RESUMO
Western hemlock (Tsuga heterophylla) is highly susceptible to Annosus root and butt rot disease, caused by Heterobasidion occidentale across its native range in western North America. Understanding molecular mechanisms of tree defense and dissecting genetic components underlying disease resistance will facilitate forest breeding and disease control management. The aim of this study was to profile host transcriptome reprogramming in response to pathogen infection using RNA-seq analysis. Inoculated seedlings were clearly grouped into three types: quantitative resistant (QR), susceptible (Sus), and un-infected (Uif), based on profiles of H. occidentale genes expressed in host tissues. Following de novo assembly of a western hemlock reference transcriptome with more than 33,000 expressed genes, the defensive transcriptome reprogramming was characterized and a set of differentially expressed genes (DEGs) were identified with gene ontology (GO) annotation. The QR seedlings showed controlled and coordinated molecular defenses against biotic stressors with enhanced biosynthesis of terpenoids, cinnamic acids, and other secondary metabolites. The Sus seedlings showed defense responses to abiotic stimuli with a few biological processes enhanced (such as DNA replication and cell wall organization), while others were suppressed (such as killing of cells of other organism). Furthermore, non-synonymous single nucleotide polymorphisms (ns-SNPs) of the defense- and resistance-related genes were characterized with high genetic variability. Both phylogenetic analysis and principal coordinate analysis (PCoA) revealed distinct evolutionary distances among the samples. The QR and Sus seedlings were well separated and grouped into different phylogenetic clades. This study provides initial insight into molecular defense and genetic components of western hemlock resistance against the Annosus root and butt rot disease. Identification of a large number of genes and their DNA variations with annotated functions in plant resistance and defense promotes the development of genomics-based breeding strategies for improved western hemlock resistance to H. occidentale.
RESUMO
Osteoarthritis (OA) is the most common joint disorder characterised by bone remodelling and cartilage degradation and associated with chondrocyte apoptosis. These processes were investigated at 10, 16, 24, and 30 weeks in Dunkin Hartley (DH) and Bristol Strain 2 (BS2) guinea pigs that develop OA spontaneously. Both strains had a more pronounced chondrocyte apoptosis, cartilage degradation, and subchondral bone changes in the medial than the lateral side of the tibia, and between strains, the changes were always greater and faster in DH than BS2. In the medial side, a significant increase of chondrocyte apoptosis and cartilage degradation was observed in DH between 24 and 30 weeks of age preceded by a progressive thickening and stiffening of subchondral bone plate (Sbp). The Sbp thickness consistently increased over the 30-week study period but the bone mineral density (BMD) of the Sbp gradually decreased after 16 weeks. The absence of these changes in the medial side of BS2 may indicate that the Sbp of DH was undergoing remodelling. Chondrocyte apoptosis was largely confined to the deep zone of articular cartilage and correlated with thickness of the subchondral bone plate suggesting that cartilage degradation and chondrocyte apoptosis may be a consequence of continuous bone remodelling during the development of OA in these animal models of OA.