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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Plant Sciences".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 12975

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Special Issue Editors

Prof. Dr. Huiquan Liu

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Guest Editor

College of Plant Protection, Northwest A&F University, Yangling, China
Interests: Fusarium graminearum; Fusarium head blight (FHB); plant-fungus interactions; plant immunity; mycotoxin; epigenetics; evolutionary biology; bioinformatics

Prof. Dr. Cong Jiang

E-Mail Website
Guest Editor

College of Plant Protection, Northwest A&F University, Xianyang, China
Interests: Fusarium graminearum; phytopathogens; fungal sensing; signaling pathways; histone modification; plant-fungus interactions; plant immunity; mycotoxin
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Prof. Dr. Guotian Li

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Guest Editor

College of Plant Science & Technology, Huazhong Agricultural University, Wuhan, China
Interests: Magnaporthe oryzae; rice blast; rice immunity; plant-fungus interactions; plant phospholipid; pathogenicity; signaling pathways; genomics

Special Issue Information

Dear Colleagues,

Phytopathogenic fungi are among the most dominant causal agents of crop diseases. Fungal diseases lead to a significant reduction in crop yield and quality, thereby posing a significant risk to global food security and economic development. The most devastating fungal disease is rice blast caused by Magnaporthe oryzae, resulting in losses of up to 10–30% of the global yield of rice worldwide. In addition to causing yield and quality losses, many fungal pathogens, such as Fusarium graminearum, produce mycotoxins during infection that pose great threats to human and animal health. As the global climate and tillage system change, fungal diseases are emerging on new hosts and in new places. In order to develop sustainable management strategies for crop protection and improve crop resistance to fungal diseases, we must understand the pathogen biology, host–pathogen interactions, and host resistance to diseases, as well as epidemiology and disease management.

The aim of this Special Issue is to cover the research on fungal diseases in crops. We welcome manuscripts on the following subtopics, but not limited to: 1) biology of fungal pathogens towards gaining more insights into the infection process and the weak spots in the disease cycles; 2) host–pathogen interaction and plant immunity to fungal pathogens; 3) diseases caused by emerging and re-emerging fungal populations or species; 4) population diversity and adaptive evolution revealed by genomics and population genomics. Manuscripts addressing epidemiology, the impact of climate change, and novel strategies to control fungal diseases and/or mycotoxin contamination are also welcome.

We invite you to submit research articles, as well as reviews and short communications related to state-of-the-art research on fungal diseases in crops.

Prof. Dr. Huiquan Liu
Prof. Dr. Cong Jiang
Prof. Dr. Guotian Li
Guest Editors

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Keywords

crop disease
fungi
pathogenesis
plant immunity
host–pathogen interaction
mycotoxin
disease cycle

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Published Papers (5 papers)

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Research

16 pages, 6036 KiB

Open AccessArticle

A Chloroplast-Localized Glucose-6-Phosphate Dehydrogenase Positively Regulates Stripe Rust Resistance in Wheat

by Xiaobo Wei, Xueling Huang, Weiling Yang, Xinran Wang, Tao Guan, Zhensheng Kang and Jie Liu

Int. J. Mol. Sci. 2023, 24(1), 459; https://doi.org/10.3390/ijms24010459 - 27 Dec 2022

Cited by 5 | Viewed by 2244

Abstract

Glucose-6-phosphate dehydrogenase (G6PDH), the rate-limiting enzyme of the pentose phosphate pathway (PPP), plays a pivotal role in plant stress responses. However, the function and mechanism of G6PDHs in crop plants challenged by fungal pathogens remain poorly understood. In this study, a wheat G6DPH gene responding to infection by Puccinia striiformis f. sp. tritici (Pst), designated TaG6PDH2, was cloned and functionally identified. TaG6PDH2 expression was significantly upregulated in wheat leaves inoculated with Pst or treated with abiotic stress factors. Heterologous mutant complementation and enzymatic properties indicate that TaG6PDH2 encodes a G6PDH protein. The transient expression of TaG6PDH2 in Nicotiana benthamiana leaves and wheat protoplasts revealed that TaG6PDH2 is a chloroplast-targeting protein. Silencing TaG6PDH2 via the barley stripe mosaic virus (BSMV)-induced gene silencing (VIGS) system led to compromised wheat resistance to the Pst avirulent pathotype CYR23, which is implicated in weakened H₂O₂ accumulation and cell death. In addition, TaG6PDH2 was confirmed to interact with the wheat glutaredoxin TaGrxS4. These results demonstrate that TaG6PDH2 endows wheat with increased resistance to stripe rust by regulating reactive oxygen species (ROS) production. Full article

(This article belongs to the Special Issue Fungal Diseases in Crops)

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18 pages, 5062 KiB

Open AccessArticle

Ontogenetic Variation in Macrocyclic and Hemicyclic Poplar Rust Fungi

by Zhongdong Yu, Zijia Peng, Mei Qi and Wei Zheng

Int. J. Mol. Sci. 2022, 23(21), 13062; https://doi.org/10.3390/ijms232113062 - 27 Oct 2022

Viewed by 2241

Abstract

Melampsora larici-populina (Mlp), M. medusae (Mmed), M. magnusiana (Mmag), and M. pruinosae (Mpr) are epidemic rust fungi in China. The first two are macrocyclic rust fungi distributed in temperate humid environments. The latter two are hemicyclic rusts, mainly distributed in arid and semi-arid areas. Ontogenetic variation that comes with this arid-resistance is of great interest—and may help us predict the influence of a warmer, drier, climate on fungal phylogeny. To compare the differences in the life history and ontogeny between the two types of rust, we cloned mating type genes, STE3.4 and STE3.3 using RACE-smart technology. Protein structures, functions, and mutant loci were compared across each species. We also used microscopy to compare visible cytological differences at each life stage for the fungal species, looking for variation in structure and developmental timing. Quantitative PCR technology was used to check the expression of nuclear fusion and division genes downstream of STE3.3 and STE3.4. Encoding amino acids of STE3.3 and STE3.4 in hemicyclic rusts are shorter than these in the macrocyclic rusts. Both STE3.3 and STE3.4 interact with a protein kinase superfamily member EGG12818 and an E3 ubiquitin protein ligase EGG09709 directly, and activating G-beta conformational changes. The mutation at site 74th amino acid in the conserved transmembrane domain of STE3.3 ascribes to a positive selection, in which alanine (Ala) is changed to phenylalanine (Phe) in hemicyclic rusts, and a mutation with Tyr lost at site 387th in STE3.4, where it is the binding site for β-D-Glucan. These mutants are speculated corresponding to the insensitivity of hemicyclic rust pheromone receptors to interact with MFa pheromones, and lead to Mnd1 unexpressed in teliospora, and they result in the diploid nuclei division failure and the sexual stage missing in the life cycle. A Phylogenic tree based on STE3.4 gene suggests these two rust types diverged about 14.36 million years ago. Although these rusts share a similar uredia and telia stage, they show markedly different wintering strategies. Hemicyclic rusts overwinter in the poplar buds endophytically, their urediniospores developing thicker cell walls. They form haustoria with a collar-like extrahaustorial membrane neck and induce host thickened callose cell walls, all ontogenetic adaptations to arid environments. Full article

(This article belongs to the Special Issue Fungal Diseases in Crops)

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16 pages, 4921 KiB

Open AccessArticle

FgCsn12 Is Involved in the Regulation of Ascosporogenesis in the Wheat Scab Fungus Fusarium graminearum

by Hang Jiang, Yuhan Zhang, Wanshan Wang, Xinyu Cao, Huaijian Xu, Huiquan Liu, Junshan Qi, Cong Jiang and Chenfang Wang

Int. J. Mol. Sci. 2022, 23(18), 10445; https://doi.org/10.3390/ijms231810445 - 9 Sep 2022

Cited by 4 | Viewed by 2333

Abstract

Fusarium head blight (FHB), caused by the fungal pathogen Fusarium graminearum, is a destructive disease worldwide. Ascospores are the primary inoculum of F. graminearum, and sexual reproduction is a critical step in its infection cycle. In this study, we characterized the functions of FgCsn12. Although the ortholog of FgCsn12 in budding yeast was reported to have a direct interaction with Csn5, which served as the core subunit of the COP9 signalosome, the interaction between FgCsn12 and FgCsn5 was not detected through the yeast two-hybrid assay. The deletion of FgCSN12 resulted in slight defects in the growth rate, conidial morphology, and pathogenicity. Instead of forming four-celled, uninucleate ascospores, the Fgcsn12 deletion mutant produced oval ascospores with only one or two cells and was significantly defective in ascospore discharge. The 3′UTR of FgCsn12 was dispensable for vegetative growth but essential for sexual reproductive functions. Compared with those of the wild type, 1204 genes and 2240 genes were up- and downregulated over twofold, respectively, in the Fgcsn12 mutant. Taken together, FgCsn12 demonstrated an important function in the regulation of ascosporogenesis in F. graminearum. Full article

(This article belongs to the Special Issue Fungal Diseases in Crops)

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25 pages, 7588 KiB

Open AccessArticle

PKR Protects the Major Catalytic Subunit of PKA Cpk1 from FgBlm10-Mediated Proteasome Degradation in Fusarium graminearum

by Chen Gong, Daiying Xu, Daiyuan Sun and Xue Zhang

Int. J. Mol. Sci. 2022, 23(18), 10208; https://doi.org/10.3390/ijms231810208 - 6 Sep 2022

Viewed by 2833

Abstract

For optimal proteolytic function, the proteasome core (CP or 20S) must associate with activators. The cAMP-PKA pathway is reported to affect the activity of the proteasome in humans. However, the relationship between the proteasome and PKA is not well characterized. Our results showed that the major catalytic subunit Cpk1 was degraded without the protection of Pkr. Eleven (out of 67) pkr suppressors had FgBlm10 C-terminal truncation, one suppressor had an amino acid change mutation in the PRE6 ortholog (FGRRES_07282), and one in the PRE5 ortholog (FGRRES_05222). These mutations rescued the defects in growth and conidial morphology, Cpk1 stability, and PKA activities in the pkr mutant. The interaction of FgBlm10 with FgPre5 and FgPre6 were detected by co-immunoprecipitation, and the essential elements for their interaction were characterized, including the FgBlm10 C-terminus, amino acid D82 of FgPre6 and K62 of FgPre5. Additional FgBlm10-interacting proteins were identified in the wild type and pkr mutant, suggesting that PKA regulates the preference of FgBlm10-mediated proteasome assembly. In addition, PKA indirectly affected the phosphorylation of FgBlm10, and its localization in the nucleus. The truncation of the FgBlm10 C terminus also enhanced nuclear import and bleomycin resistance, suggesting its role in proteasome assembly at DNA damage sites. Collectively, our data demonstrated that regulation between PKA and proteasome degradation is critical for the vegetative growth of F. graminearum. Full article

(This article belongs to the Special Issue Fungal Diseases in Crops)

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21 pages, 3353 KiB

Open AccessArticle

Stage-Specific Genetic Interaction between FgYCK1 and FgBNI4 during Vegetative Growth and Conidiation in Fusarium graminearum

by Jindong Zhu, Denghui Hu, Qianqian Liu, Rui Hou, Jin-Rong Xu and Guanghui Wang

Int. J. Mol. Sci. 2022, 23(16), 9106; https://doi.org/10.3390/ijms23169106 - 14 Aug 2022

Cited by 5 | Viewed by 2454

Abstract

CK1 casein kinases are well conserved in filamentous fungi. However, their functions are not well characterized in plant pathogens. In Fusarium graminearum, deletion of FgYCK1 caused severe growth defects and loss of conidiation, fertility, and pathogenicity. Interestingly, the Fgyck1 mutant was not stable and often produced fast-growing spontaneous suppressors. Suppressor mutations were frequently identified in the FgBNI4 gene by sequencing analyses. Deletion of the entire FgBNI4 or disruptions of its conserved C-terminal region could suppress the defects of Fgyck1 in hyphal growth and conidiation, indicating the genetic relationship between FgYCK1 and FgBNI4. Furthermore, the Fgyck1 mutant showed defects in polarized growth, cell wall integrity, internalization of FgRho1 and vacuole fusion, which were all partially suppressed by deletion of FgBNI4. Overall, our results indicate a stage-specific functional relationship between FgYCK1 and FgBNI4, possibly via FgRho1 signaling for regulating polarized hyphal growth and cell wall integrity. Full article

(This article belongs to the Special Issue Fungal Diseases in Crops)

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