Michael Kobor


Research Interests

Social Epigenetics
molecular biology
Chromatin Biology

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Graduate Student Supervision

Doctoral Student Supervision (Jan 2008 - May 2019)
DNA methylation variation across the human life course (2018)

Aging is a multifaceted process occurring in all living organisms, and it involves the breakdown of biological robustness. Although much research has revealed fascinating features of cellular mechanisms related to aging and lifespan, we have yet to understand the underpinnings driving this inevitable progression. Epigenetics is one area of aging research that has developed significant interest as certain modifications, such as DNA methylation, have been proposed to mediate the relationship between the environment and gene expression as well as have age-associated patterns. Interestingly, predictors of age based on DNA methylation of
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Tissue-specific investigations of DNA methylation variation in human neurobiological diseases (2018)

No abstract available.

Epigenetic signatures of prenatal alcohol exposure (2017)

Prenatal alcohol exposure (PAE) can alter the development, function, and regulation of neurobiological and physiological systems, causing lasting cognitive alterations, behavioral deficits, immune dysfunction, and increased vulnerability to mental health problems. In humans, the spectrum of these deficits is known as fetal alcohol spectrum disorder (FASD). Although the molecular underpinnings are not fully elucidated, epigenetic mechanisms are a prime candidate for the programming of physiological systems by PAE, as they may bridge environmental stimuli and neurodevelopmental outcomes. DNA methylation is also emerging as a potential biomarker of early-life events, which may aid in earlier FASD diagnoses. Thus, my overarching aim was to identify epigenetic mechanisms that may contribute to the deficits associated with FASD and act as biosignatures of PAE. Specifically, I used genome-wide approaches to assess underlying gene expression programs and epigenomic profiles in a rat model of PAE and clinical cohorts of individuals with FASD. In the rat model, I identified alterations to gene expression programs in the brain of adult PAE females under steady-state and immune challenge conditions. Building on these long-term alterations to transcriptomic programs, I identified altered DNA methylation patterns persisting from birth to weaning in the hypothalamus PAE animals, suggestive of early reprogramming of neurobiological systems. In parallel, I found concordant alterations to DNA methylation profiles in the hypothalamus and white blood cells of PAE animals, which may reflect systemic effects and potential biomarkers of PAE. To complement the animal model, I also investigated DNA methylation patterns in two clinical cohorts of FASD, where I identified an epigenetic signature of FASD in buccal epithelial cells. As these results raised the possibility of an epigenetic biomarker, I investigated the relevance of DNA methylation as a diagnostic method for PAE, and successfully generated a predictive algorithm that could classify individuals with FASD versus controls. Overall, these findings provide evidence for the biological embedding of PAE’s effects through changes in gene expression and DNA methylation, while setting the stage for the development of novel biomarkers. Ultimately, these may aid in the development of targeted interventions and early screening tools to mitigate the deficits associated with FASD.

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Diverse mechanisms of transcription regulation by RNA polymerase II in saccharomyces ceresisiae (2015)

No abstract available.

Functional characterization of Rtt107 in the DNA damage response in Saccharomyces cerevisiae (2014)

No abstract available.

Deciphering the function of chromatin modifiers in genome regulation and maintenance in saccharomyces cerevisiae (2012)

No abstract available.

Genome-wide analysis of chromatin modification patterns and their functional associations with major cellular processes in Saccharomyces cerevisiae (2010)

No abstract available.

Master's Student Supervision (2010 - 2018)
Genome-wide analysis of DNA methylation variance in healthy human subjects (2015)

DNA methylation is a type of epigenetic modification that modulates gene expression by acting as an intermediate between genes and environment; this in turn could trigger phenotypic changes with widespread implications in both disease and population models. Unlike DNA sequence, which is relatively stable and finite, DNA methylation presents itself differently in different tissues, and it is described as the sum of interactions affecting attachment of methyl groups to DNA mostly as a result of development and aging, with minor influences from stochastic variability, and environmental factors. Most studies involving DNA methylation focus on finding epigenetic changes related to pathogenicity or disease, as a result, there are certain foundational questions that remain unanswered. In order to translate the current knowledge into reliable insights, it is important to answer these questions, then standardize research methods and establish reference epigenomes. Here we begin to address this challenge through two avenues: epigenomic characterization and environmental interaction. To characterize the epigenome, we monitored the peripheral blood mononuclear cell DNA methylation levels from healthy subjects over a circadian day, a month, and under prolonged sample storage. We also investigated tissue specific variability in DNA methylation by comparing matched peripheral blood mononuclear and buccal epithelial cell samples from healthy subjects. Lastly, we analyzed the impact of diesel exhaust on the DNA methylation. We discovered that while overall DNA methylation was stable within a circadian day, certain loci demonstrated significant changes over the course of a month. Prolonged sample storage, on the other hand, had an even larger effect on DNA methylation. When we compared differences across tissues, we found that although both tissues showed extensive probe-wise variability, the specific regions and magnitude of that variability differed strongly between tissues. Lastly, in light of environmental influences, we observed that DNA methylation was sensitive to even short-term exposure to diesel exhaust, and we identified associated CpG sites across the functional genome, as well as in Alu and LINE1 repetitive elements, with most of these exposure sensitive sites demonstrating loss of DNA methylation.

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