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 Based on published literature and unpublished work in progress, we have reviewed the qualitative effects of climate change on pathogens that cause disease of four major food crops: wheat, rice, soybean and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.

Zymoseptoria tritici is a globally distributed fungal pathogen which causes Septoria tritici blotch on wheat. Management of the disease is attempted through the deployment of resistant wheat cultivars and the application of fungicides. However, fungicide resistance is commonly observed in Z. tritici populations, and continuous monitoring is required to detect breakdowns in fungicide efficacy. We recently reported azole-resistant isolates in Australia; however, it remained unknown whether resistance was brought into the continent through gene flow or whether resistance emerged independently. To address this question, we screened 43 isolates across five Australian locations for azole sensitivity and performed wholegenome sequencing on 58 isolates from seven locations to determine the genetic basis of resistance. Population genomic analyses showed extremely strong differentiation between the Australian population recovered after azoles began to be used and both Australian populations recovered before azoles began to be used and populations on different continents. The apparent absence of recent gene flow between Australia and other continents suggests that azole fungicide resistance has evolved de novo and subsequently spread within Tasmania. Despite the isolates being distinct at the whole-genome level, we observed combinations of nonsynonymous substitutions at the CYP51 locus identical to those observed elsewhere in the world. We observed nine previously reported nonsynonymous mutations as well as isolates that carried a combination of the previously reported L50S, S188N, A379G, I381V, Y459DEL, G460DEL, and N513K substitutions. Assays for the 50% effective concentration against a subset of isolates exposed to the tebuconazole and epoxiconazole fungicides showed high levels of azole resistance. The rapid, parallel evolution of a complex CYP51 haplotype that matches a dominant European haplotype demonstrates the enormous potential for de novo resistance emergence in pathogenic fungi.

Grain hardness is a major determinant of the classification and end-use of wheat. Two genes, Pina-D1 and Pinb-D1, have a major effect on this trait, so for wheat breeding programs it is important to identify the alleles of these genes present in elite germplasm. This study was conducted to identify the alleles present in southern Australian germplasm, and to determine if they affected quality characteristics other than grain hardness.Only 3 genotypes were identified. These were Pina-D1a/Pinb-D1a producing soft grain, Pina-D1a/Pinb-D1b producing moderately hard grain, and Pina-D1b/Pinb-D1a producing very hard grain. WW15 was the probable source of Pina-D1a/Pinb-D1b in most cultivars; however, Halberd represented another source. An important source of Pina-D1b/Pinb-D1a was the CIMMYT line Pavon, with sources from the old Australian cultivars Gabo and Falcon probably still present in modern germplasm.In an analysis of grain quality data from the Victorian Institute for Dryland Agriculture breeding program, the Pina-D1b/Pinb-D1a genotype had a significantly higher water absorption and significantly lower milling yield than the Pina-D1a/Pinb-D1b genotype, which indicates that these genes will impede the development of hard-grained cultivars that combine high water absorption and high milling yield.

We identify an esterase isozyme in Drosophila melanogaster, EST 23, which shares biochemical, physiological, and genetic properties with esterase E3, which is involved in resistance to organophosphate insecticides in Lucilia cuprina. Like E3, the D. melanogaster EST 23 is a membrane-bound alpha-esterase which migrates slowly toward the anode at pH 6.8. Both enzymes have similar preferences for substrates with shorter acid side chain lengths. Furthermore, on the basis of their high sensitivity to inhibition by paraoxon and their insensitivity to inhibition by eserine sulfate, both enzymes were classified as subclass I carboxylesterases. The activity of each enzyme peaks early in development and, again, in the adult stage. Both enzymes are found in the male reproductive system and larval and adult digestive tissues, the latter being consistent with a role for these enzymes in organophosphate resistance. Fine structure deficiency mapping localized Est 23 to cytological region 84D3 to E1-2 on the right arm of chromosome 3. Moreover, we show that the genes encoding three other esterase phenotypes also map to the same region; these phenotypes involve allozymic differences in EST 9 (formerly EST C), ali-esterase activity, defined by the hydrolysis of methyl butyrate, and malathion carboxylesterase activity, defined by hydrolysis of the organophosphate malathion. This cluster corresponds closely to that encompassing E3 and malathion carboxylesterase on chromosome 4 in L. cuprina, the homologue of chromosome 3R in D. melanogaster.

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