Bacterial effectors target the plant cell nucleus to subvert host transcription

Abstract

In order to promote virulence, Gram-negative bacteria have evolved the ability to inject so-called type III effector proteins into host cells. The plant cell nucleus appears to be a subcellular compartment repeatedly targeted by bacterial effectors. In agreement with this observation, mounting evidence suggests that manipulation of host transcription is a major strategy developed by bacteria to counteract plant defense responses. It has been suggested that bacterial effectors may adopt at least three alternative, although not mutually exclusive, strategies to subvert host transcription. T3Es may (1) act as transcription factors that directly activate transcription in host cells, (2) affect histone packing and chromatin configuration, and/or (3) target host transcription factor activity. Here, we provide an overview on how all these strategies may lead to host transcriptional re-programming and, as a result, to improved bacterial multiplication inside plant cells.

Figure 1. Schematic representation of different bacterial strategies to subvert host transcription following nuclear targeting of type III effectors. Using the type III secretion system, Gram-negative bacteria are able to inject effectors into the plant cell. Some effector proteins are targeted to the plant cell nucleus where they may display a range of molecular activities. (A) Effectors mimicking host transcriptional activators. TAL effectors from Xanthomonas spp are able to mimic eukaryotic TFs and directly activate transcription by binding to target host promoters. Although structurally distinct from TAL effectors, HsvG from P. agglomerans is also able to bind host promoters and activate transcription. (B) Effectors altering chromatin configuration. It has been proposed that bacterial effectors such as XopD from X. campestris, PopP2 from R. solanacearum and HopAI1 from P. syringae may affect histone post-translational modification and chromatin remodelling in a process that may modify the access to DNA of host TFs or the recruitment of transcription-associated components, thereby affecting transcription. (C) Effectors directly targeting host TFs. XopD from X. campestris physically interacts with the Arabidopsis TF AtMYB30, thereby repressing activation of AtMYB30 target gene expression and suppressing AtMYB30-mediated defense. Similarly, the interaction between PopP2 from R. solanacearum and the WRKY domain-containing Arabidopsis R protein RRS1-R may affect RRS1-R-mediated transcription and/or transcriptional activation by additional TFs. T3E, type III effector; TF, transcription factor.