- Email: [email protected]
Attach, adhere, “appress”, attack
ARTICLE IN PRESS
Physiological and Molecular Plant Pathology 70 (2007) 97–98 www.elsevier.com/locate/pmpp
Editorial
Attach, adhere, ‘‘appress’’, attack Ample evidence exists that demonstrates infection of plants by fungi requires fungal spore attachment to the plant surface. This is then followed by germination and, in many cases, the formation of an appressorium [1,2]. This attachment is important as it prevents the spore from being dislodged prior to attempted invasion into the plant. Even though the need for attachment is general, the mechanisms of attachment are quite variable [1,2]. A variety of adhesive materials have been observed in spore attachment to leaf surfaces. These include polysaccharides, glycoproteins and even cutinolytic enzymes [1,2]. The mechanism of spore attachment that utilize these materials can either be passive or active. For example, attachment of Magnaporthe grisea conidia occurs via the passive extrusion of a mucilage containing droplet from the spore tip as a result of contact with the plant surface [3]. Release of cutinase from Blumeria graminis condidia is associated with attachment [4,5] as is the release of cutinase and other esterases from the matrix that surrounds the Uromyces vicia-fabae urediniospores [6]. Other fungi, such as Colletotrichum graminicola, require active metabolism for attachment as shown by the observations that cycloheximide reduces the efficiency of attachment [7,8]. Once attachment occurs, the fungal spore must germinate and, in many cases, form an appressorium at the tip of a germ tube [1]. The formation of the appressorium also requires a number of developmental steps which include the attachment of this structure to the plant surface. Both chemical and physical signals have been shown to be involved in triggering appressorium formation and, for example, include surface topography and leaf wax components, respectively [1,2]. In this issue, Rawlings et al. [9] report on the role of the Colletotrichum lindemuthianum spore coat in the early events of pathogenesis. C. lindemuthianum, the cause of anthracnose on Phaseolus, is capable of causing disease on aerial plant parts such as leaves and green pods. Thus, understanding the factors that control the early stages of infection is needed to know how this pathogen causes disease [10]. Previous studies [reviewed in 9] have shown that C. lindemuthianum has spore coat that is composed of densely packed fibers and contains polysaccharides and a smaller amount of glycoprotein. A monoclonal antibody 0885-5765/$ - see front matter r 2007 Published by Elsevier Ltd. doi:10.1016/j.pmpp.2007.10.005
specific for one of the glycoproteins was able to inhibit the attachment of spores to polystyrene. Thus, the spore coat appears to play a very important role in attachment to surfaces. In their report, Rawlings et al. [9] were able to demonstrate that the adhesion of C. lindemuthianum spores is a two-step process: this was characterized as passive adhesion that was followed by secretion of glycoproteins. Using monoclonal antibodies, the authors we able to show that the monoclonal antibody specific proteins were located at the spore apex within an hour of attachment to an artificial surface and were also present on the germ tubes and appressoria that subsequently formed. The requirement of the spore coat for adhesion was further demonstrated by treatment with a protease that removes the spore coat. However, removal of the spore coat had no effect on the ability of the conidia to release glycoproteins needed for the second phase of adhesion. What was most interesting, however, was the apparent need for the spore coat for appressorium formation. Although protease treatment to remove the spore coat had no effect on germination, the germinated spores did not form appressoria. In further support of the spore coat’s role in appressorium formation, treatment of conidia with monoclonal antibodies that bind glycoproteins of the extracellular matrix had no effect on subsequent appressorium formation on a hydrophobic surface. Although studies on artificial surfaces can begin to define which components are needed for attachment and further development of infection structures, the true test is to determine if these factors are needed for infection. Treatment of the spores with protease resulted in an inhibition of appressorium formation and a lack of disease development on bean leaves. Similar to studies on polystyrene, treatment with monoclonal antibody specific for a spore coat glycoprotein did no effect appressorium formation. This treatment also did not inhibit disease development. Taken in total, the authors conclude that the C. lindemuthianum spore coat plays a role in both attachment and as part of the process that leads to appressorium formation and thus the ability of this pathogen to attack its host. It will be of great interested to learn how these processes are controlled by the spore coat.
ARTICLE IN PRESS 98
Editorial / Physiological and Molecular Plant Pathology 70 (2007) 97–98
References [1] Mendgen K, Hahn M, Deising H. Morphogenesis and mechanisms of penetration by plant pathogenic fungi. Ann Rev Phytopathol 1996;34:367–86. [2] Tucker SL, Talbot NJ. Surface attachment and pre-penetration state development by plant pathogenic fungi. Ann Rev Phytopathol 2001;39:385–417. [3] Hamer JE, Howard RJ, Chumley FG, Valent B. A mechanism for surface attachment of spores of a plant pathogenic fungus. Science 1987;239:288–90. [4] Nielsen KA, Nicholson RL, Carver TLW, Kunoh H, Oliver RP. First touch: An immediate response to surface recognition in conidia of Blumeria graminis. Physiol Mol Plant Pathol 2000;56:63–70. [5] Pascholati SF, Yoshikawa K, Kunoh H, Nicholson RL. Preparation of the infection courts by Erysiphe graminis f.sp. hordei.–cutinase is a component of the conidial exudates. Physiol Mol Plant Pathol 1992;41:53–9. [6] Deising H, Nicholson RL, Haug M, Howard RJ, Mengen K. Adhesion pad formation and the involvement of cutinase and
[7]
[8]
[9]
[10]
esterases in the attachment of uredospores to the host cuticle. Plant Cell 1992;4:1101–11. Mercure EW, Kunoh H, Nicholson RL. Adhesion of Colletotrichum graminicola conidia to corn leaves. A requirement for disease development. Physiol Mol Plant Pathol 1994;45:407–20. Mercure EW, Leite B, Nicholson RL. Adhesion of ungerminated conidia of Colletotrichum graminicola to artificial hydrophobic surfaces. Physiol Mol Plant Pathol 1994;45:421–40. Rawlings SL, O’Connell RJ, Green JR. The spore coat of the bean anthracnose fungus Colletotrichum lindemuthianum is required for adhesion, appressorium formation and pathogenicity. Physiol Mol Plant Pathol 2007;70:108–17. Agrios GN. Plant Pathology. 5th ed. New York: Elsevier; 2005. p. 487–8.
R. Hammerschmidt Department of Plant Pathology, 107 CIPS Bldg Michigan State University, East Lansing, MI 48824–1311, USA E-mail address: [email protected]
Physiological and Molecular Plant Pathology 70 (2007) 97–98 www.elsevier.com/locate/pmpp
Editorial
Attach, adhere, ‘‘appress’’, attack Ample evidence exists that demonstrates infection of plants by fungi requires fungal spore attachment to the plant surface. This is then followed by germination and, in many cases, the formation of an appressorium [1,2]. This attachment is important as it prevents the spore from being dislodged prior to attempted invasion into the plant. Even though the need for attachment is general, the mechanisms of attachment are quite variable [1,2]. A variety of adhesive materials have been observed in spore attachment to leaf surfaces. These include polysaccharides, glycoproteins and even cutinolytic enzymes [1,2]. The mechanism of spore attachment that utilize these materials can either be passive or active. For example, attachment of Magnaporthe grisea conidia occurs via the passive extrusion of a mucilage containing droplet from the spore tip as a result of contact with the plant surface [3]. Release of cutinase from Blumeria graminis condidia is associated with attachment [4,5] as is the release of cutinase and other esterases from the matrix that surrounds the Uromyces vicia-fabae urediniospores [6]. Other fungi, such as Colletotrichum graminicola, require active metabolism for attachment as shown by the observations that cycloheximide reduces the efficiency of attachment [7,8]. Once attachment occurs, the fungal spore must germinate and, in many cases, form an appressorium at the tip of a germ tube [1]. The formation of the appressorium also requires a number of developmental steps which include the attachment of this structure to the plant surface. Both chemical and physical signals have been shown to be involved in triggering appressorium formation and, for example, include surface topography and leaf wax components, respectively [1,2]. In this issue, Rawlings et al. [9] report on the role of the Colletotrichum lindemuthianum spore coat in the early events of pathogenesis. C. lindemuthianum, the cause of anthracnose on Phaseolus, is capable of causing disease on aerial plant parts such as leaves and green pods. Thus, understanding the factors that control the early stages of infection is needed to know how this pathogen causes disease [10]. Previous studies [reviewed in 9] have shown that C. lindemuthianum has spore coat that is composed of densely packed fibers and contains polysaccharides and a smaller amount of glycoprotein. A monoclonal antibody 0885-5765/$ - see front matter r 2007 Published by Elsevier Ltd. doi:10.1016/j.pmpp.2007.10.005
specific for one of the glycoproteins was able to inhibit the attachment of spores to polystyrene. Thus, the spore coat appears to play a very important role in attachment to surfaces. In their report, Rawlings et al. [9] were able to demonstrate that the adhesion of C. lindemuthianum spores is a two-step process: this was characterized as passive adhesion that was followed by secretion of glycoproteins. Using monoclonal antibodies, the authors we able to show that the monoclonal antibody specific proteins were located at the spore apex within an hour of attachment to an artificial surface and were also present on the germ tubes and appressoria that subsequently formed. The requirement of the spore coat for adhesion was further demonstrated by treatment with a protease that removes the spore coat. However, removal of the spore coat had no effect on the ability of the conidia to release glycoproteins needed for the second phase of adhesion. What was most interesting, however, was the apparent need for the spore coat for appressorium formation. Although protease treatment to remove the spore coat had no effect on germination, the germinated spores did not form appressoria. In further support of the spore coat’s role in appressorium formation, treatment of conidia with monoclonal antibodies that bind glycoproteins of the extracellular matrix had no effect on subsequent appressorium formation on a hydrophobic surface. Although studies on artificial surfaces can begin to define which components are needed for attachment and further development of infection structures, the true test is to determine if these factors are needed for infection. Treatment of the spores with protease resulted in an inhibition of appressorium formation and a lack of disease development on bean leaves. Similar to studies on polystyrene, treatment with monoclonal antibody specific for a spore coat glycoprotein did no effect appressorium formation. This treatment also did not inhibit disease development. Taken in total, the authors conclude that the C. lindemuthianum spore coat plays a role in both attachment and as part of the process that leads to appressorium formation and thus the ability of this pathogen to attack its host. It will be of great interested to learn how these processes are controlled by the spore coat.
ARTICLE IN PRESS 98
Editorial / Physiological and Molecular Plant Pathology 70 (2007) 97–98
References [1] Mendgen K, Hahn M, Deising H. Morphogenesis and mechanisms of penetration by plant pathogenic fungi. Ann Rev Phytopathol 1996;34:367–86. [2] Tucker SL, Talbot NJ. Surface attachment and pre-penetration state development by plant pathogenic fungi. Ann Rev Phytopathol 2001;39:385–417. [3] Hamer JE, Howard RJ, Chumley FG, Valent B. A mechanism for surface attachment of spores of a plant pathogenic fungus. Science 1987;239:288–90. [4] Nielsen KA, Nicholson RL, Carver TLW, Kunoh H, Oliver RP. First touch: An immediate response to surface recognition in conidia of Blumeria graminis. Physiol Mol Plant Pathol 2000;56:63–70. [5] Pascholati SF, Yoshikawa K, Kunoh H, Nicholson RL. Preparation of the infection courts by Erysiphe graminis f.sp. hordei.–cutinase is a component of the conidial exudates. Physiol Mol Plant Pathol 1992;41:53–9. [6] Deising H, Nicholson RL, Haug M, Howard RJ, Mengen K. Adhesion pad formation and the involvement of cutinase and
[7]
[8]
[9]
[10]
esterases in the attachment of uredospores to the host cuticle. Plant Cell 1992;4:1101–11. Mercure EW, Kunoh H, Nicholson RL. Adhesion of Colletotrichum graminicola conidia to corn leaves. A requirement for disease development. Physiol Mol Plant Pathol 1994;45:407–20. Mercure EW, Leite B, Nicholson RL. Adhesion of ungerminated conidia of Colletotrichum graminicola to artificial hydrophobic surfaces. Physiol Mol Plant Pathol 1994;45:421–40. Rawlings SL, O’Connell RJ, Green JR. The spore coat of the bean anthracnose fungus Colletotrichum lindemuthianum is required for adhesion, appressorium formation and pathogenicity. Physiol Mol Plant Pathol 2007;70:108–17. Agrios GN. Plant Pathology. 5th ed. New York: Elsevier; 2005. p. 487–8.
R. Hammerschmidt Department of Plant Pathology, 107 CIPS Bldg Michigan State University, East Lansing, MI 48824–1311, USA E-mail address: [email protected]