Chemotaxis of amphibian pathogen batrachochytrium dendrobatidis in the presence and absence of antifungal metabolites produced by amphibian skin bacteria

Chytridiomycosis is an amphibian skin disease that threatens amphibian biodiversity worldwide. The infectious fungal agent of chytridiomycosis, Batrachochytrium dendrobatidis, can affect amphibians differently in that some amphibian populations can co-exist with the fungus and others quickly succumb to disease. Amphibians in populations that co-exist with the B. dendrobatidis are shown to have sub-lethal infections on their skins. Several co-existing populations have also been shown to have higher proportions of individuals with antifungal skin bacteria suggesting the role of skin bacteria in disease outcome. Little is known about the mechanism(s) that antifungal skin bacteria use to ameliorate the effects of B. dendrobatidis. In this study I identified that a B. dendrobatidis isolate JEL 310 zoospores (motile infectious phase) displays chemotaxis in the presence of two bacterially-produced metabolites (2,4-diacetylphloroglucinol and indole-3-carboxaldehyde). In the presence of either metabolite, B. dendrobatidis (JEL 310) zoospores are more likely to move away from the metabolites. Another B. dendrobatidis isolate JEL 423 did not display chemotaxis in the presence of violacein (bacterially-produced metabolite). Using parameters estimated from my B. dendrobatidis chemotaxis study, a mathematical model illustrates that B. dendrobatidis JEL 310 zoospores will disperse onto the source containing no metabolite if zoospores initially start both away from the source and on the source. The model illustrates that in the presence of a bacterially-produced 2,4-DAPG, B. dendrobatidis JEL 310 zoospores will disperse away from the source. These results suggest that amphibians that have skin bacteria that produce 2,4-DAPG might be able to keep B. dendrobatidis infections below the lethal threshold and thus be able to co-exist with the fungus

Association of CNVs with methylation variation.

Germline copy number variants (CNVs) and single-nucleotide polymorphisms (SNPs) form the basis of inter-individual genetic variation. Although the phenotypic effects of SNPs have been extensively investigated, the effects of CNVs is relatively less understood. To better characterize mechanisms by which CNVs affect cellular phenotype, we tested their association with variable CpG methylation in a genome-wide manner. Using paired CNV and methylation data from the 1000 genomes and HapMap projects, we identified genome-wide associations by methylation quantitative trait locus (mQTL) analysis. We found individual CNVs being associated with methylation of multiple CpGs and vice versa. CNV-associated methylation changes were correlated with gene expression. CNV-mQTLs were enriched for regulatory regions, transcription factor-binding sites (TFBSs), and were involved in long-range physical interactions with associated CpGs. Some CNV-mQTLs were associated with methylation of imprinted genes. Several CNV-mQTLs and/or associated genes were among those previously reported by genome-wide association studies (GWASs). We demonstrate that germline CNVs in the genome are associated with CpG methylation. Our findings suggest that structural variation together with methylation may affect cellular phenotype