An Oomycete CRN Effector Reprograms Expression of Plant HSP Genes by Targeting their Promoters

Abstract

Oomycete pathogens produce a large number of CRN effectors to manipulate plant immune responses and promote infection. However, their functional mechanisms are largely unknown. Here, we identified a Phytophthora sojae CRN effector PsCRN108 which contains a putative DNA-binding helix-hairpin-helix (HhH) motif and acts in the plant cell nucleus. Silencing of the PsCRN108 gene reduced P. sojae virulence to soybean, while expression of the gene in Nicotiana benthamiana and Arabidopsis thaliana enhanced plant susceptibility to P. capsici. Moreover, PsCRN108 could inhibit expression of HSP genes in A. thaliana, N. benthamiana and soybean. Both the HhH motif and nuclear localization signal of this effector were required for its contribution to virulence and its suppression of HSP gene expression. Furthermore, we found that PsCRN108 targeted HSP promoters in an HSE- and HhH motif-dependent manner. PsCRN108 could inhibit the association of the HSE with the plant heat shock transcription factor AtHsfA1a, which initializes HSP gene expression in response to stress. Therefore, our data support a role for PsCRN108 as a nucleomodulin in down-regulating the expression of plant defense-related genes by directly targeting specific plant promoters.

Random mutagenesis screen shows that Phytophthora capsici CRN83_152‐mediated cell death is not required for its virulence function(s)

“…Thus, it appears that chromatin re‐localization capacities are not sufficient per se for PcCRN83_152 virulence functions. Recently, two CRN effectors have been shown to directly bind DNA to achieve their virulence functions (Ramirez‐Garcés et al ., ; Song et al ., ). In addition, the targeting of DNA‐related processes has been predicted to be a conserved feature of CRN effectors (Zhang et al ., ), making further investigation into the mechanisms involved in PcCRN83_152‐mediated chromatin re‐localization of upmost importance.…”

“…CRN effectors, however, have received considerably less attention (Amaro et al ., ). Recently, some studies have provided new insights into CRN virulence functions (Ramirez‐Garcés et al ., ; Song et al ., ; Zhang et al ., ), but the role of CRN‐mediated cell death has remained mostly elusive.…”

“…Furthermore, over‐expression of P. sojae PsCRN108 enhanced Arabidopsis and N. benthamiana susceptibility to P. capsici infections. In addition, silencing of PsCRN108 reduced P. sojae virulence on soybean (Song et al ., ). Similarly, ectopic expression of the P. infestans effector PiCRN8 in N. benthamiana leaves led to an increase in susceptibility to P. infestans (van Damme et al ., ).…”

“…More detailed CRN virulence function is known for P. sojae PsCRN108. This CRN has been shown to enhance pathogen virulence by targeting the promotor regions of genes encoding for heat shock proteins (HSPs) and thereby reducing their expression (Song et al ., ). The P. sojae effector PsCRN63 has also been suggested to increase pathogen virulence by direct interaction and destabilization of host catalases (Zhang et al ., ).…”

A Phytophthora capsici effector suppresses plant immunity via interaction with EDS1

“…For protoplast transfection in Arabidopsis , coding sequences of desired genes were amplified and cloned into the pUC19‐35S‐FLAG/HA‐RBS vector (Li et al , ). For transient expression in N. benthamiana , PcAvh103 was PCR‐amplified and inserted into pBinGFP2 vector (Song et al , ). For prokaryotic expression of recombinant proteins, EDS1 , PAD4, and PcAvh103 were amplified and cloned into pGEX‐6P‐1, pET‐28a and pBAD/gIII, respectively.…”