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Review
. 2023 Jan 21;24(3):2141.
doi: 10.3390/ijms24032141.

Appressoria-Small but Incredibly Powerful Structures in Plant-Pathogen Interactions

Ting-Ting Shi  1 , Guo-Hong Li  1 , Pei-Ji Zhao  1
Affiliations
Review

Appressoria-Small but Incredibly Powerful Structures in Plant-Pathogen Interactions

Ting-Ting Shi et al. Int J Mol Sci. .

Abstract

Plant-pathogenic fungi are responsible for many of the most severe crop diseases in the world and remain very challenging to control. Improving current protection strategies or designating new measures based on an overall understanding of molecular host-pathogen interaction mechanisms could be helpful for disease management. The attachment and penetration of the plant surface are the most important events among diverse plant-fungi interactions. Fungi evolved as small but incredibly powerful infection structure appressoria to facilitate attachment and penetration. Appressoria are indispensable for many diseases, such as rusts, powdery mildews, and blast diseases, as well as devastating oomycete diseases. Investigation into the formation of plant-pathogen appressoria contributes to improving the understanding of the molecular mechanisms of plant-pathogen interactions. Fungal host attachment is a vital step of fungal pathogenesis. Here, we review recent advances in the molecular mechanisms regulating the formation of appressoria. Additionally, some biocontrol agents were revealed to act on appressorium. The regulation of fungal adhesion during the infective process by acting on appressoria formation is expected to prevent the occurrence of crop disease caused by some pathogenic fungi.

Keywords: appressoria; interaction; pathogenic fungi; plant.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Several signaling pathways related to appressorium formation in Magnaporthe oryzae. The sensor proteins Msb2 and Sho1 activate the Pmk1 MAPK pathway; Whi2 interacts with Psr1, participating in the regulation of the cAMP levels and the Tor signaling pathway; Som1 functions downstream of the cAMP-PKA pathway, which may regulate the Pmk1 MAPK pathway through Som1. Rgs1 regulates G-protein signaling; the normal process of G-protein MoMagA-cAMP signaling depends on a condition of steadiness among Rgs1, Ckb2, and Emc2; Opy2 participates in the Mps1 MAPK pathway by interacting with Mst50; Ral2 interacts with Smo1, Scd1, and Mst50 to regulate the activation of the Mst11-Mst7-Pmk1 MAPK pathway by Ras2; Pmk1 pathway activation involves Mgb1, Ras2, and Cdc42; Mst50 activates Pmk1 through its interaction with Smo1, Cdc42, Scd1, Ral2; Pmk1 also requires the Mst7 and Mst11, which both bind to Mst50; Mka1, which interacts with Mst50, functions upstream of the MAPK pathway; Pal1 interacts with Sla1 and functions upstream of both cAMP and Pmk1–MAPK signaling pathways; Whi2 interacts with Psr1, participating the regulation of appressoria formation through the regulation of the cAMP levels and the target of rapamycin (Tor) signaling pathway; Ubp3 regulates GTPase-activating protein Smo1.
Figure 2
Figure 2
Concept of plant infection by appressorium-forming fungi. (A): A spore secretes an adhesive extracellular matrix that allows it to attach firmly to the host surface, then the infection begins. (B,C): Subsequently, the spore tapering end develops a single, polarized hypha, which grows along the host plant surface, and finally differentiates into an appressorium. (D): Formed appressoria adhere firmly to the host surface and subsequently secrete extracellular enzymes or produce physical force (or use a combination of both factors) to facilitate cuticle penetration. Cellular turgor is translated into mechanical force by penetration peg, forcing it through the leaf cuticle. (E): The pegs differentiate invasive hyphae to colonize rapidly epidermal and mesophyll tissues and secrete effectors and sequester nutrients from living host cells. The fungus ramifies intra- and intercellularly in susceptible host tissue upon penetration. Lesion formation is initiated with host cell death starting 4 to 5 days after infection. (F): The next generation of conidia is then produced.
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Grants and funding

This research was supported by the National Natural Science Foundation of China (grant no. 31970060 (P.-J.Z.) and 32270132 (P.-J.Z.)) and the Yunnan Science and Technology Special Project (202102AA100013 and 202001BB050061).