Abstract. In this review, we summarise factors contributing to plant availability of magnesium (Mg) in soils, the role of Mg in plant physiological processes related to yield formation and abiotic stress tolerance, and soil and fertiliser parameters related to Mg leaching in fertilised soils. Mg is a common constituent in many minerals, comprising 2% of Earth's crust; however, most soil Mg (90-98%) is incorporated in the crystal lattice structure of minerals and thus not directly available for plant uptake. Plants absorb Mg from the soil solution, which is slowly replenished by soil reserves. Duration and intensity of weathering, soil moisture, soil pH, and root-microbial activity in soil are key factors that determine plant-available Mg release from soils. On the other hand, the amount of Mg released from soil minerals is generally small compared with the amounts needed to sustain high crop yield and quality. Thus, in many agro-ecosystems, application of Mg fertilisers is crucial. Magnesium is involved in many physiological and biochemical processes; it is an essential element for plant growth and development and plays a key role in plant defence mechanisms in abiotic stress situations. An early effect of Mg deficiency in plants is the disturbed partitioning of assimilates between roots and shoots because the supply of sink organs with photosynthetic products is impaired, and sugars accumulate in source leaves. Thus, optimal supply of Mg is required to improve crop tolerance to various stresses and to increase yield and quality parameters of harvested products. Unlike other cations, Mg is very mobile in soils because it is less bound to the soil charges. Therefore, Mg losses by leaching might occur in sandy soils with high water conductivity. Leaching of Mg in soils when applied with various water-soluble fertilisers may also vary depending on the fertiliser's chemical composition, granule size, and effect on soil pH and cation balance, as we discuss in detail.

As part of a successful agronomic strategy, adequate nutrient management of the potato crop is essential throughout the whole growth period. In this review, the importance of balanced fertilisation for potato yield formation and yield security is addressed by taking advantage of the results of field trials and existing literature. The most important roles of the macronutrients nitrogen, phosphorous, potassium, magnesium, calcium and sulphur in the plant and their importance for yield formation in potato are reviewed. Fertilisation practices in potato production are discussed. Due to their various functions in plant metabolism, the impact of plant nutrients on potato yield is complex. Therefore, interactions with abiotic and biotic factors, for instance interactions between two different plant nutrients in the soil and the plant, are taken into account.

The term 'quality' is a complex parameter in the field of potato production, and the desired quality traits depend on the intended use. Important internal quality traits for potatoes are tuber flesh discolouration, dry matter, and starch content. External quality traits include tuber size and shape as well as resistance against mechanical stress during and after harvest. These quality traits are closely interrelated and genetically controlled. It has been demonstrated that all these parameters are also linked to the nutrient status of the plant and/or the tubers. For instance, the susceptibility of tubers for discolouration of both fresh market and processed cultivars is closely related not only to the nutrient supply but also to post-harvest treatment. Besides, the potential to form carcinogenic compounds like acrylamide from precursors during the deep-frying of potato products and the accumulation of toxic substances like glycoalkaloids are important quality criteria in terms of food safety. The influence of the supply of nutrients on potato tuber quality depends initially on their physiological functions, but the ratio to other nutrient needs should also be taken into account.

The D1 Leu(218) Val substitution in C. album confers significant resistance to triazinones. This suggests that Leu(218) Val is involved in the binding of triazinones. First establishment of the resistance profiles of the three psbA mutations suggests that these mutations have been independently selected.

P25, a Beet necrotic yellow vein virus (BNYVV) pathogenicity factor, interacts with a sugar beet protein with high homology to Arabidopsis thaliana kelch repeat containing F-box family proteins (FBK) of unknown function in yeast. FBK are members of the Skp1-Cullin-F-box (SCF) complex that mediate protein degradation. Here, we confirm this sugar beet FBK-P25 interaction in vivo and in vitro and provide evidence for in planta interaction and similar subcellular distribution in Nicotiana tabacum leaf cells. P25 even interacts with an FBK from A. thaliana, a BNYVV nonhost. FBK functional classification was possible by demonstrating the interaction with A. thaliana orthologs of Skp1-like (ASK) genes, a member of the SCF E3 ligase. By means of a yeast two-hybrid bridging assay, a direct effect of P25 on SCF-complex formation involving ASK1 protein was demonstrated. FBK transient Agrobacterium tumefaciens-mediated expression in N. benthamiana leaves induced a hypersensitive response. The full-length F-box protein consists of one F-box domain followed by two kelch repeats, which alone were unable to interact with P25 in yeast and did not lead to cell-death induction. The results support the idea that P25 is involved in virus pathogenicity in sugar beet and suggest suppression of resistance response.

Beet necrotic yellow vein virus (BNYVV) induces the most important disease threatening sugar beet. The growth of partially resistant hybrids carrying monogenic dominant resistance genes stabilize yield but are unable to entirely prevent virus infection and replication. P25 is responsible for symptom development and previous studies have shown that recently occurring resistance-breaking isolates possess increased P25 variability. To better understand the viral pathogenicity factor's interplay with plant proteins and to possibly unravel the molecular basis of sugar beet antivirus resistance, P25 was applied in a yeast two-hybrid screen of a resistant sugar beet cDNA library. This screen identified candidate proteins recognized as orthologues from other plant species which are known to be expressed following pathogen infection and involved in plant defense response. Most of the candidates potentially related to host-pathogen interactions were involved in the ubiquitylation process and plants response to stress, and were part of cell and metabolism components. The interaction of several candidate genes with P25 was confirmed in Nicotiana benthamiana leaf cells by transient agrobacterium-mediated expression applying bimolecular fluorescence complementation assay. The putative functions of several of the candidates identified support previous findings and present first targets for understanding the BNYVV pathogenicity and antivirus resistance mechanism.

Rhizomania of sugar beet, caused by Beet necrotic yellow vein virus (BNYVV), is characterized by excessive lateral root (LR) formation leading to dramatic reduction of taproot weight and massive yield losses. LR formation represents a developmental process tightly controlled by auxin signaling through AUX/IAA-ARF responsive module and LATERAL ORGAN BOUNDARIES DOMAIN (LBD) transcriptional network. Several LBD transcription factors play central roles in auxin-regulated LR development and act upstream of EXPANSINS (EXPs), cell wall (CW)-loosening proteins involved in plant development via disruption of the extracellular matrix for CW relaxation and expansion. Here, we present evidence that BNYVV hijacks these auxin-regulated pathways resulting in formation LR and root hairs (RH). We identified an AUX/IAA protein (BvAUX28) as interacting with P25, a viral virulence factor. Mutational analysis indicated that P25 interacts with domains I and II of BvAUX28. Subcellular localization of co-expressed P25 and BvAUX28 showed that P25 inhibits BvAUX28 nuclear localization. Moreover, root-specific LBDs and EXPs were greatly upregulated during rhizomania development. Based on these data, we present a model in which BNYVV P25 protein mimics action of auxin by removing BvAUX28 transcriptional repressor, leading to activation of LBDs and EXPs. Thus, the evidence highlights two pathways operating in parallel and leading to uncontrolled formation of LRs and RHs, the main manifestation of the rhizomania syndrome.

The method allows exhaustive surveys screening C. album leaf or seed samples for the occurrence of the D1 Ser264Gly mutation to confirm or disprove metamitron resistance in the case of unsatisfactory control.