The expression of potato expansin A3 (StEXPA3) and extensin4 (StEXT4) genes with distribution of StEXPAs and HRGPs-extensin changes as an effect of cell wall rebuilding in two types of PVYNTN–solanum tuberosum interactions

Katarzyna Otulak-Kozieł, Edmund Kozieł, Benham E.L. Lockhart, Józef J. Bujarski

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

The plant cell wall acts not only as a physical barrier, but also as a complex and dynamic structure that actively changes under different biotic and abiotic stress conditions. The question is, how are the different cell wall compounds modified during different interactions with exogenous stimuli such as pathogens? Plants exposed to viral pathogens respond to unfavorable conditions on multiple levels. One challenge that plants face under viral stress is the number of processes required for differential cell wall remodeling. The key players in these conditions are the cell wall genes and proteins, which can be regulated in specific ways during the interactions and have direct influences on the rebuilding of the cell wall structure. The cell wall modifications occurring in plants during viral infection remain poorly described. Therefore, this study focuses on cell wall dynamics as an effect of incompatible interactions between the potato virus Y (PVYNTN) and resistant potatoes (hypersensitive plant), as well as compatible (susceptible plant) interactions. Our analysis describes, for the first time, the expression of the potato expansin A3 (StEXPA3) and potato extensin 4 (StEXT4) genes in PVYNTN-susceptible and -resistant potato plant interactions. The results indicated a statistically significant induction of the StEXPA3 gene during a susceptible response. By contrast, we demonstrated the predominantly gradual activation of the StEXT4 gene during the hypersensitive response to PVYNTN inoculation. Moreover, the in situ distributions of expansins (StEXPAs), which are essential cell wall-associated proteins, and the hydroxyproline-rich glycoprotein (HRGP) extensin were investigated in two types of interactions. Furthermore, cell wall loosening was accompanied by an increase in StEXPA deposition in a PVYNTN-susceptible potato, whereas the HRGP content dynamically increased during the hypersensitive response, when the cell wall was reinforced. Ultrastructural localization and quantification revealed that the HRGP extensin was preferably located in the apoplast, but deposition in the symplast was also observed in resistant plants. Interestingly, during the hypersensitive response, StEXPA proteins were mainly located in the symplast area, in contrast to the susceptible potato where StEXPA proteins were mainly observed in the cell wall. These findings revealed that changes in the intracellular distribution and abundance of StEXPAs and HRGPs can be differentially regulated, depending on different types of PVYNTN–potato plant interactions, and confirmed the involvement of apoplast and symplast activation as a defense response mechanism.

Original languageEnglish (US)
Article number66
JournalViruses
Volume12
Issue number1
DOIs
StatePublished - Jan 5 2020

Bibliographical note

Funding Information:
Funding: The work was financed by National Science Center, Poland, NCN project number: 2018/02/X/NZ9/00832 given to K. O.-K.

Funding Information:
The work was financed by National Science Center, Poland, NCN project number: 2018/02/X/NZ9/00832 given to K. O.-K. The authors would like to thank A. Przewodowska and Dorota Micha?owska (IHAR-PIB, Bonin, Poland) for kindly providing potato tubers, and E. Znojek for her excellent ultramicrotome work. The authors would like to express sincere thanks to Emily A. Wilkes for English editing process.

Publisher Copyright:
© 2020 by the authors.

Keywords

  • Expansin
  • Extensin
  • Hypersensitive response
  • Plant cell wall
  • Potato virus Y-host interaction

Fingerprint

Dive into the research topics of 'The expression of potato expansin A3 (StEXPA3) and extensin4 (StEXT4) genes with distribution of StEXPAs and HRGPs-extensin changes as an effect of cell wall rebuilding in two types of PVYNTN–solanum tuberosum interactions'. Together they form a unique fingerprint.

Cite this