Academic mentors are a critical resource for our students. Academic Mentors contribute formally and informally to graduate student training. They advise first year students on their Fall core courses, rotation lab choices and upon transitioning into their chosen research lab. They develop an individualized educational plan in conjunction with the student and their Research Mentor. They track student progress through individual meetings with the students and review of DAC reports.
Michael S. Cohen, PhD
The overall interests of my lab are in two main areas: 1. uncovering new roles for nicotinamide adenine dinucleotide (NAD+) regulation in cells and 2. elucidating the function of post-translational modifications (PTMs) by enzymes that use NAD+ as a substrate. A current focus in on the evolutionarily conserved PTM known as ADP-ribosylation. We seek to understand the impact ADP-ribosylation on cell function as a strategy for therapeutic development. ADP-ribosylation is catalyzed by a family of enzymes known as poly-ADP-ribose polymerases (PARPs, 17 in humans; also referred to as ARTDs), and involves the transfer of ADP-ribose from NAD+ to amino acids in target proteins. Despite being called PARPs, most of the family members catalyze mono-ADP-ribosylation (MARylation) and not poly-ADP-ribosylation (PARylation). Over the past eight years we have developed novel chemical tools and approaches, including orthogonal NAD+ analogue-enzyme pairs and selective PARP inhibitors, which have provided insights into the function of PARP-mediated MARylation in ways not attainable with conventional methods. Our studies have kindled a number of collaborations with other researchers in the PARP field that are using our selective PARP inhibitors and knowledge gained from our chemical genetic studies to understand how MARylation regulates protein function in cells.
I am deeply passionate about mentoring and training graduate students, both in the lab and in the classroom. Graduate students are the catalyst for academic research and I am committed to training the next generation of PhD scientists. I have been involved in all aspects of graduate student education: from teaching in graduate courses to mentoring graduate students in my lab and serving on dissertation advisory committees. I am enthusiastic about the opportunity to contribute more formally to graduate student training as an Academic Mentor. One of my main priorities will be to make sure students feel supported and can achieve their educational and career goals.
Cheryl L. Maslen, PhD
Dr. Maslen is a professor in the Knight Cardiovascular Institute and the Department of Molecular and Medical Genetics. In PBMS, she is a member of the Genome Sciences hub. She has been on the faculty at OHSU for nearly 30 years. Dr. Maslen’s area of research is on the etiology and pathogenesis of congenital cardiovascular diseases, with an emphasis on genetic, genomic and epigenetic underpinnings of disease. Her current focus in on the causes of cardiovascular manifestations in Turner syndrome, which is caused by deficiency of the second sex chromosome. Understanding why individuals with Turner syndrome have a greatly increased risk for congenital heart defects and acquired cardiovascular-related diseases will help improve medical management for Turner syndrome, but will also provide insights into how sex chromosome genes influence cardiovascular health in all people.
In addition, Dr. Maslen is also an expert in graduate education. She is the former director of the PhD Program in Molecular and Cellular Bioscience (PMCB), which preceded PBMS. She is the current director of the NIH-supported Program in Enhanced Research Training (PERT), which is a training grant that supports selected PBMS second year student and provides a specialized curriculum in professional development in scientific careers. As an experience mentor, Dr. Maslen is pleased to be a PBMS Academic Mentor and looks forward to guiding PBMS trainees in the early stages of their graduate education.
Mathew Thayer, PhD
I am a Professor in the Department of Chemical Physiology and Biochemistry at OHSU where my focus is on the mechanisms that control chromosome-wide replication timing, mono-allelic gene expression, and structural stability of mammalian chromosomes. I have also been very active in graduate education here at OHSU for the past 27 years. I have received several Teaching and Mentoring Awards, including the John A. Resko Faculty Research Achievement Award in 2017, which is the highest academic honor awarded at OHSU. I was the inaugural Director of the Cancer Biology Graduate Program (CANB) at OHSU, where I was responsible for developing the CANB Program; including development of new course work, establishing a Journal club, and a seminar series. I was also responsible for writing and presenting the CANB Program to the Oregon University System site visit in 2009, and we were granted PhD degree granting status in 2010. I continue to be active in all aspects of graduate education at OHSU and I am currently an Academic Mentor and I am on the Steering Committee for the new OHSU graduate Program in Biomedical Sciences.
My lab uses classical cytogenetic and state of the art molecular genetic approaches to characterize an abnormal chromosomal phenotype associated with genomic instability in cancer cells. This abnormal phenotype affects the entire chromosome and is characterized by delayed replication timing (DRT), which is represents a >3 hour delay in both the initiation as well as the completion of DNA synthesis along the entire length of the chromosome. Chromosomes with DRT also display a significant delay in mitotic chromosome condensation (DMC) that is characterized by an under-condensed appearance during mitosis. My lab found that Cre/loxP-mediated deletion of a large non-coding RNA gene, which we named asynchronous replication and autosomal RNA on chromosome 6 (ASAR6), caused DRT/DMC of the entire chromosome. We went on to show that the ASAR6 locus shares many characteristics with the X inactivation center: 1) mono-allelic expression of large non-coding RNAs, 2) random asynchronous replication timing between alleles, 3) regulation of mono-allelic gene expression in cis, and 4) regulation of the replication timing of an entire chromosome. More recently, we identified a second lncRNA gene, ASAR15, that when disrupted results in delayed replication of human chromosome 15. Importantly, ASAR15 shares many physical and functional characteristics with XIST and ASAR6, including: random mono-allelic expression of lncRNAs, asynchronous replication between alleles that is coordinated with other mono-allelic genes in cis, and the ability to delay replication timing of entire chromosomes following ectopic integration of transgenes. We are currently using ectopic integration of transgenes into human and mouse chromosomes to further map the functional sequences of ASAR6 and ASAR15. Thus, our most recent work defined the first cis-acting loci responsible for chromosome-wide replication timing, monoallelic gene expression, and structural stability of human autosomes.