tter medium was prepared by homogenising leaves of B. napus cv. Westar in a waring blender in a final volume of 1 L of water. The homogenate was centrifuged at 2000 g for 20 min and the resulting supernatant was filter sterilised. Plant growth and infection conditions Brassica napus cv. Westar was used for all infection assays; it has no known resistance genes. Seedlings were grown in a glasshouse maintained at 25uC under natural lighting. Wounded cotyledons were infected with conidia or water, at 10 days post sowing as described previously. Extraction of RNA and gene expression analysis For RNA-seq analysis, B. napus cotyledons were infected with Lmb, Lbc or water, and at 7 and 14 days post inoculation tissue around the inoculation site was harvested using a cork borer and then placed into liquid nitrogen before freeze drying and subsequent grinding under liquid nitrogen. Tissue samples were prepared in biological triplicate. RNA was extracted using Trizol reagent from infected tissue and from mycelia of Lmb and Lbc from 7-day still cultures grown in oilseed rape medium. RNA was then DNAase-treated and cleaned up. The two biological replicates of each sample with 
the highest RNA integrity number values were sequenced with Illumina TruSeq version 3 chemistry on an Illumina HiSeq2000 sequencer at the Australian Genome Research Facility. In vitro derived RNA was sequenced with 100 bp paired-end reads in order to aid gene annotation, and in planta derived RNA was sequenced with 100 bp single-end reads. A total of 15.5 Gbp sequence was generated from the in vitro libraries of the two fungi, and 72 Gbp sequence was generated from 12 in planta libraries . Reads were trimmed to a minimum phred quality score of 20 using Nesoni sequence software, orphaned members of pairs were retained, adaptor sequences were removed, and reads shorter than 20 bp were rejected. Trimmed reads were aligned to PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19657843 a reference genome sequence with Tophat v1.4.1 splice-junction mapper. Multiple genome-wide association studies have replicated a link between common Elesclomol site single nucleotide polymorphisms in the CLU gene and increased susceptibility for late-onset Alzheimer’s disease . In addition, rare CLU variants revealed by next-generation sequencing have also been associated with AD risk. However, the mechanisms by which modifications in clusterin expression and/or function alter disease risk are not yet clear. Clusterin is synthesized as a 6080 kD precursor protein that undergoes internal cleavage generating a- and b-chains joined by disulfide bonds. This glycosylated heterodimeric CLU is constitutively secreted and referred to as soluble clusterin, or as apolipoprotein J, when found in association with lipoproteins. Shorter forms of the precursor CLU have been detected intracellularly and named cytosolic, truncated or nuclear CLU. Alternative splicing, internal translation initiation, mistranslocation of sCLU, and impaired proteasomal degradation all appear to contribute to the pool of cytosolic CLU isoforms. The function of intracellular CLU is not completely understood. Studies in cancer biology have linked iCLU to Baxmediated apoptosis. Of relevance to AD, it has been recently shown that iCLU levels increase quickly in cultured primary neurons exposed to amyloid-b peptides, and that this iCLU elevation is required for the neurotoxic downstream signaling effects of Ab. CLU expression is highest in the brain and is markedly upregulated under situations of stress and inflam