 64, 65, 73–76]. Since infection processes may be initiated soon after contact, prepenetration phenomena necessary for infection can easily be overlooked. One of these early prepenetration events is adhesion. The mechanisms of fungal adhesion are not as well understood as are those for bacterial adhesion [76]. Nicholson and Epstein [51] reviewed adhesion by plant pathogenic fungi and discussed mechanisms known to be involved in adhesion, as well as the broader topic of extracellular fungal matrices. The purpose of this review is to address cytological aspects of extracellular materials associated with fungal adhesion, and the subject of recognition between fungal and host cells.

The initial process of attachment of fungal propagules to a host plant is essential to the successful establishment of pathogenesis. Attachment may be involved in recognition of the host surface, serve as a base around which the infection court can be altered, and may include adhesion of the propagule. It was considered initially that attachment was purely a chance event resulting from physical entrapment of the propagule or germling. We know now that attachment involves an active process of secretion of adhesive materials by the fungus that in some cases are highly specific for the recognition of, and binding to, a particular host species. Adhesive production may occur at a specific stage of conidium or germling development, but may best be considered a general phenomenon for the establishment of the fungus prior to penetration.

Sorghum produces phytoalexins that are 3-deoxyanthocyanidin flavonoids. The compounds inhibit the growth of phytopathogenic fungi in vitro. The phytoalexins appear to be synthesized in subcellular inclusions within a host epidermal cell that is about to be penetrated by a fungus. This site-restricted synthesis suggests that the phytoalexin response occurs initially in the first cells that come under fungal attack and is not simply a response of cells that surround the original infection site.

Professor Emeritus Richard M. Lister died 10 September 1998 in Yeovil, England, after a brief illness. Richard was born on 14 November 1928 in Sheffield, England, and was educated there. He graduated with honors from the University of Sheffield and obtained a diploma in agricultural science from Cambridge University. He received training in tropical plant agriculture at the Imperial College of Tropical Agriculture in Trinidad, British West Indies. Following this, Richard worked on the cocoa swollen shoot disease in West Africa for 4 years as a plant pathologist with the West African Cocoa Research Institute. He then did research at the Scottish Horticultural Research Institute. In 1964, Richard earned a Ph.D. degree from the University of St. Andrews, St. Andrews, Fife, Scotland. In this work, Dr. Lister investigated the transmission of a group of polyhedral viruses through seed and by nematodes in strawberry. During 1964, Dr. Lister spent a sabbatical year in the Department of Botany and Plant Pathology at Purdue University in West Lafayette, IN. In 1966, he accepted an appointment to the faculty in that department, where he continued to work until his retirement in 1994. Dr. Lister began his work at Purdue on viruses that infected apple. He succeeded in isolating and characterizing major groups of filamentous viruses in apple and other tree fruits. Dr. Lister was one of the early adopters of rapid serological methods for the detection of viruses in apples, which replaced the much slower and more tedious indexing techniques that were in common use. He also showed that tobacco streak virus consisted of particles of different sizes and showed how this information could be used to provide an important understanding of virus structure. In the early 1960s, it was recognized that tobacco rattle virus produced both long and short particles in infected plants, but the significance of this phenomenon was not understood. Dr. Lister showed that if plants were inoculated with only the long particles, the RNA of the long particles was replicated but no coat protein was produced. Inoculations with only the short particles were never successful, but he showed that the presence of the short particles was necessary for the production of coat protein for particles of both sizes. In 1966, Dr. Lister hypothesized that the RNA of the short particles contained the information required for synthesis of coat protein but lacked the information required for infection. He validated this hypothesis in a series of experiments and laid the groundwork for recognition of the multicomponent phenomenon in plant viruses. This concept, now basic to considerations of divided genome viruses, is considered a major contribution to the field. During the latter part of his career at Purdue, Dr. Lister was a leader in the application of enzyme-linked immunosorbent assay (ELISA) for the detection of plant viruses. He worked extensively on barley yellow dwarf virus and used ELISA to study the epidemiology of this important disease of small grain cereals and to characterize genetic resistance in these crops. Dr. Lister taught plant virology at the graduate level for many years and attracted students from several disciplines. Initially, his teaching was part of a series of “methods” courses and consisted primarily of laboratory exercises as the basis of learning. As the science of plant virology blossomed during the past 30 years, this course was greatly expanded to include both lectures and laboratory experience. Dr. Lister was an effective teacher with a gift for providing clear and concise explanations of plant viruses and the diseases they cause. Dr. Lister served as the major professor for more than 35 graduate students, from both the United States and other countries. In addition, during his career, he served as the mentor of numerous young researchers at the postdoctoral level of training. Dr. Lister was the author of more than 100 research papers as well as numerous reviews and book chapters that covered a variety of subjects in the field of plant virology. Dr. Lister was a member of The American Phytopathological Society, and in 1973, was named a Fellow of the Society. In 1986, he received the Society’s prestigious Ruth Allen Award for outstanding contributions to the science of plant pathology. Among many other positions, Dr. Lister also was a member of the editorial committee for the Annual Review of Phytopathology (1975– 1979), a council member for the Association of Applied Biology (1962–1964), a member and chairman of The American Phytopathological Society Plant Virus Committee (1971–1975), chairman for the Luteovirus Working Group (1988), associate editor for the Journal of General Virology and Virology (1979–1983), and senior editor for Phytopathology (1976–1977). Richard was an avid gardener. A few years before his retirement from Purdue, he and his wife bought a home with a large, wooded yard west of the Purdue campus. He spent many hours creating a delightful garden, and he enjoyed discussing gardening with colleagues and friends. Richard was especially fond of daylilies and made numerous crosses and selections of these popular perennials. Richard and his wife traveled a great deal after his retirement. Their trips included visits to children and grandchildren and “overwintering” in the Tucson, AZ, area during the past few winters. During the summer of 1998, the Listers arranged an extended vacation in England. It was during this visit that Richard was unexpectedly stricken with an aneurysm, which proved fatal. Surviving are his wife, Jean; son, John Lister of Chicago; daughters, Rosalind Lister of Ellensburg, WA, Susan Madhavan of Morgantown, WV, and Christina Sanford of Reston, VA; brothers, Wilfred Lister and Brian Lister; and four grandsons.

Infection of the juvenile sorghum leaf by Colletotrichum graminicola (a pathogen) and Helminthosporium maydis (a non-pathogen) resulted in the rapid accumulation of a phytoalexin pigment complex previously identified from the sorghum mesocotyl. The principal pigments have been identified as the 3-deoxyanthocyanidins, apigeninidin and luteolinidin, but the complex includes several as yet unidentified pigment components. After the onset of penetration, components of the complex rapidly accumulated to nanogram levels within a highly restricted area at the infection site. Because of the speed of synthesis, occurrence in response to attempted infection, and previously reported fungitoxicity of the components, we propose that synthesis of the pigment complex constitutes a defense response in the juvenile sorghum leaf. The results show that the preformed cyanogenic glycoside, dhurrin, is not the only source of resistance of sorghum seedlings to fungal infection.

Cultural studies were undertaken on three isolates of Coletotrichum graminicola obtained from anthracnose infected sorghum ( Sorghum vulgare ), shattercane ( Sorghum bicolor ) and corn ( Zea mays ). Radial growth and sporulation of these isolates were compared on 7 culture media. The effect of culture age on germination of the spores was also determined. Oatmeal agar was found to be a good medium for vegetative growth and sporulation. Better sporulation was obtained on media containing sucrose as a carbon source.

Phenolic compounds inhibitory to the germination of spores of Colletotrichum graminicola were shown to leach from necrotic lesions on corn leaves caused by the fungus. Primary components of the phenolic mixture were identified as esters and glycosides of p -coumaric and ferulic acids as well as the free compounds themselves. Spores of C. graminicola produced in acervuli on infected leaves were shown to be surrounded by a mucilaginous matrix as is the case when the fungus is cultured in vitro . It is suggested that the mucilage protects spores from the inhibitory effects of the phenols by the presence of proline-rich proteins that have been shown to have a high binding affinity for a variety of phenols.

Phenylalanine ammonia-lyase (E.C. 4.3.1.5) (PAL) and hydroxycinnamate:CoA ligase (E.C. 6.2.1.12) activities were measured in extracts from maize mesocotyls resistant and susceptible to Helminthosporium maydis and resistant to H. carbonum . CoA ligase activity increased in response to infection with H. maydis in both the resistant and susceptible cultivars. Activity began to increase between 6 and 9 h after inoculation and in the resistant cultivar continued to increase throughout a 48-h period. In susceptible cultivars activity ceased to increase at approximately 12 h after inoculation. The results demonstrate that the increase in CoA ligase activity is detectable as early as the onset of penetration by the fungus. No significant change in PAL activity was observed in either resistant or susceptible combinations with H. maydis , suggesting that PAL and CoA ligase are not coordinately regulated in interactions involving this fungus. Neither enzyme was found to change as a result of inoculation of any cultivar with H. carbonum .

The effect of a toxin extract of Helminthosporium maydis, race T on K(+) ((86)Rb) uptake by excised root segments of normal (N) and Texas cytoplasmic male-sterile (T) versions of corn inbred W64A was investigated. The uptake of K(+) was inhibited in both N and T roots by the toxin. This was true for both basal (freshly excised) and augmented (pretreated with aeration) K(+) uptake. Augmented uptake was more toxin-sensitive than basal uptake (irrespective of cytoplasm type), and the augmented uptake in T roots was seven to eight times more toxin-sensitive than in N roots.Specific zones of roots differed in their basal and augmented K(+) uptake rates as well as their toxin sensitivities. The root apex of T was more sensitive to toxin than the apex of N roots when basal K(+) uptake was measured. In mature zones of the root, T was more sensitive than N when augmented rates were measured. During the development of the augmented K(+) uptake capacity in either N or T roots, the sensitivity to the toxin did not change; uptake in N roots was inhibited by 10 to 25% and uptake in T roots was inhibited by 70 to 80%.The difference in toxin sensitivity of K(+) uptake between N and T roots may be due to N possessing a protective mechanism which is deficient in T.

As the seedling primary root of maize inbred W64A elongates, basal and augmented K+(86Rb) uptake rates increase in regions increasingly distant from the apex and in regions at a fixed distance from the advancing apex. The pH-dependent process of augmentation requires aeration, begins without a lag period at pH 6, and is linear for 90 to 120 min. The augmentation potential of W64A(N) midzone root segments is minimal at 0.5 mM external K+ concentration and increases toward higher and lower external K+ concentrations. Augmentation is prevented at pH 4 in the Texas cytoplasmic male-sterile (T) version of inbred W64A but not in the male-fertile (N) version.Protein synthesis is required for development of K+(86Rb) uptake augmentation and probably also for maintenance of the augmented rate after development but apparently not for its expression. Inhibition of the maintenance of the augmented rate by low concentrations of chloramphenicol or cycloheximide does not prevent subsequent augmentation in their absence.Augmentation of amino acid uptake is not inhibited by 100 μg/ml chloramphenicol or 10 μg/ml cycloheximide, but augmentation of amino acid incorporation is inhibited by each. Augmentation of amino acid influx is sensitive to the toxin of Helminthosporium maydis, race T, in T roots but not in N roots, whereas augmentation of amino acid incorporation is only slightly more toxin-sensitive in T than in N root segments.

Changes in the activity of chalcone synthase relative to the time of accumulation of 3-deoxyanthocyanidin phytoalexins in etiolated sorghum mesocotyls inoculated with Colletotrichum graminicola were investigated. The deoxyanthocyanidin, apigeninidin, began to accumulate in tissue between 3 and 6 h after the initial increase in the level of the enzyme. The level of chalcone synthase in uninoculated tissue was not affected by exposure of the tissue to light, indicating that the increase in enzyme activity was the direct result of fungal infection. The results are discussed with reference to apparent differences between sorghum, a monocotyledon, and various dicotyledonous species where chalcone synthase is an integral factor in expression of resistance to fungal infection.

We devised a procedure to propagate selectively the vegetative and asexual-reproductive states of Helminthosporium carbonum so that we could characterize morphological and subcellular events associated with the onset of conidiation. Solidified agar media were uniformly inoculated with an overlay of conidia suspended in molten agar. After the overlay solidified, it was covered with a sheet of Miracloth. When incubated in the dark, cultures produced abundant aerial hyphae that grew through the Miracloth layer and conidiation was suppressed for 48 to 50 h. Hyphae were easily harvested from the surface of the Miracloth with a spatula. When cultures were placed in the light after 38 h of growth in the dark, differentiation was detected in 90% of the hyphal tips within 8 to 10 h. The initial response of the hyphal tips, comprising early stages in conidiophore development, was rapid and highly synchronized. The behavior of nuclei during conidiogenous cell development and the initiation of conidia was similar to that reported for other fungi that form blastic conidia. One-dimensional gel electrophoresis of in vitro translation products confirmed differences in poly(A) RNA populations from dark-grown and light-induced cultures.

The release of esterase enzyme activity by conidia of Erysiphe graminis is described as a tropic response to the stimulus of contact with leaf or cellophane surfaces. The release of esterase was completed within 30 minutes of the contact stimulus, and activity was released in two stages. The first began within 2 minutes of conidium contact and the second began between 10 and 15 minutes after contact. A portion of the esterase activity was solubilized in aqueous buffer and a portion remained bound to the conidial wall. Preparations of soluble proteins containing esterase activity were separated by sodium dodecyl sulfate-polyacrylamide and native gel electrophoresis which revealed the presence of several proteins and three zones that possessed esterase activity. The release of enzyme activity was correlated with changes in surface morphology described to occur within the first 30 minutes of initiation by the contact stimulus. The results are discussed in the context of cuticular degradation and preparation of the infection court by the fungus prior to the time of conidium germination.

A comparison was made of patterns of 4-hydroxycinnamic acid: CoA ligase (CoA ligase, E.C.6.2.1.12) activities in near isogenic maize cultivars with differential resistance (B73Ht rkm) and susceptibility (B73Ht) to Helminthosporium maydis. CoA ligase activity was assayed with p-coumaric, caffeic and ferulic acids as substrates in fractions collected after molecular sieve column chromatography of protein extracts from maize mesocotyls. All CoA ligase activity eluted between a molecular size range of 42–77 kilodaltons. The CoA ligase elution profiles distinguished multiple peaks of activity and were different in uninoculated susceptible and resistant cultivars. Inoculation with H. maydis changed the elution profiles of the enzyme activities from the respective cultivars. The multiple peaks of enzyme activity in the elution profiles and their shift in response to infection indicate CoA ligase isoenzyme responses in these host-parasite interactions.

The timing of papilla formation in the epidermis of the maize mesocotyl was followed after inoculation with Helminthosporium maydis and Colletotrichum graminicola . Histochemical tests showed the presence of phenols and lignin in papillae and the surrounding cell wall material. Peroxidase (E.C.1.11.1.7) enzyme activity was detected histochemically in the granules which appear prior to papilla formation and in the papillae themselves. Soluble and ionically bound peroxidases were extracted from epidermal tissue during the time of papilla formation. The pattern of soluble anionic isozymes in epidermis which had been undergoing papilla formation was different from the pattern of isozymes from uninoculated epidermis or inoculated epidermis which had not yet started to form papillae. Eight isozymes were present in the soluble peroxidase fraction of uninoculated tissue and tissue inoculated but not yet forming papillae. Two new isozymes were detected in tissue in which papillae had been formed but in which fungal penetration had not yet occurred. The identical isozyme pattern was found in two maize cultivars during papilla formation in response to two different pathogenic fungi, suggesting that the occurrence of isozymes was part of a non-specific host response to attempted fungal penetration.

With age, callus tissue of sorghum forms relatively large amounts ofphenolic materials. Among those present are polyphenols which strongly bind and precipitate proteins and which strongly bind and precipitate proteins and which respond to tests for condensed tannins (proanthocyanidins).

Infection of the sorghum mesocotyl by Helminthosporium maydis (a nonpathogen) and Colletotrichum graminicola (a pathogen) resulted in the rapid accumulation of a pigment complex by two sorghum cultivars. The components of the complex were fungitoxic. The principal compounds have been identified as the 3-deoxyanthocyanidins apigeninidin and luteolinidin. Apigeninidin accumulated in both sorghum cultivars in response to infection and was the predominant pigment. Luteolinidin accumulated in only one of the cultivars. Because of the speed of synthesis, occurrence only in response to inoculation, and fungitoxicity of the individual components, we propose that synthesis of the pigment complex constitutes a defense response and that the compounds apigeninidin and luteolinidin should be considered as phytoalexins.

Basal K + uptake in the root midzone region (cm 2 + 3 + 4) of N and T cytoplasmic versions of each of four maize inbreds was equally sensitive to the toxin(s) of Helminthosporium maydis , race T. Basal K + uptake in the root apex (0-1 cm) and augmented K + uptake in the root midzone were more toxin-sensitive in inbreds W64A(T) and Mo17(T) than in inbreds W64A(N) and Mo17(N). This differential response of N and T cytoplasms to toxins was not found for corresponding cytoplasms of inbreds WF9 and B37. Development of the augmented K + uptake rate in midzone segments of W64A(T) was blocked by a toxin concentration which did not affect augmentation development in W64A(N). Augmentation development was more toxin-sensitive in T than in N cytoplasmic versions of all inbreds tested. Fertility-restoring nuclear loci decreased but did not eliminate the toxin sensitivity of augmentation developments as observed in root midzones of inbred A619(T). Chloramphenicol-and/or cycloheximide-sensitive protein synthesis was required for augmentation development, but not for expression of either basal or augmented K + uptake.

We have investigated the basis of adhesion of uredospores of the obligately parasitic rust fungus Uromyces viciae-fabae to leaves of its broad bean host. Upon contact with an aqueous environment, spores form a structure that we have termed an adhesion pad. The adhesion pad is formed by both living and autoclaved spores, but only adhesion pads formed by living spores adhered to the cuticle of leaves of the host plant. Treatment of living spores with the serine-esterase inhibitor diisopropyl fluorophosphate prevented the adhesion of the pad to the leaf surface, suggesting a functional role for esterase or cutinase in the process of adhesion. A cutinase and two nonspecific serine-esterases were found to be localized on the surface of spores. These enzymes were released rapidly from the spore surface upon contact with an aqueous environment. The addition of the cutinase and the nonspecific esterases to autoclaved spores restored their ability to adhere to the host cuticle. Thus, whereas pad formation appears to be a passive response to the aqueous environment, the actual adhesion of pads to the host cuticle appears to depend on the cutinase and esterases associated with the spore surface. These results suggest a new role for cutinases and serine-esterases in the fungal infection process.