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<jats:title>Abstract</jats:title><jats:sec> <jats:title>Main conclusion</jats:title> <jats:p>The cumulative action of combinations of alleles at several loci on the wheat genome is associated with different levels of resistance to late maturity α-amylase in bread wheat.</jats:p> </jats:sec><jats:sec> <jats:title>Abstract</jats:title> <jats:p>Resistance to late maturity α-amylase (LMA) in bread wheat (<jats:italic>Triticum aestivum</jats:italic> L.) involves a complex interaction between the genotype and the environment. Unfortunately, the incidence and severity of LMA expression is difficult to predict and once the trait has been triggered an unacceptably low falling number, high grain α-amylase may be the inevitable consequence. Wheat varieties with different levels of resistance to LMA have been identified but whilst some genetic loci have been reported, the mechanisms involved in resistance and the interaction between resistance loci requires further research. This investigation was focused on mapping resistance loci in populations derived by inter-crossing resistant wheat varieties or crossing resistant lines with a very susceptible line and then mapping quantitative trait loci. In addition to the previously reported locus on chromosome 7B for which a candidate gene has been proposed, loci were mapped on chromosomes 1B, 2A, 2B, 3A, 3B, 4A, 6A and 7D. These loci have limited effects on their own but have a cumulative effect in combination with each other. Further research will be required to determine the nature of the causal genes at these loci, to develop diagnostic markers and determine how the genes fit into the pathway that leads to the induction of <jats:italic>α-AMY1</jats:italic> transcription in the aleurone of developing wheat grains. Depending on the target environmental conditions, different combinations of alleles may be required to achieve a low risk of LMA expression.</jats:p> </jats:sec>

<jats:title>Abstract</jats:title><jats:sec> <jats:title>Main conclusion</jats:title> <jats:p>NO releases caryopsis dormancy in <jats:italic>Avena fatua</jats:italic>, the effect being dependent on the level of dormancy. The NO effect involves also the reduction of caryopsis sensitivity to ABA and to a decrease in the ABA to GA<jats:sub>s</jats:sub> ratio due to a decrease in ABA levels and the lack of effect on GA<jats:sub>s</jats:sub> levels before germination is completed.</jats:p> </jats:sec><jats:sec> <jats:title>Abstract</jats:title> <jats:p>Nitric oxide (NO) from various donors (i.e. SNP, GSNO and acidified KNO<jats:sub>2</jats:sub>), applied to dry caryopses or during initial germination, released primary dormancy in caryopses. Dormancy in caryopses was gradually lost during dry storage (after-ripening) at 25 °C, enabling germination at 20 °C in the dark. The after-ripening effect is associated with a decrease in NO required for germination. In addition, NO decreased the sensitivity of dormant caryopses to exogenous abscisic acid (ABA) and decreased the embryos’ ABA content before germination was completed. However, NO did not affect the content of bioactive gibberellins (GA<jats:sub>s</jats:sub>) from non-13-hydroxylation (GA<jats:sub>4</jats:sub>, GA<jats:sub>7</jats:sub>) and 13-hydroxylation (GA<jats:sub>1</jats:sub>, GA<jats:sub>3</jats:sub>, GA<jats:sub>6.</jats:sub>) pathways. Paclobutrazol (PAC), commonly regarded as a GA<jats:sub>s</jats:sub> biosynthesis inhibitor, counteracted the dormancy-releasing effect of NO and did not affect the GA<jats:sub>s</jats:sub> level; however, it increased the ABA content in embryos before germination was completed. Ascorbic acid, sodium benzoate and tiron, scavengers of reactive oxygen species (ROS), reduced the stimulatory effect of NO on caryopsis germination. This work provides new insight on the participation of NO in releasing <jats:italic>A. fatua</jats:italic> caryopses dormancy and on the relationship of NO with endogenous ABA and GA<jats:sub>s</jats:sub>.</jats:p> </jats:sec>

<jats:title>Abstract</jats:title><jats:sec> <jats:title>Main conclusion</jats:title> <jats:p>PGPRs: <jats:italic>P. fluorescens</jats:italic> Ms9N and <jats:italic>S. maltophilia</jats:italic> Ll4 inhibit in vitro growth of three legume fungal pathogens from the genus <jats:italic>Fusarium</jats:italic>. One or both trigger up-regulation of some genes (<jats:italic>CHIT, GLU, PAL, MYB, WRKY</jats:italic>) in <jats:italic>M. truncatula</jats:italic> roots and leaves in response to soil inoculation.</jats:p> </jats:sec><jats:sec> <jats:title>Abstract</jats:title> <jats:p><jats:italic>Pseudomonas fluorescens</jats:italic> (referred to as Ms9N; GenBank accession No. MF618323, not showing chitinase activity) and <jats:italic>Stenotrophomonas maltophilia</jats:italic> (Ll4; GenBank accession No. MF624721, showing chitinase activity), previously identified as promoting growth rhizobacteria of <jats:italic>Medicago truncatula</jats:italic>, were found, during an in vitro experiment, to exert an inhibitory effect on three soil-borne fungi: <jats:italic>Fusarium culmorum</jats:italic> Cul-3, <jats:italic>F. oxysporum</jats:italic> 857 and <jats:italic>F. oxysporum</jats:italic> f. sp<jats:italic>. medicaginis</jats:italic> strain CBS 179.29, responsible for serious diseases of most legumes including <jats:italic>M. truncatula</jats:italic>. <jats:italic>S. maltophilia</jats:italic> was more active than <jats:italic>P. fluorescens</jats:italic> in suppressing the mycelium growth of two out of three <jats:italic>Fusarium</jats:italic> strains. Both bacteria showed β-1,3-glucanase activity which was about 5 times higher in <jats:italic>P. fluorescens</jats:italic> than in <jats:italic>S. maltophilia.</jats:italic> Upon soil treatment with a bacterial suspension, both bacteria, but particularly <jats:italic>S. maltophilia</jats:italic>, brought about up-regulation of plant genes encoding chitinases (<jats:italic>MtCHITII, MtCHITIV, MtCHITV),</jats:italic> glucanases<jats:italic> (MtGLU)</jats:italic> and phenylalanine ammonia lyases<jats:italic> (MtPAL2</jats:italic>, <jats:italic>MtPAL4, MtPAL5).</jats:italic> Moreover, the bacteria up-regulate some genes from the <jats:italic>MYB</jats:italic> (<jats:italic>MtMYB74</jats:italic>, <jats:italic>MtMYB102</jats:italic>) and <jats:italic>WRKY</jats:italic> (<jats:italic>MtWRKY6</jats:italic>, <jats:italic>MtWRKY29</jats:italic>, <jats:italic>MtWRKY53</jats:italic>, <jats:italic>MtWRKY70</jats:italic>) families which encode TFs in <jats:italic>M. truncatula</jats:italic> roots and leaves playing multiple roles in plants, including a defense response. The effect depended on the bacterium species and the plant organ. This study provides novel information about effects of two <jats:italic>M</jats:italic>. <jats:italic>truncatula</jats:italic> growth-promoting rhizobacteria strains and suggests that both have a potential to be candidates for PGPR inoculant products on account of their ability to inhibit in vitro growth of <jats:italic>Fusarium</jats:italic> directly and indirectly by up-regulation of some defense priming markers such as <jats:italic>CHIT, GLU</jats:italic> and <jats:italic>PAL</jats:italic> genes in plants. This is also the first study of the expression of some <jats:italic>MYB</jats:italic> and <jats:italic>WRKY</jats:italic> genes in roots and leaves of <jats:italic>M. truncatula</jats:italic> upon soil treatment with two PGPR suspensions.</jats:p> </jats:sec>