Leaf senescence is an essential developmental process that impacts dramatically on crop yields and involves altered regulation of thousands of genes and many metabolic and signaling pathways, resulting in major changes in the leaf. The regulation of senescence is complex, and although senescence regulatory genes have been characterized, there is little information on how these function in the global control of the process. We used microarray analysis to obtain a highresolution time-course profile of gene expression during development of a single leaf over a 3-week period to senescence. A complex experimental design approach and a combination of methods were used to extract high-quality replicated data and to identify differentially expressed genes. The multiple time points enable the use of highly informative clustering to reveal distinct time points at which signaling and metabolic pathways change. Analysis of motif enrichment, as well as comparison of transcription factor (TF) families showing altered expression over the time course, identify clear groups of TFs active at different stages of leaf development and senescence. These data enable connection of metabolic processes, signaling pathways, and specific TF activity, which will underpin the development of network models to elucidate the process of senescence.

The genomes of a representative world-wide collection of 32 Turnip mosaic virus (TuMV) isolates were sequenced and these, together with six previously reported sequences, were analysed. At least one-fifth of the sequences were recombinant. In phylogenetic analyses, using genomic sequences of Japanese yam mosaic virus as an outgroup, the TuMV sequences that did not show clear recombination formed a monophyletic group with four well-supported lineages. These groupings correlated with differences in pathogenicity and provenance; the sister group to all others was of Eurasian B-strain isolates from nonbrassicas, and probably represents the ancestral TuMV population, and the most recently 'emerged' branch of the population was probably that of the BR-strain isolates found only in east Asia. Eight isolates, all from east Asia, were clear recombinants, probably the progeny of recent recombination events, whereas a similar number, from other parts of the world, were seemingly older recombinants. This difference indicates that the presence of clear recombinants in a subpopulation may be a molecular signature of a recent 'emergence'.

Aphid transmitted in the non-persistent manner, by at least 89 species, including Myzus persicae and Brevicoryne brassicae. Useful website: http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/57010072.htm.

The genetic structure of populations of Turnip mosaic virus in Eurasia was assessed by making host range and gene sequence comparisons of 142 isolates. Most isolates collected in West Eurasia infected Brassica plants whereas those from East Eurasia infected both Brassica and Raphanus plants. Analyses of recombination sites (RSs) in five regions of the genome (one third of the full sequence) showed that the protein 1 (P1 gene) had recombined more frequently than the other gene regions in both subpopulations, but that the RSs were located in different parts of the genomes of the subpopulations. Estimates of nucleotide diversity showed that the West Eurasian subpopulation was more diverse than the East Eurasian subpopulation, but the Asian-BR group of the genes from the latter subpopulation had a greater nonsynonymous/synonymous substitution ratio, especially in the P1, viral genome-linked protein (VPg) and nuclear inclusion a proteinase (NIa-Pro) genes. These subpopulations seem to have evolved independently from the ancestral European population, and their genetic structure probably reflects founder effects.

The Brassica napus differential line 165 is resistant to infection by Turnip mosaic virus (TuMV) isolates belonging to pathotypes 1 and 3. Nucleotide sequences of resistance-breaking mutants of pathotype 1 (UK 1), pathotype 3 (CHN 12), and wild-type isolates have been determined. When the mutations identified were introduced into an infectious clone of UK 1, a single mutation in the viral P3 protein induced a hypersensitive (necrotic) response in inoculated leaves of line 165 plants. Full systemic nonnecrotic infection was only possible when another mutation (in the cylindrical inclusion protein) was introduced. Tests on segregating populations derived from line 165 indicated that the two viral genes were pathogenicity determinants for two different resistance genes in line 165. One gene responsible for an extreme form of resistance (no symptoms seen) was epistatic to a second responsible for the hypersensitive reaction. These results help to explain the relative stability of the resistance in line 165 and to further define the genetic basis of the TuMV pathotyping system.