Relevant Thesis-Based Degree Programs
Affiliations to Research Centres, Institutes & Clusters
Complete these steps before you reach out to a faculty member!
- Familiarize yourself with program requirements. You want to learn as much as possible from the information available to you before you reach out to a faculty member. Be sure to visit the graduate degree program listing and program-specific websites.
- Check whether the program requires you to seek commitment from a supervisor prior to submitting an application. For some programs this is an essential step while others match successful applicants with faculty members within the first year of study. This is either indicated in the program profile under "Admission Information & Requirements" - "Prepare Application" - "Supervision" or on the program website.
- Identify specific faculty members who are conducting research in your specific area of interest.
- Establish that your research interests align with the faculty member’s research interests.
- Read up on the faculty members in the program and the research being conducted in the department.
- Familiarize yourself with their work, read their recent publications and past theses/dissertations that they supervised. Be certain that their research is indeed what you are hoping to study.
- Compose an error-free and grammatically correct email addressed to your specifically targeted faculty member, and remember to use their correct titles.
- Do not send non-specific, mass emails to everyone in the department hoping for a match.
- Address the faculty members by name. Your contact should be genuine rather than generic.
- Include a brief outline of your academic background, why you are interested in working with the faculty member, and what experience you could bring to the department. The supervision enquiry form guides you with targeted questions. Ensure to craft compelling answers to these questions.
- Highlight your achievements and why you are a top student. Faculty members receive dozens of requests from prospective students and you may have less than 30 seconds to pique someone’s interest.
- Demonstrate that you are familiar with their research:
- Convey the specific ways you are a good fit for the program.
- Convey the specific ways the program/lab/faculty member is a good fit for the research you are interested in/already conducting.
- Be enthusiastic, but don’t overdo it.
G+PS regularly provides virtual sessions that focus on admission requirements and procedures and tips how to improve your application.
ADVICE AND INSIGHTS FROM UBC FACULTY ON REACHING OUT TO SUPERVISORS
These videos contain some general advice from faculty across UBC on finding and reaching out to a potential thesis supervisor.
Graduate Student Supervision
Doctoral Student Supervision
Dissertations completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest dissertations.
Maintaining energy homeostasis is essential for survival in a changing environment. When dietary energy is abundant, animals store excess energy and when dietary energy is scarce, animals mobilize energy stores to support biological functions. In most animals, fat is the main form of stored energy. One important factor that regulates fat metabolism is biological sex. In many animals, females store more fat and have decreased fat breakdown compared with males. Several studies have investigated how sex chromosomes and hormones establish the male-female differences in fat metabolism; however, the metabolic effectors acting downstream of sex chromosomes and hormones are understudied. To better understand the sex-specific regulation of fat metabolism, I used Drosophila as a model to identify metabolic genes and pathways which contribute to sex differences in fat metabolism. In Chapter 2, I identified male-biased regulation of the triglyceride lipase brummer (bmm) and showed how this regulation contributes to the male-female differences in fat storage and breakdown. Further, I found that bmm functions in the neurons and somatic cells of the gonads to influence these sex differences. However, sex-specific regulation of bmm does not fully account for the male-female differences in fat metabolism. Therefore, in Chapter 3, I investigated the role of sex determination gene transformer (tra) in establishing the male-female differences in fat storage and breakdown. I demonstrated that tra establishes the sex difference in fat storage via the sex-specific regulation of the adipokinetic hormone (Akh) signaling pathway, a major lipolytic pathway. In Chapter 4, I explored the role of the Akh pathway in regulating fat breakdown in females and males. Here, I demonstrated that Akh pathway activity post-starvation has differential effects on fat breakdown in females and males.By investigating the role of metabolic effectors in both sexes, I identified sex-limited effects on fat metabolism in both males and females, highlighting the importance of considering both sexes in experimental design and execution. Overall, my work sets the foundation for future studies aimed at identifying conserved mechanisms underlying sex-specific regulation of fat metabolism, and thus allow for a more comprehensive understanding of fat metabolism and metabolic diseases associated with dysregulated fat metabolism.
Sexual size dimorphism (SSD) is common throughout the animal kingdom. Inthe fruit fly, Drosophila melanogaster, females are ~30% larger than males. Over thepast two decades, studies in Drosophila have expanded our knowledge of thegenetic and dietary requirements for growth. However, it remains incompletelyunderstood how males and females differ in the regulation of growth. Theinsulin/insulin-like growth factor signaling pathway (IIS) was found to be a keyregulator of nutrient-dependent growth and body size. The appropriate coupling ofgrowth with dietary nutrients is known as body size plasticity. Recent studies haveimplicated both dietary nutrients and IIS in establishing SSD, but the mechanismremains poorly understood. To better understand how males and females differ ingrowth, I used Drosophila to perform a series of studies examining the contributionof nutrients and IIS on growth in both sexes.In Chapter 2, I found that IIS activity is required for increased female bodysize. Further, genetically augmenting IIS in males is sufficient for increased bodysize. In Chapter 3, I build upon this characterization and identify that in a high proteindietary context, females increase IIS activity and body size more than males. Thisresults in increased female body size plasticity. Specifically, when dietary protein isabundant, females produce high levels of the insulinotropic factor Stunted whichpromotes increased IIS and larger body size. This mechanism was dependent onthe sex determination gene transformer. These findings elucidate a molecularmechanism underlying the sex difference in body size plasticity. In Chapter 4, Ipresent evidence that in a low-sugar dietary context both sexes increase growth viadistinct mechanisms to achieve the same phenotype. Specifically, males increaseIIS activity whereas females increase target of rapamycin (TOR) signaling to reach alarger body size. Together, my thesis provides novel mechanistic insight into howmales and females differ in their phenotypic response to genetic manipulation anddietary manipulation. This work provides the basis for future studies to identifyconserved sex differences in the regulation of nutrient-responsive pathways, andultimately will inform our knowledge of the sex-biased risk of human metabolicdisease.
Master's Student Supervision
Theses completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest theses.
The risk of developing type 2 diabetes (T2D) is ~40% higher in men than in pre-menopausal women. While lifestyle and cultural factors play a role in this male-biased risk of T2D, studies across animal species suggest biological sex contributes significantly to the sex difference in developing T2D. Large-scale gene expression studies suggest sex differences in pancreatic β cells play a role in the differential T2D risk between men and women. Yet, we lack a comprehensive understanding of β cell dysfunction between the sexes in both normal and pathological contexts. Here, we examined scRNA-seq data of human insulin-producing pancreatic β cells from non-diabetic (ND) and T2D men and women, revealing profound sex-specific changes to β cell gene expression in T2D. To gain deeper insight into sex-specific β cell responses in T2D, we sought a detailed understanding of β cell gene expression in normal physiological conditions. Unbiased pathway analysis of our well-powered islet RNAseq dataset from 20-week-old male and female mice with equivalent insulin sensitivity revealed a sex difference in the enrichment of UPR pathway-associated genes under basal conditions. Because female islets had higher expression of genes involved in protein synthesis, folding, and processing compared with males, we hypothesized female islets would be more resilient to acute ER stress induction with thapsigargin. Indeed, we found female islets resolved ER stress-induced protein synthesis repression faster than males and showed less cell death. These differences were significant for β cell function, as female islets maintained better insulin secretion than males in an ER stress context. Given the profound differences that we observed between the sexes in the transcriptional response to thapsigargin and the known links between ER stress and T2D pathogenesis, these findings provide additional insight into potential mechanisms underlying the differential risk of T2D between men and women.