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Chapter 37 : and Rice Blast Disease

Authors: Chang Hyun Khang1, Barbara Valent2
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Affiliations: 1: Department of Plant Pathology, Kansas State University, Manhattan, KS 66506-5502; 2: Department of Plant Pathology, Kansas State University, Manhattan, KS 66506-5502
Content Type: Monograph
Publication Year: 2010

Category: Microbial Genetics and Molecular Biology; Fungi and Fungal Pathogenesis

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Abstract:

The species complex includes pathogens of more than 50 grass species. was recently segregated as a distinct species from based on a multilocus phylogenetic analysis and on mating properties of the strains. isolates are pathogenic on crabgrass, , and related grasses, and is associated with pathogens of diverse grasses with agricultural significance. Evolution of host-specific populations is an important topic that can be addressed within the species complex. The abundance of transposable elements in the rice isolates from the field suggests that lacks the repeat-induced point mutation (RIP) mechanism described in the related pyrenomycete . Fluorescent effectors remained localized to the biotrophic interfacial complex (BIC) region as long as invasive hyphae (IH) continued to grow in the rice cell. Secreted effector fusions partially colocalized with an aggregation of plant endocytotic membranes that labeled with FM4-64. Some of the blast fungal metabolites, such as tenuazonic acid (TA) and picolinic acid, were demonstrated to be hypersensitive-response elicitors, inducing resistance responses in rice. For rice blast disease, the increasing numbers of avirulence (AVR)-like genes that control host specificity and the large number of R proteins that are predicted to be localized in the rice cytoplasm are consistent with the hypothesis that translocates many effectors into the host cytoplasm.

Citation: Hyun Khang C, Valent B. 2010. and Rice Blast Disease, p 593-606. In Borkovich K, Ebbole D (ed), Cellular and Molecular Biology of Filamentous Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555816636.ch37

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Magnaporthe oryzae and Rice Blast Disease
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Citation: Hyun Khang C, Valent B. 2010. and Rice Blast Disease, p 593-606. In Borkovich K, Ebbole D (ed), Cellular and Molecular Biology of Filamentous Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555816636.ch37
/content/10.1128/9781555816636.ch37.ch37fig01
FIGURE 1
A sporulating leaf blast lesion on rice. Fully susceptible lesions first become visible ~5 days postinoculation (dpi) and mature ~7 dpi. Such lesions range from 0.5 to >1 cm in length depending on the rice variety and plant maturity in the field, and they produce several thousand conidia a day for about 2 weeks (Ou, 1985). (Photo courtesy of J. M. Bonman.)
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Image of FIGURE 1
FIGURE 1

A sporulating leaf blast lesion on rice. Fully susceptible lesions first become visible ~5 days postinoculation (dpi) and mature ~7 dpi. Such lesions range from 0.5 to >1 cm in length depending on the rice variety and plant maturity in the field, and they produce several thousand conidia a day for about 2 weeks (Ou, 1985). (Photo courtesy of J. M. Bonman.)

Citation: Hyun Khang C, Valent B. 2010. and Rice Blast Disease, p 593-606. In Borkovich K, Ebbole D (ed), Cellular and Molecular Biology of Filamentous Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555816636.ch37
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FIGURE 2
Asexual and sexual cycles of the rice blast fungus. (A) A conidium (25 to 30 by 9 to 12 μm) adheres to the leaf surface by using spore tip mucilage, produces a germ tube that senses the inductive surface, and differentiates an appressorium. A mature appressorium uses osmotically generated pressure to force a penetration peg through the plant cuticle and cell wall. (B) Inside the host cell lumen, the penetration peg becomes a filamentous primary hypha, accompanied by migration of cellular contents from the appressorium into the primary hypha. The primary hypha invaginates the host plasma membrane and secretes effectors, which are visualized by translational fusion of effector polypeptides with enhanced green fluorescent protein (GFP), into the membranous cap BIC at its tip at 22 to 25 h postinoculation (hpi). By 26 to 30 hpi, primary hyphae have differentiated into bulbous IH, which are sealed in an EIHM compartment. The BIC has moved beside the first differentiated IH, where it accumulates fluorescent effector proteins as long as IH grow in the cell. By 36 to 40 hpi, IH have undergone extreme constriction to cross the plant cell wall. In neighbor cells, the fungus first grows as filamentous IH secreting effector:GFP fusion proteins into tip BICs and then differentiates into bulbous IH with fluorescent side BICs. Subsequent cell invasions follow the same pattern. (C) Conidiogenesis in is holoblastic such that expansion and swelling of the conidiophore apex gives rise to a conidium, followed by a septum being formed to delimit the forming conidium ( ). The apex then grows to the side to produce the next conidium, resulting in three to five conidia borne sympodially on a conidiophore. (D) Sexual cycle: strains of opposite mating type mate to form pigmented perithecia (500 to 1,200 μm in length) with spherical bases (80 to 260 μm in diameter) and long cylindrical necks. Unordered asci contain eight hyaline, fusiform ascospores (16 to 25 by 4 to 8 μm), each with four cells and a single nucleus per cell.
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10.1128/9781555816636/f0595-01.gif
Image of FIGURE 2
FIGURE 2

Asexual and sexual cycles of the rice blast fungus. (A) A conidium (25 to 30 by 9 to 12 μm) adheres to the leaf surface by using spore tip mucilage, produces a germ tube that senses the inductive surface, and differentiates an appressorium. A mature appressorium uses osmotically generated pressure to force a penetration peg through the plant cuticle and cell wall. (B) Inside the host cell lumen, the penetration peg becomes a filamentous primary hypha, accompanied by migration of cellular contents from the appressorium into the primary hypha. The primary hypha invaginates the host plasma membrane and secretes effectors, which are visualized by translational fusion of effector polypeptides with enhanced green fluorescent protein (GFP), into the membranous cap BIC at its tip at 22 to 25 h postinoculation (hpi). By 26 to 30 hpi, primary hyphae have differentiated into bulbous IH, which are sealed in an EIHM compartment. The BIC has moved beside the first differentiated IH, where it accumulates fluorescent effector proteins as long as IH grow in the cell. By 36 to 40 hpi, IH have undergone extreme constriction to cross the plant cell wall. In neighbor cells, the fungus first grows as filamentous IH secreting effector:GFP fusion proteins into tip BICs and then differentiates into bulbous IH with fluorescent side BICs. Subsequent cell invasions follow the same pattern. (C) Conidiogenesis in is holoblastic such that expansion and swelling of the conidiophore apex gives rise to a conidium, followed by a septum being formed to delimit the forming conidium ( ). The apex then grows to the side to produce the next conidium, resulting in three to five conidia borne sympodially on a conidiophore. (D) Sexual cycle: strains of opposite mating type mate to form pigmented perithecia (500 to 1,200 μm in length) with spherical bases (80 to 260 μm in diameter) and long cylindrical necks. Unordered asci contain eight hyaline, fusiform ascospores (16 to 25 by 4 to 8 μm), each with four cells and a single nucleus per cell.

Citation: Hyun Khang C, Valent B. 2010. and Rice Blast Disease, p 593-606. In Borkovich K, Ebbole D (ed), Cellular and Molecular Biology of Filamentous Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555816636.ch37
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FIGURE 3
The EIHM tightly wraps the IH and prevents the endocytotic tracker dye FM4-64 from reaching IH membranes. At 29 hpi, an IH of a fungal transformant expressing cytoplasmic enhanced yellow fluorescent protein (YFP) is viewed by bright-field optics (left panel) and by YFP (middle panel) and FM4-64 (right panel) fluorescence (both shown as white). At this site, the primary hypha (P) extending from the appressorial penetration site (PS) had lost viability after IH formed (observed in ~50% of all infection sites). A BIC (arrow) beside the first IH cell is rich in FM4-64-stained membranes that are continuous with EIHM. Bars, 5 μm.
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10.1128/9781555816636/f0599-01.gif
Image of FIGURE 3
FIGURE 3

The EIHM tightly wraps the IH and prevents the endocytotic tracker dye FM4-64 from reaching IH membranes. At 29 hpi, an IH of a fungal transformant expressing cytoplasmic enhanced yellow fluorescent protein (YFP) is viewed by bright-field optics (left panel) and by YFP (middle panel) and FM4-64 (right panel) fluorescence (both shown as white). At this site, the primary hypha (P) extending from the appressorial penetration site (PS) had lost viability after IH formed (observed in ~50% of all infection sites). A BIC (arrow) beside the first IH cell is rich in FM4-64-stained membranes that are continuous with EIHM. Bars, 5 μm.

Citation: Hyun Khang C, Valent B. 2010. and Rice Blast Disease, p 593-606. In Borkovich K, Ebbole D (ed), Cellular and Molecular Biology of Filamentous Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555816636.ch37
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FIGURE 4
IH exhibit extreme constriction as they cross the rice cell wall at 32 hpi. YFP fluorescence in the fungal cytoplasm (in white) is shown alone to highlight the constriction (arrows). Bar, 5 μm. Reproduced with permission from .
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10.1128/9781555816636/f0600-01.gif
Image of FIGURE 4
FIGURE 4

IH exhibit extreme constriction as they cross the rice cell wall at 32 hpi. YFP fluorescence in the fungal cytoplasm (in white) is shown alone to highlight the constriction (arrows). Bar, 5 μm. Reproduced with permission from .

Citation: Hyun Khang C, Valent B. 2010. and Rice Blast Disease, p 593-606. In Borkovich K, Ebbole D (ed), Cellular and Molecular Biology of Filamentous Fungi. ASM Press, Washington, DC. doi: 10.1128/9781555816636.ch37
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