Air Power’s Cyber Risk: How Operational Causes will have Strategic Consequences

This thesis argues that air power's cyber risk which has emerged from operational causes will create profound strategic consequences. Through a comprehensive examination of existing literature, it challenges prevailing perspectives by highlighting a critical gap in knowledge: a failure to map the link between operational causes and strategic consequences of air power’s cyber risk which, when realised, will threaten the roles and, in extremis, survival of states. While acknowledging the risks emergent nature and situational specificity with not all states reliant on air power and size inverse to severity, the thesis asserts that the realisation of these strategic consequences is a matter of 'when', not 'if'. Developed within a risk management framework, supported by literature reviews and case studies, and leading to observations and recommendations, the thesis responds by offering a pathway for further research which can mitigate air power’s cyber risk. If embraced, an opportunity exists for academia and practitioners to act in synergy, fill the identified gap in knowledge and address the risk proactively. Conversely, if ignored and the pathway is not followed, the implications will, the thesis predicts, result in the unmitigated strategic consequences of air power’s cyber risk reshaping the geopolitical landscape of the 21st century

Independent deletions of a pathogen-resistance gene in Brassica and Arabidopsis

Plant disease resistance (R) genes confer race-specific resistance to pathogens and are genetically defined on the basis of intra-specific functional polymorphism. Little is known about the evolutionary mechanisms that generate this polymorphism. Most R loci examined to date contain alternate alleles and/or linked homologs even in disease-susceptible plant genotypes. In contrast, the resistance to Pseudomonas syringae pathovar maculicola (RPM1) bacterial resistance gene is completely absent (rpm1-null) in 5/5 Arabidopsis thaliana accessions that lack RPM1 function. The rpm1-null locus contains a 98-bp segment of unknown origin in place of the RPM1 gene. We undertook comparative mapping of RPM1 and flanking genes in Brassica napus to determine the ancestral state of the RPM1 locus. We cloned two B. napus RPM1 homologs encoding hypothetical proteins with ≈81% amino acid identity to Arabidopsis RPM1. Collinearity of genes flanking RPM1 is conserved between B. napus and Arabidopsis. Surprisingly, we found four additional B. napus loci in which the flanking marker synteny is maintained but RPM1 is absent. These B. napus rpm1-null loci have no detectable nucleotide similarity to the Arabidopsis rpm1-null allele. We conclude that RPM1 evolved before the divergence of the Brassicaceae and has been deleted independently in the Brassica and Arabidopsis lineages. These results suggest that functional polymorphism at R gene loci can arise from gene deletions

Molecular genetics of the Streptomyces plasmid SCP2

SIGLEAvailable from British Library Document Supply Centre- DSC:D52297/84 / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Genetic control of immunity to turnip mosaic virus (TuMV) pathotype 1 in Brassica rapa (Chinese cabbage)

Turnip mosaic virus (TuMV) is the major virus infecting crops of the genus Brassica worldwide. A dominant resistance gene, TuRB01b, that confers immunity to the virus isolate UK 1 (a representative pathotype 1 isolate of TuMV) on Brassica rapa was identified in the Chinese cabbage cultivar Tropical Delight. The TuRB01b locus was mapped to a 2.9-cM interval on B. rapa chromosome 6 (A6) that was flanked by RFLP markers pN101e1 and pW137e1. This mapping used a first backcross (B1) population segregating for the resistance gene at TuRB01b and sets of RFLP markers employed in previous mapping experiments in Brassica. Virus–plant interaction phenotypes were assayed in inbred progeny derived from B1 individuals to allow different virus isolates to be tested. Comparative mapping confirmed that A6 of B. rapa was equivalent to chromosome 6 of Brassica napus (A6) and that the map position of TuRB01b in B. rapa could be identical to that of TuRB01 in B. napus. Detailed evaluation of plant–virus interactions showed that TuRB01 and TuRB01b had indistinguishable specificities to a range of TuMV isolates. The possibility that TuRB01 and TuRB01b represent similar or identical alleles at the same A genome resistance locus suggests that B. napus acquired TuRB01 from the B. rapa gene pool