Genetic Dissection ofVerticilliumWilt Resistance Mediated by Tomato Ve1      

Abstract

Vascular wilt diseases caused by soil-borne pathogens are among the most devastating plant diseases worldwide. The Verticillium genus includes vascular wilt pathogens with a wide host range. Although V. longisporum infects various hosts belonging to the Cruciferaceae, V. dahliae and V. albo-atrum cause vascular wilt diseases in over 200 dicotyledonous species, including economically important crops. A locus responsible for resistance against race 1 strains of V. dahliae and V. albo-atrum has been cloned from tomato (Solanum lycopersicum) only. This locus, known as Ve, comprises two closely linked inversely oriented genes, Ve1 and Ve2, that encode cell surface receptor proteins of the extracellular leucine-rich repeat receptor-like protein class of disease resistance proteins. Here, we show that Ve1, but not Ve2, provides resistance in tomato against race 1 strains of V. dahliae and V. albo-atrum and not against race 2 strains. Using virus-induced gene silencing in tomato, the signaling cascade downstream of Ve1 is shown to require both EDS1 and NDR1. In addition, NRC1, ACIF, MEK2, and SERK3/ BAK1 also act as positive regulators of Ve1 in tomato. In conclusion, Ve1-mediated resistance signaling only partially overlaps with signaling mediated by Cf proteins, type members of the receptor-like protein class of resistance proteins.

Cotton WRKY1 Mediates the Plant Defense-to-Development Transition during Infection of Cotton byVerticillium dahliaeby ActivatingJASMONATE ZIM-DOMAIN1Expression

“…[See online article for color version of this figure. ] potato (Solanum tuberosum; Zhou et al, 2006;Klosterman et al, 2009). Typical symptoms caused by V. dahliae include leaf necrosis, premature defoliation, altered flowering time, and severe growth stunting (Veronese et al, 2003;Fradin et al, 2009;Xu et al, 2011b). Recent studies have identified signaling pathways that play essential roles in cotton resistance to V. dahliae (Xu et al, 2011b;Gao et al, 2013;Zhang et al, 2013), but how plants orchestrate development under V. dahliae infection remains elusive.…”

“…The cDNA sequence of GbWRKY1 was cloned into the TRV plasmid using BamHI and KpnI to construct the TRV:GbWRKY1 VIGS vector and was then transformed into Agrobacterium tumefaciens GV3101 via electroporation as described previously (Fradin et al, 2009). The TRV:00 (control) and TRV: GbWRKY1 vectors were agroinfiltrated into the cotyledons of 10-d-old cv YZ1 plants using a needleless syringe as described previously .…”

Cautionary Notes on the Use of C-Terminal BAK1 Fusion Proteins for Functional Studies

“…affect (in a nonmutually exclusive manner) phosphorylation events within the PRR-BAK1 complex, association and/or dissociation with downstream components, and phosphorylation events with direct substrates. It is becoming increasingly clear that, in addition to their role in BR responses, BAK1 and other SERKs in Arabidopsis and other plant species are master regulators of plant innate immunity (Heese et al, 2007;Shan et al, 2008;Fradin et al, 2009Fradin et al, , 2011Santos et al, 2009;Bar et al, 2010;Krol et al, 2010;Chaparro-Garcia et al, 2011;Mantelin et al, 2011;Roux et al, 2011;Yang et al, 2011) as well as of cell death control Kemmerling et al, 2007;Gao et al, 2009;Wang et al, 2011), pollen development (Albrecht et al, 2005;Colcombet et al, 2005), and organ abscission (Lewis et al, 2010). One must not assume that the model based on analyses between BRI1 and BAK1 is universal, and, in light of our results, it is essential that researchers analyze in detail and quantify the impact of modifying the SERK proteins in transgenic approaches when studying SERKdependent signaling pathways.…”

Brassinosteroids inhibit pathogen-associated molecular pattern–triggered immune signaling independent of the receptor kinase BAK1

“…Additional SERKs can be recruited by FLS2 with BKK1 as major regulator besides BAK1 (13). BAK1 also positively regulates other PRR-dependent pathways (12,(14)(15)(16). However, innate immune responses triggered by PAMPs such as fungal chitin do not depend on BAK1 (14,17).…”