scholarly journals Transcriptomic Analysis Reveals Candidate Genes Responding Maize Gray Leaf Spot Caused by Cercospora zeina

Plants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2257
Author(s):  
Wenzhu He ◽  
Yonghui Zhu ◽  
Yifeng Leng ◽  
Lin Yang ◽  
Biao Zhang ◽  
...  

Gray leaf spot (GLS), caused by the fungal pathogen Cercospora zeina (C. zeina), is one of the most destructive soil-borne diseases in maize (Zea mays L.), and severely reduces maize production in Southwest China. However, the mechanism of resistance to GLS is not clear and few resistant alleles have been identified. Two maize inbred lines, which were shown to be resistant (R6) and susceptible (S8) to GLS, were injected by C. zeina spore suspensions. Transcriptome analysis was carried out with leaf tissue at 0, 6, 24, 144, and 240 h after inoculation. Compared with 0 h of inoculation, a total of 667 and 419 stable common differentially expressed genes (DEGs) were found in the resistant and susceptible lines across the four timepoints, respectively. The DEGs were usually enriched in ‘response to stimulus’ and ‘response to stress’ in GO term analysis, and ‘plant–pathogen interaction’, ‘MAPK signaling pathways’, and ‘plant hormone signal transduction’ pathways, which were related to maize’s response to GLS, were enriched in KEGG analysis. Weighted-Genes Co-expression Network Analysis (WGCNA) identified two modules, while twenty hub genes identified from these indicated that plant hormone signaling, calcium signaling pathways, and transcription factors played a central role in GLS sensing and response. Combing DEGs and QTL mapping, five genes were identified as the consensus genes for the resistance of GLS. Two genes, were both putative Leucine-rich repeat protein kinase family proteins, specifically expressed in R6. In summary, our results can provide resources for gene mining and exploring the mechanism of resistance to GLS in maize.

Plant Disease ◽  
1999 ◽  
Vol 83 (10) ◽  
pp. 884-895 ◽  
Author(s):  
Julian M. J. Ward ◽  
Erik L. Stromberg ◽  
David C. Nowell ◽  
Forrest W. Nutter

Plant Disease ◽  
2005 ◽  
Vol 89 (6) ◽  
pp. 624-630 ◽  
Author(s):  
P. A. Paul ◽  
G. P. Munkvold

Controlled environment studies were conducted to determine the effects of temperature on the expansion of lesions of gray leaf spot, and the effects of temperature and relative humidity on the sporulation of Cercospora zeae-maydis on maize (Zea mays). For the lesion expansion experiment, potted maize plants were spray inoculated at growth stage V6, bagged, and incubated at 25 to 28°C and 100% relative humidity for 36 to 40 h. Symptomatic plants were transferred to growth chambers and exposed to constant temperatures of 25, 30, and 35°C. Lesion area (length by width) was measured at 4-day intervals for 17 days. For sporulation studies, lesions were excised from naturally infected maize leaves, measured, and incubated at constant temperature (20, 25, 30, or 35°C) and relative humidity (70, 80, 90, or 100%) for 72 h. Sporulation was estimated as the number of conidia per square centimeter of diseased leaf tissue. A quadratic function was used to model the relationship between log-transformed conidia per square centimeter at 100% relative humidity and temperature. Temperature had a significant effect on lesion expansion (P ≤ 0.05). At 25 and 30°C, the rate of lesion expansion was significantly higher than at 35°C (P ≤ 0.05). The largest lesions and the highest mean rate of lesion expansion were observed at 30°C; however, the mean lesion expansion rate at this temperature was not significantly different from that at 25°C. The interaction effect of temperature and relative humidity on the log of conidia per square centimeter of diseased tissue was significant (P ≤ 0.05). At 100% relative humidity, the effect of temperature on sporulation was significant (P ≤ 0.05), with maximum spore production occurring at 25 and 30°C. The quadratic model explained between 49 and 80% of the variation in the log of conidia per square centimeter at 100% with variation in temperature. These results suggest that the rapid increase in gray leaf spot severity generally observed during mid- and late summer may be due to favorable conditions for lesion expansion during this period. When relative humidity is >95%, expanding lesions may serve as a source of inoculum for secondary infections.


Plant Disease ◽  
2003 ◽  
Vol 87 (9) ◽  
pp. 1072-1076 ◽  
Author(s):  
Philip F. Harmon ◽  
Larry D. Dunkle ◽  
Richard Latin

Gray leaf spot caused by Magnaporthe oryzae is a serious disease of perennial ryegrass in the midwestern United States. Symptoms of gray leaf spot can be confused with those caused by other fungal diseases that also are common during periods of high temperatures and ample moisture. Because turf managers must select appropriate fungicides for remedial treatment, accurate and timely identification of the pathogen is essential for efficient and effective disease management. We developed and evaluated a polymerase chain reaction (PCR)-based method to detect M. oryzae in infected perennial ryegrass tissue. The method utilizes a commercially available kit that is used for isolation and amplification of plant DNA from leaf tissue. The kit protocol was modified and found to be reliable for the extraction of M. oryzae DNA from infected perennial ryegrass. Primers were designed to amplify a 687-bp fragment of the Pot2 transposon that is found in multiple copies in the genome of the pathogen. The protocol amplified amounts of purified DNA as low as 5 pg and consistently and specifically detected M. oryzae in single diseased leaf blades as well as in field samples of infected perennial ryegrass. The total time required for detection was approximately 4 to 8 h.


Plant Disease ◽  
2012 ◽  
Vol 96 (8) ◽  
pp. 1227-1227 ◽  
Author(s):  
A. Nasehi ◽  
J. B. Kadir ◽  
M. A. Zainal Abidin ◽  
M. Y. Wong ◽  
F. Abed Ashtiani

Symptoms of gray leaf spot were first observed in June 2011 on pepper (Capsicum annuum) plants cultivated in the Cameron Highlands and Johor State, the two main regions of pepper production in Malaysia (about 1,000 ha). Disease incidence exceeded 70% in severely infected fields and greenhouses. Symptoms initially appeared as tiny (average 1.3 mm in diameter), round, orange-brown spots on the leaves, with the center of each spot turning gray to white as the disease developed, and the margin of each spot remaining dark brown. A fungus was isolated consistently from the lesions using sections of symptomatic leaf tissue surface-sterilized in 1% NaOCl for 2 min, rinsed in sterile water, dried, and plated onto PDA and V8 agar media (3). After 7 days, the fungal colonies were gray, dematiaceous conidia had formed at the end of long conidiophores (19.2 to 33.6 × 12.0 to 21.6 μm), and the conidia typically had two to six transverse and one to four longitudinal septa. Fifteen isolates were identified as Stemphylium solani on the basis of morphological criteria described by Kim et al. (3). The universal primers ITS5 and ITS4 were used to amplify the internal transcribed spacer region (ITS1, 5.8, and ITS2) of ribosomal DNA (rDNA) of a representative isolate (2). A 570 bp fragment was amplified, purified, sequenced, and identified as S. solani using a BLAST search with 100% identity to the published ITS sequence of an S. solani isolate in GenBank (1). The sequence was deposited in GenBank (Accession No. JQ736024). Pathogenicity of the fungal isolate was tested by inoculating healthy pepper leaves of cv. 152177-A. A 20-μl drop of conidial suspension (105 spores/ml) was used to inoculate each of four detached, 45-day-old pepper leaves placed on moist filter papers in petri dishes (4). Four control leaves were inoculated similarly with sterilized, distilled water. The leaves were incubated at 25°C at 95% relative humidity for 7 days. Gray leaf spot symptoms similar to those observed on the original pepper plants began to develop on leaves inoculated with the fungus after 3 days, and S. solani was consistently reisolated from the leaves. Control leaves did not develop symptoms and the fungus was not reisolated from these leaves. Pathogenicity testing was repeated with the same results. To our knowledge, this is the first report of S. solani causing gray leaf spot on pepper in Malaysia. References: (1) S. F. Altschul et al. Nucleic Acids Res. 25:3389, 1997. (2) M. P. S. Camara et al. Mycologia 94:660, 2002. (3) B. S. Kim et al. Plant Pathol. J. 15:348, 1999. (4) B. M. Pryor and T. J. Michailides. Phytopathology 92:406, 2002.


2020 ◽  
Vol 71 (1) ◽  
pp. 327-353 ◽  
Author(s):  
Miguel A. Blázquez ◽  
David C. Nelson ◽  
Dolf Weijers

This review focuses on the evolution of plant hormone signaling pathways. Like the chemical nature of the hormones themselves, the signaling pathways are diverse. Therefore, we focus on a group of hormones whose primary perception mechanism involves an Skp1/Cullin/F-box-type ubiquitin ligase: auxin, jasmonic acid, gibberellic acid, and strigolactone. We begin with a comparison of the core signaling pathways of these four hormones, which have been established through studies conducted in model organisms in the Angiosperms. With the advent of next-generation sequencing and advanced tools for genetic manipulation, the door to understanding the origins of hormone signaling mechanisms in plants beyond these few model systems has opened. For example, in-depth phylogenetic analyses of hormone signaling components are now being complemented by genetic studies in early diverging land plants. Here we discuss recent investigations of how basal land plants make and sense hormones. Finally, we propose connections between the emergence of hormone signaling complexity and major developmental transitions in plant evolution.


2015 ◽  
Vol 40 (6) ◽  
pp. 368-374 ◽  
Author(s):  
Danilo L. Neves ◽  
Cleiltan N. Silva ◽  
Carolina B. Pereira ◽  
Hercules D. Campos ◽  
Dauri J. Tessmann

2017 ◽  
Vol 30 (9) ◽  
pp. 710-724 ◽  
Author(s):  
Velushka Swart ◽  
Bridget G. Crampton ◽  
John B. Ridenour ◽  
Burt H. Bluhm ◽  
Nicholas A. Olivier ◽  
...  

Gray leaf spot (GLS), caused by the sibling species Cercospora zeina or Cercospora zeae-maydis, is cited as one of the most important diseases threatening global maize production. C. zeina fails to produce cercosporin in vitro and, in most cases, causes large coalescing lesions during maize infection, a symptom generally absent from cercosporin-deficient mutants in other Cercospora spp. Here, we describe the C. zeina cercosporin toxin biosynthetic (CTB) gene cluster. The oxidoreductase gene CTB7 contained several insertions and deletions as compared with the C. zeae-maydis ortholog. We set out to determine whether complementing the defective CTB7 gene with the full-length gene from C. zeae-maydis could confer in vitro cercosporin production. C. zeina transformants containing C. zeae-maydis CTB7 were generated by Agrobacterium tumefaciens–mediated transformation and were evaluated for in vitro cercosporin production. When grown on nitrogen-limited medium in the light—conditions conducive to cercosporin production in other Cercospora spp.—one transformant accumulated a red pigment that was confirmed to be cercosporin by the KOH assay, thin-layer chromatography, and ultra performance liquid chromatography-quadrupole-time-of-flight mass spectrometry. Our results indicated that C. zeina has a defective CTB7, but all other necessary machinery required for synthesizing cercosporin-like molecules and, thus, C. zeina may produce a structural variant of cercosporin during maize infection.


2019 ◽  
Vol 47 ◽  
pp. 64-72 ◽  
Author(s):  
John L Bowman ◽  
Liam N Briginshaw ◽  
Tom J Fisher ◽  
Eduardo Flores-Sandoval

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