Display options
Cite
Chang SP, Jeon YH, Kim YH. Defense-Related Responses in Fruit of the Nonhost Chili Pepper against Xanthomonas axonopodis pv. glycines Infection. Plant Pathol J. 2016;32(4):311-20doi: 10.5423/PPJ.OA.12.2015.0256.
Chang, S. P., Jeon, Y. H., & Kim, Y. H. (2016). Defense-Related Responses in Fruit of the Nonhost Chili Pepper against Xanthomonas axonopodis pv. glycines Infection. The plant pathology journal, 32(4), 311-20. https://doi.org/10.5423/PPJ.OA.12.2015.0256
Chang, Sung Pae, et al. "Defense-Related Responses in Fruit of the Nonhost Chili Pepper against Xanthomonas axonopodis pv. glycines Infection." The plant pathology journal vol. 32,4 (2016): 311-20. doi: https://doi.org/10.5423/PPJ.OA.12.2015.0256
Chang SP, Jeon YH, Kim YH. Defense-Related Responses in Fruit of the Nonhost Chili Pepper against Xanthomonas axonopodis pv. glycines Infection. Plant Pathol J. 2016 Aug;32(4):311-20. doi: 10.5423/PPJ.OA.12.2015.0256. Epub 2016 Aug 01. PMID: 27493606; PMCID: PMC4968641.
Copy Download .nbib Format: NLM
Share it on

Plant Pathol J. 2016 Aug;32(4):311-20. doi: 10.5423/PPJ.OA.12.2015.0256. Epub 2016 Aug 01.

Defense-Related Responses in Fruit of the Nonhost Chili Pepper against Xanthomonas axonopodis pv. glycines Infection.

The plant pathology journal

Sung Pae Chang, Yong Ho Jeon, Young Ho Kim

Affiliations

  1. Department of Agricultural Biotechnology and Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Korea; Animal and Plant Quarantine Agency, Anyang 14089, Korea.
  2. Department of Bioresource Sciences, Andong National University, Andong 36729, Korea.
  3. Department of Agricultural Biotechnology and Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Korea.

PMID: 27493606 PMCID: PMC4968641 DOI: 10.5423/PPJ.OA.12.2015.0256

Abstract

Xanthomonas axonopodis pv. glycines (Xag ) is a necrotrophic bacterial pathogen of the soybean that causes bacterial pustules and is a nonhost pathogen of the chili pepper. In the current study, chili pepper fruit wound inoculated in planta with Xag 8ra formed necrotic lesions on the fruit surface and induced several structural and chemical barriers systemically in the fruit tissue. The initial defense response included programmed cell death of necrotizing and necrotized cells, which was characterized by nuclear DNA cleavage, as detected by TUNEL-confocal laser scanning microscopy (CLSM), and phosphatidylserine exposure on cell walls distal to the infection site, as detected by Annexin V FLUOS-CLSM. These two responses may facilitate cell killing and enhance transportation of cell wall materials used for cell wall thickening, respectively. The cells beneath the necrotic tissue were enlarged and divided to form periclinal cell walls, resulting in extensive formation of several parallel boundary layers at the later stages of infection, accompanying the deposition of wall fortification materials for strengthening structural defenses. These results suggest that nonhost resistance of chili pepper fruit against the nonhost necrotrophic pathogen Xag 8ra is activated systematically from the initial infection until termination of the infection cycle, resulting in complete inhibition of bacterial pathogenesis by utilizing organ-specific in situ physiological events governed by the expression of genes in the plant fruit organ.

Keywords: Xanthomonas axonopodis pv. glycines; chili pepper; hypersensitive response; programmed cell death

References

  1. Sci Prog. 1998;81 ( Pt 1):35-68 - PubMed
  2. Int Rev Cytol. 1980;68:251-306 - PubMed
  3. Cytometry. 1998 Jan 1;31(1):1-9 - PubMed
  4. Nature. 1980 Apr 10;284(5756):555-6 - PubMed
  5. Exp Cell Res. 1997 Sep 15;235(2):421-30 - PubMed
  6. J Ultrastruct Res. 1969 Jan;26(1):31-43 - PubMed
  7. Plant J. 2007 Aug;51(4):604-16 - PubMed
  8. Chromosoma. 2006 Apr;115(2):89-97 - PubMed
  9. Curr Opin Plant Biol. 2000 Aug;3(4):315-9 - PubMed
  10. Trends Biotechnol. 2003 Apr;21(4):178-83 - PubMed
  11. Plant J. 2015 Jan;81(1):81-94 - PubMed
  12. Nature. 2006 Nov 16;444(7117):323-9 - PubMed
  13. Plant Physiol. 2012 Apr;158(4):1789-802 - PubMed
  14. Nature. 2010 Nov 25;468(7323):527-32 - PubMed
  15. Annu Rev Phytopathol. 2005;43:205-27 - PubMed
  16. Science. 2011 Mar 4;331(6021):1185-8 - PubMed
  17. Plant Physiol. 2005 May;138(1):80-91 - PubMed
  18. Crit Rev Biochem Mol Biol. 2009 Sep-Oct;44(5):264-77 - PubMed
  19. Cell. 1994 May 20;77(4):551-63 - PubMed
  20. Physiol Plant. 2012 May;145(1):114-20 - PubMed
  21. Mol Plant Microbe Interact. 2008 Feb;21(2):269-82 - PubMed
  22. Phytopathology. 2002 Sep;92(9):964-9 - PubMed
  23. Annu Rev Phytopathol. 2013;51:407-27 - PubMed
  24. Plant Cell. 2000 Dec;12(12):2441-2454 - PubMed
  25. J Immunol Methods. 1991 Jun 3;139(2):271-9 - PubMed
  26. J Nematol. 1987 Apr;19(2):177-87 - PubMed
  27. Trends Plant Sci. 2004 Feb;9(2):97-104 - PubMed
  28. Toxicol Pathol. 2007 Jun;35(4):495-516 - PubMed
  29. Annu Rev Phytopathol. 2008;46:101-22 - PubMed
  30. Trends Plant Sci. 2004 May;9(5):211-4 - PubMed
  31. Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13500-5 - PubMed
  32. Clin Microbiol Rev. 1999 Oct;12(4):564-82 - PubMed
  33. Lab Invest. 1998 Aug;78(8):893-913 - PubMed
  34. Mol Plant Microbe Interact. 2014 May;27(5):403-14 - PubMed
  35. Phytopathology. 2004 Dec;94(12):1295-304 - PubMed

Publication Types