Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 -- 2276 2023-02-23 09:34:20 |
2 update references and layout Meta information modification 2276 2023-02-23 10:37:40 |

Video Upload Options

Do you have a full video?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Zhao, R.; Kang, I.; Lee, S. Xanthomonas citri pv. glycines in Soybean. Encyclopedia. Available online: https://encyclopedia.pub/entry/41580 (accessed on 16 June 2024).
Zhao R, Kang I, Lee S. Xanthomonas citri pv. glycines in Soybean. Encyclopedia. Available at: https://encyclopedia.pub/entry/41580. Accessed June 16, 2024.
Zhao, Ruihua, In-Jeong Kang, Sungwoo Lee. "Xanthomonas citri pv. glycines in Soybean" Encyclopedia, https://encyclopedia.pub/entry/41580 (accessed June 16, 2024).
Zhao, R., Kang, I., & Lee, S. (2023, February 23). Xanthomonas citri pv. glycines in Soybean. In Encyclopedia. https://encyclopedia.pub/entry/41580
Zhao, Ruihua, et al. "Xanthomonas citri pv. glycines in Soybean." Encyclopedia. Web. 23 February, 2023.
Xanthomonas citri pv. glycines in Soybean
Edit

Soybean [Glycine max (L.) Merr.] is an economically important crop with high protein and oil contents. A range of biotic stresses constantly threaten soybean production and lead to decreases in yield and quality, bacterial pustule caused by Xanthomonas citri pv. glycines (Xcg) is one of the most destructive diseases affecting worldwide soybean production.

soybean bacterial pustule diversity of Xanthomonas citri pv. glycines (Xcg)

1. Introduction

Soybean [Glycine max (L.) Merr.] is the most economically important legume crop and provides edible oil and protein used in food, feed, and industrial products worldwide [1][2][3]. The percentages of oil and protein in soybean seeds are almost 18.0% and 38.0%, respectively [4]. As estimated, almost 40.0% of the edible vegetable oil consumed worldwide is produced from soybeans [5]. Unfortunately, soybean is susceptible to numerous pests and pathogens, including aphids, beetles, mites, stinkbugs, nematodes, viruses, bacteria, oomycetes, and fungi, resulting in decreased yield and quality [6][7][8]. For example, the cumulative economic loss from 1996 to 2016 due to 23 diseases across 28 states in the United States was $73,535 per hectare [9]. These 23 diseases can be grouped into six categories: stem/root, nematode, foliar, bacteria, virus, and other diseases. Of these, infection with bacterial diseases specifically results in a $529 per hectare loss at the national level (across 28 states and 21 years) [9].
Bacterial pustule (BP) caused by Xanthomonas citri pv. glycines (Xcg) is one of the most significant bacterial diseases in susceptible soybean genotypes worldwide [10]. Over the last 120 years, the identification and distribution of Xcg has been continuously documented around the world [11][12][13][14][15][16][17][18]. Several genetic studies have identified genomic regions associated with resistance to Xcg using mapping populations and collections of soybean accessions [10][19][20][21][22][23][24][25][26][27], with a 33-kb region located on chromosome 17 often identified as a strong candidate locus [20]. Molecular markers associated with resistance to Xcg have also been reported in a few studies. Genome-wide gene expression was compared between soybean near-isogenic lines carrying either a BP-resistant or -susceptible allele following inoculation with Xcg [28]. However, resistance genes for Xcg have yet to be cloned, and much remains unknown despite these efforts. Recent research has revealed that the genetic diversity of BP isolates is increasing, and molecular evidence suggests that a population shift has occurred in Xcg during the past 20 years [13][16][29]. Climate change also increases the possibility of changes in the Xcg population, but little work has been done in the past decade to mine new genetic sources and identify resistance genes/quantitative trait loci (QTLs).

2. Bacterial Pustule and Its Causal Agent Xanthomonas citri pv. glycines

Xanthomonas citri pv. glycines (Xcg) is the causal agent of BP [30]. Hedges [31] first identified the typical pustule symptoms caused by this disease and named the causal agent Bacterium phaseoli var. sojense. The pathogen was later reclassified to Xanthomonas campestris pv. glycines [32] and then Xanthomonas axonopodis pv. glycines through DNA–DNA hybridization analysis [33] before finally receiving the name Xanthomonas citri pv. glycines [30].
Xcg is a Gram-negative, aerobic, and motile bacterium with a single polar flagellum. It is rod shaped, with sizes of 0.5–0.9 μm (width) × 1.4–2.3 μm (length). This bacterium can grow at 10–40 °C (but grows optimally at 30–33 °C in wet conditions) and at a pH of 4.0–8.0 (optimal pH = 7.0). Colonies on tryptic soy agar are small, circular, and smooth, and have entire margins. The bacterium grows slowly in culture and is known to produce auxins, cytokinin, bacteriocins, toxins, and extracellular polysaccharides, among other molecules [34][35][36][37].
Several molecular biology tools and techniques, including polymerase chain reaction (PCR) and real-time quantitative PCR (qPCR), have been used to detect Xcg directly in plant tissues and seeds. Primers for DNA hybridization and conventional PCR have been developed for the glycinecin A (glyA) gene [38][39] and the PstI fragment containing the open reading frame of the TAL gene [40]. Real-time PCR methods based on the rpoD gene can also detect the presence of Xcg and quantify the degree of Xcg contamination in seeds [41].
DNA sequences of various genes have been utilized to analyze the genetic relatedness of different species within the genus Xanthomonas, as well as that of different strains within the species X. citri. According to Constantin et al. [30], a gyrB fragment was selected as an effective target gene for the identification of Xanthomonas taxa [42].
For differentiation within Xanthomonas species, multi-locus sequence analysis (MLSA) has been used in phylogenetic analysis, and recently, 109 Xanthomonas strains were distinguished based on seven housekeeping genes (atpD, dnaK, efp, glnA, gyrB, rpoD, lepA, and lrp) [30][43]. These analyses showed that Xcg is closely related to some pathogenic bacterial species on different hosts, namely X. axonopodis pv. citri and X. citri pv. mangiferaeindicae, but it is relatively distant from X. campestris pv. syngonii and X. axonopodis pv. axonopodis [30].
Key symptoms of BP, shown in Figure 1, include small, yellowish spots that later turn reddish-brown and slightly raised pustules in the center of the lesions [44]. The pustules often arise through hypertrophic changes in the parenchymatous tissues of the host responding to the bacterial infection. Pustule production on soybean leaves is known to be accompanied by a drastic increase in indole-3-acetic acid content in host tissues [45]. These lesions often occur on the abaxial side of leaves and vary from specks to large, irregularly shaped, and mottled-brown areas, which develop when the lesions coalesce. The leaf spots can form without developing pustules.
Figure 1. Bacterial pustule symptom caused by Xanthomonas citri pv. glycines on a susceptible soybean genotype.
The etiology of BP is fairly well understood. Xcg can infect common bean and cowpea as well as soybean [46]. It overwinters in seeds, on plant debris in the soil, and in the soil itself. Xcg enters the plant through natural openings and wounds, where it multiplies intercellularly. Xcg invades and multiplies within the apoplast, causing localized leaf spots or leaf streaks [47]. Plant-to-seed infection occurs via the vascular system through the funiculus as well as through infected pods. Seeds can also get contaminated with the bacterium during threshing after harvest. Infections are more common on younger leaves, which are more susceptible than older leaves, although the disease appears at all stages of plant growth [22][48][49]. Disease incidence depends on the susceptibility of the soybean genotype, virulence of the pathogen, and favorability of weather conditions. Bacterial cells are spread by wind-blown rain, by rain splashing up from old crop residue, and during field work when the canopy is wet. For the disease to occur, soil- and seed-borne inocula must be spread during warm and humid weather, which promotes fast multiplication of the bacterium. Kang et al. [29] reported that disease severity of BP in Korea is often correlated with the amount of precipitation in August when soybean plants are at the flowering stage. Thus, especially wet conditions are likely to be one of the main factors contributing to a high incidence of BP.

3. Distribution and Population Diversity of Xcg

Xcg is widely distributed and commonly occurs in major soybean-producing countries such as Brazil, the United States, China, Korea, Thailand, Australia, and Benin [50]. In recent years, disease severities of up to 26% and incidences of up to 70% have been reported in several countries [18][51]. In addition, the bacterium was reported to be present in areas where it had not previously been found. For instance, in the United States, the disease had commonly been found in the southern region, but more recently it was also reported as far north as North Dakota [15]. In China, the disease is most severe in South China, especially in the Yangtze and Huai River Basins. The incidence of BP has been increasing due to global warming and the more frequent occurrence of storms [16][52]. It was also reported that BP occurred during all four seasons in the northern coastal region of New South Wales, Australia [53]. In Benin, Africa, BP was present in 33 of 34 sites in the Guinea Savanna, with mean incidence varying from 15 to 70% [18]. In Korea, BP occurs nationwide and can be observed from July to September. During the 1990s and 2000s, BP was so severe that it could be observed in 86–89% of all soybean fields in Korea [54].
Strains of the BP pathogen have been shown to fall into distinct races [29][42][55][56] that differ in aggressiveness [57]. Hwang et al. [42] evaluated the pathogenic variability of 63 Xcg isolates in a set of 11 differential soybean cultivars, including Chippewa, Harosoy, Mukden, Pella, and Williams. Based on the results of this experiment, they classified the isolates into five races, designated 1, 2, 3, 4, and 5. Similarly, Kaewnum et al. [57] demonstrated that 26 Xcg isolates from Thailand differed in their capability to induce disease on soybean cultivars and in their ability to induce a hypersensitive response (HR) in a range of plant species, including tobacco (Nicotiana tabacum), cucumber (Cucumis sativus), pea (Pisum sativum), and sesame (Sesamum indicum). They classified these Thai Xcg isolates into three races based on the presence of an avr gene that contributes to differential virulence on soybean cultivars. Park et al. [56] classified 155 Xcg isolates from Korea into six groups based on the number and size of genomic fragments hybridizing with an avrBs3 gene family probe, as differences in avrBs3 content are correlated with resistance and/or aggressiveness. They also identified six type strains that represent these groups. As a follow-up to that study, Kang et al. [29] characterized the diversity of a nationwide collection of 106 Korean Xcg isolates based on avrBs3 banding patterns and reported that the diversity of Xcg strains increased during the last two decades. They also documented the emergence of new type strains along with new dominant strains.

4. Molecular Mechanisms Underlying Bacterial Pustule Formation in Soybean

During disease establishment, Xanthomonas pathogens such as Xcg employ various virulence factors, including adhesins, polysaccharides, lipopolysaccharides, and degradative enzymes. One key pathogenicity factor is the type III secretion system (T3SS), which enables bacteria to directly inject effector proteins into the host cell cytosol. The type III (T3) effectors are translocated into the host cells, where they interfere with host immunity responses or facilitate the nutritional or virulence processes of the pathogen [47][58][59]. The T3SS is encoded by the hypersensitive reaction and pathogenicity (hrp), hrp-conserved (hrc), and avirulence (avr) genes and reacts with specific resistance (R) receptors. Effector proteins are encoded by hrp-dependent out protein (hop) genes [60].
Kim et al. [61] characterized the HrpT3SS and hpa (hrp-associated) virulence genes and identified HR-eliciting proteins such as HpaG in the Xcg genome. The pathogenicity island (PAI) contained seven plant-inducible promoter boxes and was composed of nine hrp, nine hrc, and eight hpa genes that are regulated by HrpG and HrpX. The Hrp PAI in Xcg resembled that of other Xanthomonas species, and the Hrp PAI core region was highly conserved.
The largest effector family found in the Xanthomonas spp. is the AvrBs3/PthA or TAL family. Xanthomonas strains express a combination of typically 20–40 T3 effectors. Xcg strains possess more than 30 T3 effectors and contain at least four homologs of avrBs3. It was reported that Korean Xcg strains display the greatest variation in avrBs3 homolog numbers, and their plasmids also carry several avrBs3 homologs [13]. According to Athinuwat et al. [55], the avrBs3 homolog avrXg1 contributes to increased bacterial establishment in soybean leaves and acts as a determinant for virulence specificity. Similarly, several TAL effectors from Xanthomonas oryzae pv. oryzae (Xoo) are essential virulence factors for the infection of rice (Oryza sativa) [47]. Meanwhile, a variety of transcription activator-like (TAL) effectors are known to be associated with pathogen virulence and disease symptoms, and the presence or absence of specific effectors can contribute to the pathogenicity on specific hosts [62]. The specificity of TAL effectors is determined by repeat-variable diresidues (RVDs), which allow binding to the promoter of the host plant [63]. Recently, whole-genome sequencing of Xcg strains revealed that the diversity and size of RVDs are limited within Xcg, and also predicted that the effector binding elements of the TAL effectors fall into six groups and are strongly overlapping in sequence [11]. This suggests that the target binding domains in soybean cultivars may evolve specifically. However, despite these studies, little is known about the corresponding host virulence targets of TAL effectors and their role in pathogenicity.
Previous research has identified candidate genes in soybean that relate to BP resistance (Table 1) [10][19][25][26][64][65]. Gene-encoding membrane proteins, zinc finger family proteins, LRR-RLK resistance proteins, Benzyl alcohol O-benzoyl transferase-like protein, MAIN-LIKE 1-like protein, Lateral organ boundaries (LOB), CASP-like protein 4A3, E3 ubiquitin-protein ligase SIS3-like, LATERAL ORGAN BOUNDARY1 and a defective hydroperoxide lyase (HPL) gene, among others, are related to BP resistance. The control of BP is complicated because many small QTLs influence plant resistance. However, soybean breeders could adopt gene cloning using the genes implicated in the disease resistance.
Table 1. Candidate genes for resistance to Xcg in the previous studies.
  Reference Chr.
(LG) a
Gene ID Position b Functional Annotation
1 Kim et al. 2010 [20] 17 (D2) Glyma.17g090100 7,020,522…7,022,065 Membrane protein At2g36330; Arabidopsis thaliana
    17 (D2) Glyma.17g090200 7,028,352…7,034,934 Zinc finger (C3HC4-type RING finger) family protein; Arabidopsis thaliana
2 Chang et al. 2016 [26] 1 (D1a) Glyma.01g197600 53,149,380…53,153,676 LRR-RLK resistance gene
    1 (D1a) Glyma.01g197800 53,170,021…53,173,875 LRR-RLK resistance gene
    11 (B1) Glyma.11g196800 27,106,029…27,107,951 LRR-RLK gene
    17 (D2) Glyma.17g090400 7,040,797…7,042,768 RLK gene
3 Zhang et al. 2018 [66] 2 (D1b) Glyma.02g108700 10,404,064…10,404,874 Calcium-binding EF-hand family protein
    2 (D1b) Glyma.02g110500 10,655,319…10,660,151 NB-ARC domain-containing disease resistance protein
    2 (D1b) Glyma.02g112300 10,900,201…10,902,765 NB-ARC domain-containing disease resistance protein
    2 (D1b) Glyma.02g120800 11,926,840…11,931,251 Leucine-rich repeat receptor-like protein kinase family protein
    17 (D2) Glyma.17g204600 33,223,552…33,226,195 Receptor-like protein 12
    17 (D2) Glyma.17g204300 33,083,927…33,090,560 Enhancer of polycomb-like transcription factor protein
    19 (L) Glyma.19g074900 27,195,325…27,202,148 LRR protein kinase family protein
4 Capobiango da Fonseca et al. 2021 [19] 3 (N) - - Benzyl alcohol O-benzoyl transferase-like (LOC100793892)
  15 (E) - - Protein MAIN-LIKE 1-like (LOC102667247)
5 Wang et al. 2020 [25] 12 (H) Glyma.12g191400 35,295,823…35,301,648 Defective hydroperoxide lyase (HPL) gene
6 Zhao et al. 2022 [10] 5 (A1) Glyma.05g040500 3,625,982…3,628,389 LBD domain-containing transcription factor
    17 (D2) Glyma.17g086300 6,660,761…6,663,277 Lateral organ boundaries (LOB) domain-containing protein 25
    17 (D2) Glyma.17g090100 7,020,522…7,022,065 CASP-like protein 4A3
    17 (D2) Glyma.17g090200 7,028,352…7,034,934 E3 ubiquitin-protein ligase SIS3-like
    17 (D2) Glyma.17g090400 7,040,797…7,042,768 Uncharacterized

a Chr., Chromosome; LG, Linkage group. b Physical positions (in base pairs) are based on the reference genome Glyma.Wm82.a2 (Glyma2).

References

  1. Lam, H.-M.; Xu, X.; Liu, X.; Chen, W.; Yang, G.; Wong, F.-L.; Li, M.-W.; He, W.; Qin, N.; Wang, B. Resequencing of 31 wild and cultivated soybean genomes identifies patterns of genetic diversity and selection. Nat. Genet. 2010, 42, 1053–1059.
  2. Gao, H.; Wang, Y.; Li, W.; Gu, Y.; Lai, Y.; Bi, Y.; He, C. Transcriptomic comparison reveals genetic variation potentially underlying seed developmental evolution of soybeans. J. Exp. Bot. 2018, 69, 5089–5104.
  3. Liu, S.; Zhang, M.; Feng, F.; Tian, Z. Toward a “green revolution” for soybean. Mol. Plant 2020, 13, 688–697.
  4. Shiriki, D.; Igyor, M.A.; Gernah, D.I. Nutritional evaluation of complementary food formulations from maize, soybean and peanut fortified with Moringa oleifera leaf powder. Food Nutr. Sci. 2015, 6, 494.
  5. Singh, G.; Dukariya, G.; Kumar, A. Distribution, importance and diseases of soybean and common bean: A review. Biotechnol. J. Int. 2020, 24, 86–98.
  6. Kumar, S. Diseases of soybean and their management. In Crop Diseases and Their Management; Apple Academic Press: New York, NY, USA, 2016; p. 295.
  7. Singh, G. The Soybean: Botany, Production and Uses; CABI: Wallingford, UK, 2010.
  8. Roth, M.G.; Webster, R.W.; Mueller, D.S.; Chilvers, M.I.; Faske, T.R.; Mathew, F.M.; Bradley, C.A.; Damicone, J.P.; Kabbage, M.; Smith, D.L. Integrated management of important soybean pathogens of the United States in changing climate. J. Integr. Pest Manag. 2020, 11, 17.
  9. Bandara, A.Y.; Weerasooriya, D.K.; Bradley, C.A.; Allen, T.W.; Esker, P.D. Dissecting the economic impact of soybean diseases in the United States over two decades. PLoS ONE 2020, 15, e0231141.
  10. Zhao, F.; Cheng, W.; Wang, Y.; Gao, X.; Huang, D.; Kong, J.; Antwi-Boasiako, A.; Zheng, L.; Yan, W.; Chang, F. Identification of novel genomic regions for bacterial leaf pustule (BLP) resistance in soybean (Glycine max L.) via integrating linkage mapping and association analysis. Int. J. Mol. Sci. 2022, 23, 2113.
  11. Wolf, B.F.A. Bacterial pustule of soybean. J. Agric. Res. 1924, 29, 57–68.
  12. Khare, U.; Khare, M.; Ansari, M. Bacterial pustule disease of soybean-present scenario and future strategies. Soybean Res. 2003, 1, 43–57.
  13. Kang, I.J.; Kim, K.S.; Beattie, G.A.; Yang, J.W.; Sohn, K.H.; Heu, S.; Hwang, I. Pan-genome analysis of effectors in Korean strains of the soybean pathogen Xanthomonas citri pv. glycines. Microorganisms 2021, 9, 2065.
  14. Kladsuwan, L.; Athinuwat, D.; Prathuangwong, S. Diversity of Xanthomonas axonopodis pv. glycines, the causal agent of bacterial pustule of soybean and specific primer for detection. J. Agric. 2018, 34, 77–87.
  15. Heitkamp, E.C.; Lamppa, R.S.; Lambrecht, P.A.; Harveson, R.M.; Mathew, F.M.; Markell, S.G. First report of bacterial pustule on soybeans in North Dakota. Plant Health Prog. 2014, 15, 155–156.
  16. Xu, Y.; Cheng, W.; Wu, H.; Zheng, L.; Zhao, T.; Gao, X. Identification of pathogen causing bacterial pustule spot of soybean and resistance evaluation of new soybean germplasm. Soybean Sci. 2015, 3, 463–469.
  17. Smith, E.F. Bacterial leaf spot diseases. Science 1904, 19, 417–418.
  18. Zinsou, V.; Afouda, L.; Zoumarou-Wallis, N.; Pate-Bata, T.; Dossou, L.; Götz, M.; Winter, S. Occurrence and characterisation of Xanthomonas axonopodis pv. glycines, causing bacterial pustules on soybean in Guinea Savanna of Benin. Afr. Crop Sci. J. 2015, 23, 203–210.
  19. Capobiango da Fonseca, P.; Maria Barbosa, M.R.; Ferreira, D.d.O.; Badel, J.L.; Schuster, I.; Vieira, R.F.; Lopes da Silva, F. Genome-wide association study reveals molecular markers and genes potentially associated with soybean (Glycine max) resistance to Xanthomonas citri pv. glycines. Plant Breed. 2021, 141, 37–48.
  20. Kim, D.H.; Kim, K.H.; Van, K.; Kim, M.Y.; Lee, S.-H. Fine mapping of a resistance gene to bacterial leaf pustule in soybean. Theor. Appl. Genet. 2010, 120, 1443–1450.
  21. Kim, K.-S.; Kim, M.Y.; Lee, S.-H. Development of molecular markers for Xanthomonas axonopodis resistance in soybean. Korean J. Crop Sci. 2004, 49, 429–433.
  22. Narvel, J.; Jakkula, L.; Phillips, D.; Wang, T.; Lee, S.-H.; Boerma, H. Molecular mapping of Rxp conditioning reaction to bacterial pustule in soybean. J. Hered. 2001, 92, 267–270.
  23. Seo, M.; Kang, S.-T.; Moon, J.-K.; Lee, S.; Kim, Y.-H.; Jeong, K.-H.; Yun, H.-T. Identification of quantitative trait loci associated with resistance to bacterial pustule (Xanthomonas axonopodis pv. glycines) in soybean. Korean J. Breed. Sci. 2009, 41, 456–462.
  24. Van, K.; Ha, B.-K.; Kim, M.Y.; Moon, J.K.; Paek, N.-C.; Heu, S.; Lee, S.-H. SSR mapping of genes conditioning soybean resistance to six isolates of Xanthomonas axonopodis pv. glycines. Genes Genom. 2004, 26, 47–54.
  25. Wang, Y.; Liu, M.; Ge, D.; Akhter Bhat, J.; Li, Y.; Kong, J.; Liu, K.; Zhao, T. Hydroperoxide lyase modulates defense response and confers lesion-mimic leaf phenotype in soybean (Glycine max (L.) Merr.). Plant J. 2020, 104, 1315–1333.
  26. Chang, H.-X.; Lipka, A.E.; Domier, L.L.; Hartman, G.L. Characterization of disease resistance loci in the USDA soybean germplasm collection using genome-wide association studies. Phytopathology 2016, 106, 1139–1151.
  27. Kim, K.H.; Park, J.-H.; Kim, M.Y.; Heu, S.; Lee, S.-H. Genetic mapping of novel symptom in response to soybean bacterial leaf pustule in PI 96188. J. Crop Sci. Biotechnol. 2011, 14, 119–123.
  28. Kim, K.H.; Kang, Y.J.; Shim, S.; Seo, M.-J.; Baek, S.-B.; Lee, J.-H.; Park, S.K.; Jun, T.H.; Moon, J.-K.; Lee, S.-H. Genome-wide RNA-seq analysis of differentially expressed transcription factor genes against bacterial leaf pustule in soybean. Plant Breed. Biotech. 2015, 3, 197–207.
  29. Kang, I.J.; Kim, K.S.; Beattie, G.A.; Chung, H.; Heu, S.; Hwang, I. Characterization of Xanthomonas citri pv. glycines population genetics and virulence in a national survey of bacterial pustule disease in Korea. Plant Pathol. J. 2021, 37, 652–661.
  30. Constantin, E.C.; Cleenwerck, I.; Maes, M.; Baeyen, S.; Van Malderghem, C.; De Vos, P.; Cottyn, B. Genetic characterization of strains named as Xanthomonas axonopodis pv. dieffenbachiae leads to a taxonomic revision of the X. axonopodis species complex. Plant Pathol. 2016, 65, 792–806.
  31. Hedges, F. Bacterial pustule of soybean. Science 1922, 56, 111–112.
  32. Nakano, K. Soybean leaf spot. J. Plant Prot. Tokyo 1919, 6, 217–221.
  33. Vauterin, L.; Hoste, B.; Kersters, K.; Swings, J. Reclassification of Xanthomonas. Int. J. Syst. Evol. Microbiol. 1995, 45, 472–489.
  34. Thowthampitak, J.; Shaffer, B.T.; Prathuangwong, S.; Loper, J.E. Role of rpfF in virulence and exoenzyme production of Xanthomonas axonopodis pv. glycines, the causal agent of bacterial pustule of soybean. phytopathology 2008, 98, 1252–1260.
  35. Fett, W.F.; Dunn, M.F.; Maher, G.T.; Maleeff, B.E. Bacteriocins and temperate phage of Xanthomonas campestris pv. glycines. Curr. Microbiol. 1987, 16, 137–144.
  36. Hwang, I.; Lim, S.; Shaw, P. Cloning and characterization of pathogenicity genes from Xanthomonas campestris pv. glycines. J. Bacteriol. 1992, 174, 1923–1931.
  37. Jones, S.B.; Fett, W. Fate of Xanthomonas campestris infiltrated into soybean leaves: An ultrastructural study. Phytopathology 1985, 75, 733–741.
  38. Oh, C.; Heu, S.; Park, Y.-C. Sensitive and pathovar-specific detection of Xanthormonas campestris pv. glycines by DNA hybridization and polymerase chain reaction analysis. Plant Pathol. J. 1999, 15, 57–61.
  39. Lee, Y.-H.; Kim, N.-G.; Yoon, Y.-N.; Lim, S.-T.; Kim, H.-T.; Yun, H.-T.; Baek, I.-Y.; Lee, Y.-K. Multiplex PCR assay for the simultaneous detection of major pathogenic bacteria in soybean. Korean J. Crop Sci. 2013, 58, 142–148.
  40. Khaeruni, A.; Suwanto, A.; Tjahjono, B.; Sinaga, M.S. Rapid detection of bacterial pustule disease on soybean employing PCR technique with specific primers. Hayati 2007, 14, 76.
  41. Watanabe, T.; Sawada, H. Detection and absolute quantification of Xanthomonas axonopodis pv. glycines from soybeans by real-time PCR. Jpn. J. Phytopathol. 2013, 79, 83–91.
  42. Hwang, I.; Lim, S. Pathogenic variability in isolates of Xanthomonas campestris pv. glycines. Plant Pathol. J. 1998, 14, 19–22.
  43. Barak, J.D.; Vancheva, T.; Lefeuvre, P.; Jones, J.B.; Timilsina, S.; Minsavage, G.V.; Vallad, G.E.; Koebnik, R. Whole-genome sequences of Xanthomonas euvesicatoria strains clarify taxonomy and reveal a stepwise erosion of type 3 effectors. Front. Plant Sci. 2016, 7, 1805.
  44. Groth, D.; Braun, E. Survival, seed transmission and epiphytic development of Xanthomonas campestris pv. glycines in the north-central United States. Plant Dis. 1989, 73, 326–330.
  45. Kim, H.-S.; Park, H.-J.; Heu, S.; Jung, J. Possible association of indole-3-acetic acid production by Xanthomonas axonopodis pv. glycines with development of pustule disease in soybean. J. Appl. Biol. Chem. 2001, 44, 173–176.
  46. Hartman, G.; Rupe, J.; Sikora, J.; Domier, L.; Davis, A.; Steffey, L. Compendium of Soybean Diseases; American Phytopathological Society: Saint Paul, MN, USA, 2015; pp. 19–20.
  47. Boch, J.; Bonas, U. Xanthomonas AvrBs3 family-type III effectors: Discovery and function. Annu. Rev. Phytopathol. 2010, 48, 419–436.
  48. Jones, S.B.; Fett, W.F. Bacterial pustule disease of soybean: Microscopy of pustule development in a susceptible cultivar. Phytopathology 1987, 77, 266–274.
  49. Phipps, P.; Koenning, S.; Rideout, S.L.; Stromberg, E.L.; Bush, E.A. Common Diseases of Soybean in the Mid-Atlantic Region; Virginia Cooperative Extension: Blacksburg, VA, USA, 2010; p. 10.
  50. Wrather, J.; Anderson, T.; Arsyad, D.; Tan, Y.; Ploper, L.D.; Porta-Puglia, A.; Ram, H.; Yorinori, J. Soybean disease loss estimates for the top ten soybean-producing counries in 1998. Can. J. Plant Pathol. 2001, 23, 115–121.
  51. Suryadi, Y.; Suhendar, M.; Akhdiya, A.; Manzila, I. Evaluation of soybean germplasm for its resistance to several foliar pathogens in Indonesia. Int. J. Agric. Technol. 2012, 8, 751–763.
  52. Zou, J.; Zhang, Z.; Yu, S.; Kang, Q.; Shi, Y.; Wang, J.; Zhu, R.; Ma, C.; Chen, L.; Wang, J. Responses of soybean genes in the substituted segments of segment substitution lines following a Xanthomonas infection. Front. Plant Sci. 2020, 11, 972.
  53. Stovold, G.; Smith, H. The prevalence and severity of diseases in the coastal soybean crop of New South Wales. Aust. J. Exp. Agric. 1991, 31, 545–550.
  54. Lee, S. Occurrence and characterization of major plant bacterial diseases in Korea. Ph.D. Thesis, Seoul National University, Seoul, Republic of Korea, 1999.
  55. Athinuwat, D.; Prathuangwong, S.; Cursino, L.; Burr, T. Xanthomonas axonopodis pv. glycines soybean cultivar virulence specificity is determined by avrBs3 homolog avrXg1. Phytopathology 2009, 99, 996–1004.
  56. Park, H.-J.; Han, S.-W.; Oh, C.-S.; Lee, S.-D.; Ra, D.-S.; Lee, S.-H.; Heu, S.-G. Avirulence gene diversity of Xanthomonas axonopodis pv. glycines isolated in Korea. J. Microbiol. Biotechnol. 2008, 18, 1500–1509.
  57. Kaewnum, S.; Prathuangwong, S.; Burr, T. Aggressiveness of Xanthomonas axonopodis pv. glycines isolates to soybean and hypersensitivity responses by other plants. Plant Pathol. 2005, 54, 409–415.
  58. Buttner, D.; He, S.Y. Type III protein secretion in plant pathogenic bacteria. Plant Physiol. 2009, 150, 1656–1664.
  59. Puhar, A.; Sansonetti, P.J. Type III secretion system. Curr. Biol. 2014, 24, R784–R791.
  60. Alfano, J.R.; Charkowski, A.O.; Deng, W.-L.; Badel, J.L.; Petnicki-Ocwieja, T.; Van Dijk, K.; Collmer, A. The Pseudomonas syringae Hrp pathogenicity island has a tripartite mosaic structure composed of a cluster of type III secretion genes bounded by exchangeable effector and conserved effector loci that contribute to parasitic fitness and pathogenicity in plants. Proc. Natl. Acad. Sci. USA 2000, 97, 4856–4861.
  61. Kim, J.-G.; Park, B.K.; Yoo, C.-H.; Jeon, E.; Oh, J.; Hwang, I. Characterization of the Xanthomonas axonopodis pv. glycines Hrp pathogenicity island. J. Bacteriol. 2003, 185, 3155–3166.
  62. Schwartz, A.R.; Potnis, N.; Timilsina, S.; Wilson, M.; Patané, J.; Martins, J., Jr.; Minsavage, G.V.; Dahlbeck, D.; Akhunova, A.; Almeida, N. Phylogenomics of Xanthomonas field strains infecting pepper and tomato reveals diversity in effector repertoires and identifies determinants of host specificity. Front. Microbiol. 2015, 6, 535.
  63. Liu, L.; Zhang, Y.; Liu, M.; Wei, W.; Yi, C.; Peng, J. Structural insights into the specific recognition of 5-methylcytosine and 5-hydroxymethylcytosine by TAL effectors. J. Mol. Biol. 2020, 432, 1035–1047.
  64. Kladsuwan, L.; Athinuwat, D.; Bogdanove, A.J.; Prathuangwong, S. AvrBs3-like genes and TAL effectors specific to race structure in Xanthomonas axonopodis pv. glycines. Thai J. Agric. Sci. 2017, 50, 121–145.
  65. Hu, Y.; Zhang, J.L.; Jia, H.G.; Sosso, D.; Li, T.; Frommer, W.B.; Yang, B.; White, F.F.; Wang, N.A.; Jones, J.B. Lateral organ boundaries 1 is a disease susceptibility gene for citrus bacterial canker disease. Proc. Natl. Acad. Sci. USA 2014, 111, 521–529.
  66. Zhang, W.; Li, Y.; Wang, C.; Sun, J.; Kang, Y.; Lin, Q.; Guo, Q. Resistance identification of soybean to bacterial rashes and QTL mapping of disease resistance. Mol. Plant Breed. 2018, 16, 5978–5986.
More
Information
Subjects: Agronomy
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : , ,
View Times: 529
Revisions: 2 times (View History)
Update Date: 23 Feb 2023
1000/1000
Video Production Service