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| Passalora fulva | |
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| Species: | P. fulva
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| Binomial name | |
| Passalora fulva (Cooke) U. Braun & Crous (2003)
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Passalora fulva is a fungal plant pathogen that causes tomato leaf mold.
Morphology and taxonomy
[edit]Colonies of P. fulva on potato dextrose agar are greenish to black colonies and slow growing with a black reverse.[1] Microscopically, the fungus grows by means of brownish, smooth-walled, branched, septate hyphae.[1] P. fulva reproduces asexually by pale yellow to olive-brown, elliptic-oblong, cylindrical conidia 11–48 x 4–11 μm in size.[1][2][3] Conidia are 1–2 (or rarely 3-) celled and borne in long, branched chains arising on conidiophores that are sparingly branched, narrow at the base but widening toward the apex.[1][4] The conidia of this species, like other species of Passalora, possess pronounced scars at the conidial attachment points, differentiating them from members of the closely related, morphologically similar genus, Cladosporium.[1] This species is a member of the ascomycete family, Mycosphaerellaceae.[1]
Physiology
[edit]Growth
[edit]The fungus thrives at >85% relative humidity, and require a temperature range between 4-34°C.[5]. However, it optimally grows at 22-24°C, which almost exclusively restricts its habitat to greenhouse plantations in the temperate regions.[6] In areas with tropical climate, the fungus is more prevalent in cool or rain season, especially since optimal sporulation takes place at 78-92% relative humidity.[5]
As a facultative biotroph[1] P. fulva could either grow in planta within a living host, or in vitro in a lab. Between seasons of tomato plant growth, the fungus can remain dormant in the form of conidia, sclerotia, or soil saprophyte for up to a year due to its ability to resist drying.[5] When the environment becomes favourable again, the conidia act as primary inocula that could either directly affect new foliage or contaminate seeds. [7] To boost dispersal, new conidia could grow from sclerotia too.[5] Conidia formation takes place on the underside of the leaves, where spore formation also takes place.[4]
Primarily, P. fulva uses sucrose in host plant as its source of carbon, but it has been suggested that they can use GABA, a non-protein amino acid produced by plant, as another source of carbon and nitrogen.[1] While nitrogen acts as both the activation and deactivation trigger for certain P. fulva genes, other compounds important for growth are alcohol dehydrogenase, alcohol oxidase, and acetaldehyde dehydrogenase in order to convert ethanol and/or methanol to hydrogen peroxide, acetaldehyde, and formaldehyde, respectively.[1]
Pathogenicity
[edit]Passalora fulva was first classified as Cladosporium fulvum by Mordecai Cubitt Cooke in 1883.[8] It is a species in the family, Mycosphaerellaceae that is a well-known agent of plant disease, penetrating plant aerial parts through natural openings such as stomata.[1] Once inside, the fungus exhibits extracellular growth between mesophyll cells instead of intercellular invasion through haustoria and lack of physical symptoms until the infection has run its course and regeneration takes place.[1]P.fulva prefers to infect healthy host. It begins infecting the host plant from the oldest leaves that are found closest to the soil, then it slowly makes its way up to the younger foliage. The primary target is the foliage, but there have been cases where the blossoms are infected and die off before it begins to fruit. Rarely will the fungus affect the fruits, but when it does it is impartial to the ripeness and turns it leathery black starting at the stem to about one half of the fruit.[1]
It was thought to have originated as a plant pathogen from Lycopersicon species in Latin America, and its long-term interaction with the only host Lycopersicon esculentum suggests a co-evolutionary association.[1] This species is a well established model for studying gene-for-gene relationship pathogen-pathogen interactions.[8] Conidia lands on the upper leaf surface, and germinates into an elongated hypha that grows across the upper leaf surface. These hyphae are thinner at the tip, and if exposed to chitinases or 1,3-β-glucanase, the hydrolase in fungal cell would initiate chitin hydrolysis that cause water pressure difference, causing tip to burst and destroy host cell.[9] After about three days, the main germ tube enters the leaf tissue through a stoma on the underside of the leaf. Successful entry allows for doubling in hyphal diameter and for the hyphal tip to grow extracellularly to spaces in between mesophyll cells. Fungal growth is directed toward plant vasculatures, following a sucrose gradient for access to this carbon source.[1] Sucrose gets converted to glucose and fructose for the fungus to use and further into polyols mannitol, glycerol, and sorbitol that the host plant cannot metabolize.[10] Then, around 9 to 10 days later stromatic bodies made up of clumps of hyphae are produced at the substomatal spaces. This is followed by the formation of aerial mycelium, through which conidiophores can protrude out of the stomata for the external release of conidial chains.[1]
It is interesting to note that although it can grow in vitro, avr and ecp genes are only highly expressed when fungus is inoculated in planta. The genes code for small proteins that contain 4, 6, or 8 cysteines connected by disulfide bridges, which allow it to be stable and functioning even in harsh, protease-rich environment of host apoplast.[1] All races of P. fulva has protein mr3186 that induces necrosis in the cells of infected leaves,[11] but there are race specific variances in modes of attack as well as matching host hypersensitivity responses too. For instance, the avr9 genes code for elicitor that contains a 28 amino acid peptide that irritate host, though in cf9 tomatoes this expression leads to electrolyte leakage and increased lipid degradation.[8] With their corresponding P. fulva strains, cf4 and cf5 plants can cause extracellular superoxide production to induce oxidation that will destroy the foreign bodies.[8] Some tomato plants are known to produce tomatine, a substance toxic to P. fulva, but the degree of its toxicity depends on the pH and nutrient condition of the soil on which the plant grows.[6]
Twelve races of this species are known, each characterized by the host plant that they infect.[7] Host preference is dependent on the types of avirulence (avr) genes that have complementary counterpart known as resistance genes in the host plant.[7] The races of P. fulva are coded as follows: race 0, 2, 2.4, 2.4.11, 2.5.9, 2.9, 4, 4.5.9, 4.9, 4.9.11, 4.11, and 9[3] and their avr gene would be called avr# (where # denotes their race number). Likewise, the corresponding resistance gene in the host plant would be called cf#.[8] It is speculated that the avr genes code for varying concentrations of pathogenic compounds, but regarding host response there is debate around whether matching cf genes activation allow for different responses or only varying intensities of the same mechanism.[8]
Host Response
[edit]In interactions where host plant does not have resistance gene, there is mild to nonexistent defense reaction. Occasionally there would be callose deposition on mesophyll cell walls to strengthen it, or the endoplasmic reticulum would move near to the plasma membrane at site of infection. In older lesions, mesophyll cell organelles (especially mitochondria and chloroplast) are degenerated. Often cytoplasmic contents are released due to damage in plasma membrane as well.[1]
If the interaction is incompatible, the fungal hypha would come back out through stomata not long after its entrance or remain inside but show no symptoms of infection in the days that follow inoculation, which suggests that there is an immune reaction activated to repulse or destroy fungal advancements. Processes of immunity includes thickening of mesophyll wall through callose deposition, secretion of hydrolytic enzymes 1,3-β-glucanase and chitinase, and phytoalexins and phytogenesis-related (PR) proteins release as well.[1] However, PR proteins are also transcribed in plants with no resistance, only much later than in those capable of hypersensitive response. Therefore, while the production of the proteins itself is unlikely the key in immunity, its timing might play a more predominant role. Another take on hypersensitivity could be to have cells surrounding site of infection undergo apoptosis, thus engulfing fungal matter in cytoplasmic content and prevent further nutrient extraction by hyphae.[1]
Ecology
[edit]The widespread distribution of tomato plants allow for equally global spread of the fungus, especially in greenhouse tomato plantations both soil grown and hydroponic. Conidia dispersal is aided by wind, water vapour, some insects, and humans, through contaminated tools and clothes of workers in the plantation.[5] P. fulva has its own parasites, such as Acsemonium strictum, Dicyma pulvinata, Trichoderma harzianum, and Trichothecum roseum. These hyperparasitic fungi coil their hyphae around that of P. fulva to inhibit its growth. [6]
Research has looked at interactions between P. fulva and non-host plants, and though penetration into stomata still takes place, the hyphae were not able to grow beyond the substomatal cavity. In some Solanum sp. hyphae can grow on young foliage tissues but not in mature tissues (actually led to necrosis instead). [1]
Symptoms
[edit]Symptoms of infection appear roughly one week after inoculation, beginning with small but expanding white to pale green to yellowish spots with indefinite margins on the upper leaf surface.[1] On the underside of the same spots will appear white to olive green patches that turn brown and velvety when sporulation happens, as the spores are fuzzy to the eye.[1] Conidiophore eruption clog the stomata, preventing leaf respiration and therefore lead to tissue damage. In many cases the leaves will wilt and fall prematurely, but in severe cases the whole plant will die.[1]
Human Impact
[edit]Typical infection reduces commercial tomato yield by 10-25%, but on a typically disastrous season it could destroy over 50% of the crop.[12] Worst reported cases of P. fulva outbreak often occurred in poorly ventilated plastic greenhouses.[7] However, severe damages have been reduced since the cf-9 resistance gene loci were introduced to commercial tomato plants in the 1970s.[1] P. fulva could be found in 28% of glasshouse tomato crops in the United Kingdom, but only 3% are severely affected.[6] In developing countries there have been efforts to expand the tomato varieties to combat the disease, as well as imposing more stringent control to prevent the spread if an infection is detected.[6]
Control
[edit]Due to its detrimental impact on tomato crops, much research has been done to control the disease. Most preventative measures are relatively simple, such as reducing indoor temperature to 16-18°C and keeping the humidity level below 85%. Reducing humidity could easily be achieved through having adequate ventilation and light, watering the plants at the soil level to prevent wetting of leaves and to water them in the morning to allow plenty of time for them to dry with daylight.[5] Keeping the plants spaced far enough from each other to avoid shading and to encourage evaporation and aeration, as well as slowing down potential spread of disease is also important.
Along the same lines, there are methods to reduce opportunity for conidial inoculation through sanitation means. Greenhouses can be sanitized though treating sections between crops with steam and then keeping greenhouse airtight at 57°C for at least 6 hours. Seeds could also be heat treated with hot water of 50°C for at least 25 minutes to kill conidial contaminants.[5] Moreover, destroying all plant material and debris after harvest before preparing the soil for the next crop generation could give the plants a fresh slate. To avoid exposing soil to potential airborne conidia, sterilized soil could be covered with plastic before planting seedlings through the holes.[6] Changing up the greenhouse building material from the conventional CA-polyethylene film to IRA-vinyl film, which absorb infrared emission released by soil and plants at night, have been shown to control the disease too.[6]
Chemical means of control such as fungicides that has chitin binding domains to cause hyphal tip to erupt prematurely can be used,[9] although there is greater push towards utilizing biologic control through deploying resistant host varieties or hyperparasites instead. Dicyma pulvinata was used as a biocontrol agent in a greenhouse experiment in 1987 and 80% of P. fulva lesions on foliage had D. pulvinata colonies too.[6] Unfortunately, D. pulvinata is not as good as dispersing as P. fulva. Other fungi that could potentially be used to control P. fulva are: Sporoticum vile, Penicillium pinophilum, and Penicillium stipitatum. The bacteria Bacillus subtilis from Rizoctonia solani also seem to have antifungal effects that could potentially be used.[6]
References
[edit]- ^ a b c d e f g h i j k l m n o p q r s t u v w x Thomma, B.P.H.J.; Van Esse, P.; Crous, P.W.; De Wit, P.J.G.M. (2005). "Cladosporium fulvum (syn. Passalora fulva), a highly specialized plant pathogen as a model for functional studies on plant pathogenic Mycosphaerellaceae". Molecular Plant Pathology. 6 (4): 379-393.
- ^ Stevens, Ph.D, F.L (1913). The fungi which cause plant disease. New York: The McMillan Company.
- ^ a b Kubota, M.; Morishima, M.; Iida, Y. (2015). "First occurrence of tomato leaf mold caused by the novel races 2.5.9 and 4.5.9 of Passalora fulva in Japan". Journal of General Plant Pathology. 81: 320-323.
- ^ a b Enya, J.; et al. (2009). "The first occurrence of leaf mold of tomato caused by races 4.9 and 4.9.11 of Passalora fulva (syn. Fulvia fulva) in Japan". Journal of General Plant Pathology. 75: 76-79.
{{cite journal}}: Explicit use of et al. in:|last2=(help) - ^ a b c d e f g Department of Crop Sciences, University of Illinois at Urbana-Champaign (1989). Report on Plant Disease: Leaf Mold of Greenhouse Tomatoes (PDF) (Report). University of Illinois. p. 1-3. Retrieved 7 November 2016.
- ^ a b c d e f g h i "Plantwise Technical Factsheet: Tomato leaf mould (Passalora fulva)". Plantwise. Retrieved 7 November 2016.
- ^ a b c d Douglas, S.M. (2003). Leaf Mold and Powdery Mildew of Tomato (PDF) (Report). Connecticut's Official State Website. p. 1-3. Retrieved 7 November 2016.
- ^ a b c d e f Joosten, M.H.A.J.; Honée, G.; Van Kan, J.A.L.; De Wit, P.J.G.M. (1997). "The gene-for-gene concept in plant-pathogen interactions: Tomato-Cladosporium fulvum". In Carroll, G.C.; Tudzynski, P. (eds.). The Mycota. Plant Relationships. Vol. V part B. Germany: Springer-Verlag. pp. 3–16. ISBN 3-540-62018-4.
- ^ a b Kobrink, E.; Somssich, I.E. (1997). "Pathogenesis-related proteins and plant defense". In Carroll, G.C.; Tudzynski, P. (eds.). The Mycota. Plant Relationships. Vol. V part A. Germany: Springer-Verlag. pp. 107–128. ISBN 3-540-58006-9.
- ^ Webster, John; Weber, Roland W.S. (2007). Introduction to fungi: 3rd Edition. New York: Cambridge University Press.
- ^ Ebel, J.; Scheel, D. (1997). "Signals in host-parasite interactions". In Carroll, G.C.; Tudzynski, P. (eds.). The Mycota. Plant Relationships. Vol. V part A. Germany: Springer-Verlag. pp. 85–105. ISBN 3-540-58006-9.
- ^ Li, S.; Zhao, T.; Li, H.; Xu, X.; Li, J. (2015). "First report of races 2.5 and 2.4.5 of Cladosporium fulvum (syn. Passalora fulva, causal fungus of tomato leaf mold disease in China". Journal of General Plant Pathology. 81: 162-165.
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