The Agrobacterium VirE2 effector interacts with multiple members of the Arabidopsis VIP1 protein family

Abstract

T-DNA transfer from Agrobacterium to its host plant genome relies on multiple interactions between plant proteins and bacterial effectors. One such plant protein is the Arabidopsis VirE2 interacting protein (AtVIP1), a transcription factor that binds Agrobacterium tumefaciens C58 VirE2, potentially acting as an adaptor between VirE2 and several other host factors. It remains unknown, however, whether the same VirE2 protein has evolved to interact with multiple VIP1 homologues in the same host, and whether VirE2 homologues encoded by different bacterial strains/species recognize AtVIP1 or its homologues. Here, we addressed these questions by systematic analysis (using the yeast two-hybrid and co-immunoprecipitation approaches) of interactions between VirE2 proteins encoded by four major representatives of known bacterial species/strains with functional T-DNA transfer machineries and eight VIP1 homologues from Arabidopsis and tobacco. We also analysed the determinants of the VirE2 sequence involved in these interactions. These experiments showed that the VirE2 interaction is degenerate: the same VirE2 protein has evolved to interact with multiple VIP1 homologues in the same host, and different and mutually independent VirE2 domains are involved in interactions with different VIP1 homologues. Furthermore, the VIP1 functionality related to the interaction with VirE2 is independent of its function as a transcriptional regulator. These observations suggest that the ability of VirE2 to interact with VIP1 homologues is deeply ingrained into the process of Agrobacterium infection. Indeed, mutations that abolished VirE2 interaction with AtVIP1 produced no statistically significant effects on interactions with VIP1 homologues or on the efficiency of genetic transformation.

Plants make galls to accommodate foreigners: some are friends, most are foes

“…Several things make the endeavor more complicated than it might seem. For example: each effector can have multiple targets – rather than a single target – in the plant cell (Lapham et al , ; Wang et al , ).…”

“…Several things make the endeavor more complicated than it might seem. For example: each effector can have multiple targetsrather than a single targetin the plant cell (Lapham et al, 2018;Wang et al, 2018). (17) The genetically transformed plant cell produces molecules that benefit Agrobacterium.…”

OsbZIP81, A Homologue of Arabidopsis VIP1, May Positively Regulate JA Levels by Directly Targetting the Genes in JA Signaling and Metabolism Pathway in Rice

“…VIP1 can bind to VRE (VIP1 response element: ACNGCT) or VRE similar sequences (AGCTGT/G, CAGCT) of promoters and control the expression of stress-related genes [23,24,26,31,32]. In addition to VIP1, numerous members of the group I subfamily can interact with C58 VirE2 (AtbZIP52, AtbZIP69, PosF21/AtbZIP59, AtbZIP29, and AtbZIP30) and they are involved in osmosensory responses (PosF21/AtbZIP59, AtbZIP69, AtbZIP29, AtbZIP30, and AtbZIP52) and vascular development (AtbZIP18, AtbZIP29, AtbZIP30, AtbZIP52, PosF21/AtbZIP59, and AtbZIP69), revealing the functional redundancy among group I members [26,33,34]. Moreover, AtbZIP29 has been defined to function in leaf and root development, PosF21/AtbZIP59 in auxin-induced callus formation and plant regeneration, DRINK ME/AtbZIP30 in growth and reproductive development regulation, and AtbZIP18 in pollen and male gametophyte development [6,27,35,36].…”

An Insight into T-DNA Integration Events in Medicago sativa

“… Sequences exceeding the borders and belonging to the so-called vector backbone (VB) are frequently transferred along with the ssT-DNA [ 3 ]; other bacterial DNA may also enter the plant cell, including plasmid DNA [ 8 , 9 ] and chromosomal DNA [ 10 , 11 , 12 ]. Coordinated activity of bacterial and host proteins are necessary for infection and T-DNA integration, the latter largely relying on host factors [ 13 , 14 ]. T-DNA integration into the plant genome follows an “illegitimate” model, that is, integration is random and not directed by sequence identity, but rather by sequence micro similarities between the borders and the genome [ 15 , 16 ].…”

“…Coordinated activity of bacterial and host proteins are necessary for infection and T-DNA integration, the latter largely relying on host factors [ 13 , 14 ].…”