How microbes evolve over time and space is central question in my research. Do certain host species act as reservoirs of microbial diversity, and are others incidental hosts? Do environmental fluctuations influence microbial population dynamics? How does the microbiome of an organism influence its fitness?
We work across a broad range of study systems and scales to address these research questions – from cone snails, plants, sewage, salt pond microbes, and more. Current projects include:
Landscape genomics of antibiotic resistance in the Central Valley of California
Increasing emergence of antibiotic resistance in pathogens is threatening our ability to treat common infectious diseases. Does the way we process our waste water influence the evolution and spread of antibiotic resistant bacteria?
Thanks to funding from UC Merced, we are currently sampling methicillin resistant Staphylococcus aureus (MRSA) and carbapenem resistant Enterobacteriaceae (CRE) from waste water treatment plants throughout the Central Valley, and using whole genome sequencing to determine the number of resistant strains circulating at each location and how they are moving through the environment.
The role of symbiotic microbes in plant responses to drought
A further study of how symbiotic microbes can affect the fitness of their hosts involves understanding how bacterial, fungal and viral communities that live in plants change in response to drought conditions. In a collaboration with the Frank and Sexton labs and supported by the Joint Genome Institute, we are exposing the Sierra Nevada endemic monkeyflower, Mimulus laciniatus to controlled drought stress in growth chambers and characterizing how the bacterial, eukaryotic and viral microbiome of the roots and leaves changes.
Hopefully this research will lead to being able to identify members of the plant microbiome interact with their host during drought conditions, and which members exacerbate or mitigate plant response to drought stress.
Using viruses to combat antibiotic resistant infections
An ongoing collaboration between myself, Dr. Ben Chan and Professor Paul Turner at Yale University is investigating the use of Virulence/Resistance Targeted Antibiotics (V/RTA’s) targeting antibiotic resistance mechanisms of bacteria with viruses of bacteria (known as bacteriophages). Utilizing natural selection, which has produced the diverse array of antibiotic resistance mechanisms and we are driving the evolution of bacteria in the opposite direction, rendering antibiotic resistant bacteria susceptible to antibiotics. Our current model for this is multi-drug resistant Pseudomonas aeruginosa. This work has resulted in FDA approval of a bacteriophage cocktail which is able to specifically target antibiotic resistance and virulence mechanisms of P. aeruginosa forcing an evolutionary trade-off between susceptibility to antibiotics and bacteriophage. My future lab work will expand these approaches to other antibiotic resistant pathogens – including Vancomycin-Resistant Enterococci and Vibrio cholerae.
Metagenomics of methanogens in restored and unrestored San Francisco Bay area wetlands
One of the most significant natural sources of the greenhouse gas methane is anaerobic bacteria which live in wetlands. In order to understand how communities of methanogenic bacteria change when wetlands are degraded and restored, a project spearheaded by graduate student Imelda Forteza, in collaboration with Dr. Susannah Tringe we are using a metagenomic approach to determine the changes in community assembly of methane producing bacteria that occur between disturbed, undisturbed and restored wetland sites. This research will help elucidate the role wetland restoration plays in climate change.
Finding new antimicrobial compounds
Development of traditional antibiotics is rapidly slowing, in the face of exponential increases in multi-drug resistant bacterial infections. It is therefore critical to discover new antimicrobial compounds for therapeutic use. We are screening lizard skin for antimicrobial activity in Vibrio cholerae, methicillin resistant Staphylococcus aureus (MRSA) and carbapenem resistant Klebsiella pneumoniae.