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SummaryIncreased tolerance of crops to low oxygen (hypoxia) during flooding is a key target for food security. In Arabidopsis thaliana (L.) Heynh., the N‐end rule pathway of targeted proteolysis controls plant responses to hypoxia by regulating the stability of group VII ethylene response factor (ERFVII) transcription factors, controlled by the oxidation status of amino terminal (Nt)‐cysteine (Cys). Here, we show that the barley (Hordeum vulgare L.) ERFVII BERF1 is a substrate of the N‐end rule pathway in vitro. Furthermore, we show that Nt‐Cys acts as a sensor for hypoxia in vivo, as the stability of the oxygen‐sensor reporter protein MCGGAIL‐GUS increased in waterlogged transgenic plants. Transgenic RNAi barley plants, with reduced expression of the N‐end rule pathway N‐recognin E3 ligase PROTEOLYSIS6 (HvPRT6), showed increased expression of hypoxia‐associated genes and altered seed germination phenotypes. In addition, in response to waterlogging, transgenic plants showed sustained biomass, enhanced yield, retention of chlorophyll, and enhanced induction of hypoxia‐related genes. HvPRT6 RNAi plants also showed reduced chlorophyll degradation in response to continued darkness, often associated with waterlogged conditions. Barley Targeting Induced Local Lesions IN Genomes (TILLING) lines, containing mutant alleles of HvPRT6, also showed increased expression of hypoxia‐related genes and phenotypes similar to RNAi lines. We conclude that the N‐end rule pathway represents an important target for plant breeding to enhance tolerance to waterlogging in barley and other cereals.

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Severe infection with Septoria tritici occurred in four of five experiments designed to create a series of different disease epidemics. These experiments successfully identified periods suitable for infection. They also indicated the effect of sprays, timed before and after these periods, on disease development and yield. Analysis of disease progress and weather records suggested that critical conditions for initial development of S. tritici occurred during early May at four sites. Heavy rain giving at least 10 mm on 1 day or a total of 10 mm or more on 2 or 3 successive days occurred at all four sites prior to the appearance of symptoms on a particular leaf layer, though less heavy rain may suffice to splash inoculum onto upper leaves in shorter, immature canopies where stem elongation is incomplete. At the fifth site, infection occurred later in May and disease failed to develop to a significant degree. At all sites, the length of the incubation period on any of the top three leaves was found to be between 396 and 496 degree days. Control of winter epidemics of S. tritici had little effect on yield, whereas spray sequences commencing later than growth stage (GS) 31 but immediately prior to the critical periods provided the best disease control and yield benefit. Regression models incorporating, as independent variables, area under the S. tritici disease progress curve for any of the top three leaves from their emergence (GS 32‐37) satisfactorily explained yield loss at the four sites where disease was severe. Consideration of leaf 2 or leaf 3 alone accounted for more than 82% of the variance at each site and a yield loss from infection of leaf 2 related to thermal time is suggested as 0.00265% per C per day from the appearance of symptoms.