Research

 

The Mohn Lab studies diverse topics related to microbial ecology and physiology. We use multi-omic approaches, process measurements and cultivation to advance knowledge of microbial catabolism, forest soil ecology and interactions between humans and their microbiomes.

 

Research Highlights:

 

Forest Soil Microbial Ecology

Soil microbial communities play fundamental roles in key forest processes including decomposition of organic matter, nutrient cycling, formation of soil, suppression of pathogens and detoxication of harmful compounds. Human and natural disturbances can induce changes in these communities, with consequences for productivity and sustainability of forest ecosystems. We are investigating the influence of forest management practices on the composition and functioning of soil microbial communities in collaboration with the Long-Term Soil Productivity Study. We are employing a combination of high-throughput sequencing and stable isotope probing approaches to investigate the effects of forest harvesting and organic matter removal on biomass decomposition and nitrogen cycling.

Forests also export carbon to adjacent ecosystems through gas exchange and dissolved organic carbon (DOC) in soil water. Through our work with the Hakai Institute we are investigating how Pacific Coastal Rainforest microbial communities prime carbon for export to the oceans, and have shown that the transport of soil microorganisms into the marine environment is a key component of marine microbial community assembly. We have partnered with researchers from the US Forest Service to conduct transboundary characterization of carbon degradation and biogeochemical cycling activity using metatranscriptomics.

 

Selected publications:

Leung, H.T.C., Maas, K.R., Wilhelm, R.C., Mohn, W.W. 2016. Long-term effects of timber harvesting on hemicellulolytic microbial populations in coniferous forest soils. ISME J. 10, 363-375.

Cardenas, E., Kranabetter, J.M., Hope, G., Mass, K.R., Hallam, S., Mohn, W.W. 2015. Forest harvesting reduces the soil metagenomic potential for biomass decomposition. ISME J. 9, 2465-2476.

VanInsberghe, D., Maas, K.R., Cardenas, E., Strachan, C.R., Hallam, S.J., Mohn, W.W. 2015. Non-symbiotic Bradyrhizobium ecotypes dominate North American forest soils. ISME J. 9, 2435-2441.

 

Microbial Steroid Metabolism

Steroids are ubiquitous in the environment and are significant growth substrates for microorganisms. Metabolism of steroids is also important for some pathogens like Mycobacterium tuberculosis, the causative agent of tuberculosis, as well as for biotechnical applications. We are studying bacterial steroid degradation using a combination of (i) culture-based molecular genetic and biochemical studies and (ii) culture-independent analyses of bacterial genomes and environmental metagenomes.

Currently, we are investigating how steroid-degrading bacteria like Rhodococcus jostii access water-insoluble steroid substrates like cholesterol, which normally occur in biological membranes. We are using a liposome-based model system with R. jostii and mutant strains. In addition, we are developing tools to explore bacterial genomes and environmental metagenomes for genes encoding steroid catabolism pathways in order to expand our knowledge of the diversity of steroid catabolism and the roles of steroid-degraders in diverse ecosystems.

 

From: Holert et al., 2018 MBio doi: 10.1128/mBio.02345-17

 

Selected Publications:

Holert J, Cardenas E, Bergstrand LH, Zaikova Z, Hahn AS,Hallam SJ, Mohn WW. Metagenomes Reveal Global Distribution of Bacterial Steroid Catabolism in Natural, Engineered, and Host Environments. MBio doi: 10.1128/mBio.02345-17

Bergstrand HL, Cardenas E, Holert J, Van Hamme JD, Mohn WW (2016) Delineation of steroid-degrading microorganisms through comparative genomic analysis. mBio doi:10.1128/mBio.00166-16


Mohn WW, Wilbrink M, Casabon I, Stewart GR, Liu J, van der Geize R, Eltis LD. 2012. Gene cluster encoding cholate catabolism in Rhodococcus spp. J. Bacteriol. 194:6712-6719.

Mohn WW, van der Geize R, Stewart GR, Okamoto S, Liu J, Dijkhuizen L, Eltis LD. 2008. The actinobacterial mce4 locus encodes a steroid transporter. J. Biol. Chem. 283:35368-35374.

 

Human Microbiome

Mammals and microbes co-exist in a tight partnership. Recent studies have shed light on the nature and relevance of this relationship, demonstrating associations between the composition and function of these microbial communities and diverse aspects of host physiology, including metabolism, immunological function, and disease.

Our research is primarily focused on the ecology of human-associated microbes, and the metabolic and immunological interactions between the microbiome and its host, which are important in health and disease. We use clinical samples to better understand the links between the microbiome and health status and mouse models to investigate the mechanisms involved. In collaboration with clinicians, microbiologists, and medical researchers, we address key areas of human microbiome research:

Early-life microbiome and childhood asthma

Relationships between microbiome structure and innate immunity

Role of geography in structuring the infant gut microbiome

Lung microbiome and chronic obstructive pulmonary disease

 

Selected Publications:

Sze MA, Dimitriu PA, Suzuki M, McDonough JE, Campbell JD, Brothers JF, Erb-Downward JR, Huffnagle GB, Hayashi S, Elliott WM, Cooper J, Sin DD, Lenburg ME, Spira A, Mohn WW, Hogg JC. 2015. The Host Response to the Lung Microbiota in Chronic Obstructive Pulmonary Disease. American Journal of Respiratory and Critical Care Medicine, 192(4):438-445.

Russell S, Gold M, Hartmann M, Willing B, Thorson L, Wlodarska M, Gill N, Blanchet M-R, Mohn WW, McNagny KM, Finlay BB. 2012. Early life antibiotic-driven changes in microbiota enhance susceptibility to allergic asthma. EMBO Reports. 13(5):440-447.

Dimitriu PA, Boyce G, Samarakoon A, Hartmann M, Johnson P, Mohn WW. 2012. Temporal stability of the mouse gut microbiota in relation to innate and adaptive immunity. Environ. Microbiol. 5:200-210.