Interaction of the Beet necrotic yellow vein virus with the auxin pathway in Beta vulgaris – Investigations on the molecular mechanism and impact on pathogenicity, symptom development and viral spread.

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Beet necrotic yellow vein virus (BNYVV) is the causal agent of Rhizomania, a viral disease of sugar beet with high economic importance transmitted by the plasmodiophorid Polymyxa betae. Upon BNYVV infection, plants display massive lateral root proliferation leading to the characteristic symptom of a “root beard” and reduced tap root weight. Auxin as the major plant hormone controls an array of developmental processes including the development of lateral roots. Therefore, it is supposed that BNYVV interacts with the auxin signaling pathway to induce lateral root proliferation but the mechanism responsible for that is still unknown. In preliminary experiments, an auxin/indole-3-acetic acid (Aux/IAA) transcription factor interacting with the pathogenicity factor of BNYVV (P25) could be identified in sugar beet. Aux/IAA proteins are transcriptional repressor that regulate the expression of auxin responsive genes in the nucleus. P25 interrupts the activity of the Aux/IAA proteins by a relocalization from the nucleus into the cytoplasma. The relocalization is followed by a massive upregulation of auxin responsive genes involved in lateral root formation. The results provide for the first time evidence that BNYVV interacts with the auxin signaling pathway in sugar beet. It is now the aim of this proposed study to investigate this interaction in detail with particular focus on the molecular mechanism and the impact on pathogenicity, symptom development and viral spread. For this purpose, all Aux/IAA proteins encoded by the sugar beet genome will be tested for an interaction with P25. Furthermore, the domain interacting with Aux/IAA proteins shall be identified in order to increase our knowledge about the multifunctional nature of viral proteins. A full length cDNA clone of BNYVV will be applied to study the effects of the interaction with the auxin signaling pathway on pathogenicity and symptom development in sugar beet. Apart from that, a virus-induced gene silencing system developed for sugar beet will be used to silence specific Aux/IAA genes in order to mimic the relocalization by P25 and to reveal the effect on lateral root formation and gene expression. Since the biological relevance of the lateral root formation for the vector P. betae is not known yet, it is also aimed to prove whether there is an effect on virus acquisition and vector propagation. The project results will provide a deep insight into the interaction between BNYVV and its host sugar beet. Moreover, the identification of plant proteins interacting with viral factors provides new targets that can be utilized to develop new resistance factors by genome editing.