Taking advantage of a pathogen: understanding how a virus alleviates plant stress response

Rena Gorovits,Iris Sobol,Ghandi Anfoka,Miasser Altaleb,Henryk Czosnek

doi:10.1186/s42483-019-0028-4

Abstract

The simplicity of Tomato yellow leaf curl virus (TYLCV) genome, encoding six proteins only, contrasts with the complexity of its impact on tomato plants. In this review, we discuss our understanding of how TYLCV proteins establish infection, and how the virus suppresses the effects of several abiotic stresses. TYLCV counteracts cell death induced by other factors, such as inactivation of HSP90 functions. Suppression of plant death is associated with the inhibition of the ubiquitin 26S proteasome degradation and with a deactivation of the heat shock transcription factor HSFA2 pathways. In order to ensure its own life cycle and spread, TYLCV protects the infected host from various unfriendly stresses, and this property can be exploited to protect crops from environmental stresses.

Highlights

In tropical and sub-tropical countries, tomatoes grown in the field in the spring and summer, are frequently exposed to temperatures of 40 o C, often in combination with Tomato yellow leaf curl virus (TYLCV) infection
We have shown that cell death was induced by the inactivation of HSP90 as well as by silencing the genes Hsp90 and Sgt1 (HSP90 co-chaperone), which led to the accumulation of damaged ubiquitinated proteins
Transcript profiling of tomato plants showed that genes affected by high temperatures included those encoding for heat shock proteins (HSPs), osmolytes, enzymes that affect the membrane fluidity and enzymes involved in reactive oxygen species (ROS) homeostasis (Frank et al 2009)

Summary

Introduction

In tropical and sub-tropical countries, tomatoes grown in the field in the spring and summer, are frequently exposed to temperatures of 40 o C (and higher), often in combination with Tomato yellow leaf curl virus (TYLCV) infection. In TYLCV infected tomatoes, a significant reduction in the levels of transcription and translation of the heat-inducible genes leads to reduced cell death. We described the suppression of host cell death, induced by inhibition of HSP90 and its co-chaperone SGT1, in tomato plants infected by TYLCV (Moshe et al 2016).

Results

Conclusion