Thirteen alleles ( L , L1 to L11 , and LH ) from the flax L locus, which encode Toll/interleukin-1 receptor homology-nucleotide binding site-leucine-rich repeat (TIR-NBS-LRR) rust resistance proteins, were sequenced and compared to provide insight into their evolution and into the determinants of gene-for-gene resistance specificity. The predicted L6 and L11 proteins differ solely in the LRR region, whereas L6 and L7 differ solely in the TIR region. Thus, specificity differences between alleles can be determined by both the LRR and TIR regions. Functional analysis in transgenic plants of recombinant alleles constructed in vitro provided further information: L10-L2 and L6-L2 recombinants, encoding the LRR of L2 , conferred L2 resistance specificity, and an L2-L10 recombinant, encoding the LRR of L10 , conferred a novel specificity. The sequence comparisons also indicate that the evolution of L alleles has probably involved reassortment of variation, resulting from accumulated point mutations, by intragenic recombination. In addition, large deletion events have occurred in the LRR-encoding regions of L1 and L8, and duplication events have occurred in the LRR-encoding region of L2 .

Thirteen alleles (L, L1 to L11, and LH) from the flax L locus, which encode Toll/interleukin-1 receptor homology-nucleotide binding site-leucine-rich repeat (TIR-NBS-LRR) rust resistance proteins, were sequenced and compared to provide insight into their evolution and into the determinants of gene-for-gene resistance specificity. The predicted L6 and L11 proteins differ solely in the LRR region, whereas L6 and L7 differ solely in the TIR region. Thus, specificity differences between alleles can be determined by both the LRR and TIR regions. Functional analysis in transgenic plants of recombinant alleles constructed in vitro provided further information: L10-L2 and L6-L2 recombinants, encoding the LRR of L2, conferred L2 resistance specificity, and an L2-L10 recombinant, encoding the LRR of L10, conferred a novel specificity. The sequence comparisons also indicate that the evolution of L alleles has probably involved reassortment of variation, resulting from accumulated point mutations, by intragenic recombination. In addition, large deletion events have occurred in the LRR-encoding regions of L1 and L8, and duplication events have occurred in the LRR-encoding region of L2.

Despite complex regional patterns of projected climate change, significant decreases in food crop yields have been predicted using the 'worst case' CO 2 emission scenario (A1FI) of the Intergovernmental Panel on Climate Change. Overall, climate change is predicted to have a progressively negative effect on the yield of food crops, particularly in the absence of efforts to mitigate global CO 2 emissions. As with all species, plant pathogens will have varying responses to climate change. Whilst the life cycle of some pathogens will be limited by increasing temperatures, e.g. Puccinia striiformis f.sp. tritici, other climatic factors such as increasing atmospheric CO 2 , may provide more favourable conditions for pathogens such as Fusarium pseudograminearum. Based on published literature and unpublished work in progress, we have reviewed the qualitative effects of climate change on pathogens that cause disease of four major food crops: wheat, rice, soybean and potato. The limited data show that the influence will be positive, negative or neutral, depending on the host-pathogen interaction. Quantitative analysis of climate change on pathogens of these crops is largely lacking, either from field or laboratory studies or from modelling-based assessments. Systematic quantitative analysis of these effects will be necessary in developing future disease management plans, such as plant breeding, altered planting schedules, chemical and biological control methods and increased monitoring for new disease threats.