Abstract

Rhizomania caused by Beet necrotic yellow vein virus (BNYVV) is characterized by excessive lateral root (LR) formation. Auxin-mediated degradation of Aux/IAA transcriptional repressors stimulates gene regulatory networks leading to LR organogenesis and involves several Aux/IAA proteins acting at distinctive stages of LR development. Previously, we showed that BNYVV p25 virulence factor interacts with BvIAA28, a transcriptional repressor acting at early stages of LR initiation. The evidence suggested that p25 inhibits BvIAA28 nuclear localization, thus, de-repressing transcriptional network leading to LR initiation. However, it was not clear whether p25 interacts with other Aux/IAA proteins. Here, by adopting bioinformatics, in vitro and in vivo protein interaction approaches we show that p25 interacts also with BvIAA2 and BvIAA6. Moreover, we confirmed that the BNYVV infection is, indeed, accompanied by an elevated auxin level in the infected LRs. Nevertheless, expression levels of BvIAA2 and BvIAA6 remained unchanged upon BNYVV infection. Mutational analysis indicated that interaction of p25 with either BvIAA2 or BvIAA6 requires full-length proteins as even single amino acid residue substitutions abolished the interactions. Compared to p25-BvIAA28 interaction that leads to redistribution of BvIAA28 into cytoplasm, both BvIAA2 and BvIAA6 remained confined into the nucleus regardless of the presence of p25 suggesting their stabilization though p25 interaction. Overexpression of p25-interacting partners (BvIAA2, BvIAA6 and BvIAA28) in Nicotiana benthamiana induced an auxin-insensitive phenotype characterized by plant dwarfism and dramatically reduced LR development. Thus, our work reveals a distinct class of transcriptional repressors targeted by p25.

Highlights

  • Beet necrotic yellow vein virus belongs to the genus Benyvirus within the family Benyviridae and is the causal agent of rhizomania disease in sugar beet (Tamada and Abe, 1989; Tamada et al, 1989; Gilmer et al, 2017)

  • The Aux/IAA protein BvIAA28 interaction with p25 was previously identified from a screening using a sugar beet cDNA library prepared from a resistant genotype that prevents efficient virus replication and massive lateral root proliferation upon Beet necrotic yellow vein virus (BNYVV) infection (Thiel and Varrelmann, 2009)

  • Since lateral root (LR) formation is controlled by auxin (Fukaki et al, 2007; Lavenus et al, 2013; Du and Scheres, 2018), it seems reasonable to assume that BNYVV interferes with the auxin signaling pathway for which experimental evidence was provided in the previous studies (Larson et al, 2008; Gil et al, 2018)

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Summary

Introduction

Beet necrotic yellow vein virus belongs to the genus Benyvirus within the family Benyviridae and is the causal agent of rhizomania disease in sugar beet (Tamada and Abe, 1989; Tamada et al, 1989; Gilmer et al, 2017). Most important are the severe symptoms induced in the infected taproots characterized by reduced size and wineglass shape, necrosis of the vascular tissue and massive lateral root (LR) proliferation, termed as root beard (Tamada and Abe, 1989). These root symptoms cause dramatic reduction of taproot weight and massive yield losses, making BNYVV to be one of the most important viral pathogens in sugar beet cultivation. The only efficient way to control rhizomania disease is the cultivation of resistant sugar beet varieties

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