Tomato plant cell death induced by inhibition of HSP90 is alleviated by Tomato yellow leaf curl virus infection

Adi Moshe, Rena Gorovits, Yule Liu, Henryk Czosnek*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

39 Scopus citations

Abstract

To ensure a successful long-term infection cycle, begomoviruses must restrain their destructive effect on host cells and prevent drastic plant responses, at least in the early stages of infection. The monopartite begomovirus Tomato yellow leaf curl virus (TYLCV) does not induce a hypersensitive response and cell death on whitefly-mediated infection of virus-susceptible tomato plants until diseased tomatoes become senescent. The way in which begomoviruses evade plant defences and interfere with cell death pathways is still poorly understood. We show that the chaperone HSP90 (heat shock protein 90) and its co-chaperone SGT1 (suppressor of the G2 allele of Skp1) are involved in the establishment of TYLCV infection. Inactivation of HSP90, as well as silencing of the Hsp90 and Sgt1 genes, leads to the accumulation of damaged ubiquitinated proteins and to a cell death phenotype. These effects are relieved under TYLCV infection. HSP90-dependent inactivation of 26S proteasome degradation and the transcriptional activation of the heat shock transcription factors HsfA2 and HsfB1 and of the downstream genes Hsp17 and Apx1/2 are suppressed in TYLCV-infected tomatoes. Following suppression of the plant stress response, TYLCV can replicate and accumulate in a permissive environment.

Original languageAmerican English
Pages (from-to)247-260
Number of pages14
JournalMolecular Plant Pathology
Volume17
Issue number2
DOIs
StatePublished - 1 Feb 2016

Bibliographical note

Publisher Copyright:
© 2015 BSPP and John Wiley & Sons Ltd.

Keywords

  • Cell death
  • Geminivirus
  • HSP90
  • Heat stress transcription factor

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