MGM SUMMER UNDERGRADUATE RESEARCH ENGAGEMENT (MGM SURE)
The Department of Molecular Genetics and Microbiology is pleased to continue for the fourth summer a 10-week summer fellowship program for Duke undergraduates. The program runs from June 3, – August 2, 2019. The deadline to apply is March 20, 2019. To download the application, click here: MGM SURE application
The goal of undergraduate research opportunity is to introduce motivated students to important questions in Genetics, Microbiology, Infectious Diseases, Virology, and RNA Biology through faculty-mentored research projects and practical lab experience. The program also includes monthly science and career development discussions with faculty and trainees (graduate students and postdocs) in MGM. The research experience culminates in MGM SURE fellows presenting their summer research project at the department’s annual retreat in early September.
Overall, the program aims to capture students who are interested in developing a research project in an MGM lab during their undergraduate years at Duke and completing their senior thesis based on this research. The program also aspires to prepare students to become scientific scholars immersed in sustained long-term pursuit of biomedical research.
Research in the Department of Molecular Genetics and Microbiology spans both model and pathogenic organisms and the full spectrum of genetics from unicellular to multicellular eukaryotic organisms. Many investigators are experts in both microbiology and genetics, including those utilizing yeasts as experimental microbial systems, and those probing the interactions of infectious agents with cellular or heterologous host model systems. Much of the history of modern molecular biology can be traced directly to genetic approaches with microbial and infectious systems, including the discoveries of DNA and RNA as the genetic material, the elucidation of the genetic code, and the development of recombinant DNA approaches based on bacterial restriction-modification systems and related enzymes. Existing areas of strength in the Department include: 1) microbiology (virology, mycology, bacteriology); 2) RNA biology and genomic expression analysis; 3) fungal genetics; 4) genetics of model systems and humans; 5) chromosome structure, function, replication, and repair, and 6) epigenetics.
Eligibility and Criteria
MGM SURE is open to Duke undergraduate students who have completed or are currently enrolled in at least one biological sciences course. With the exception of graduating seniors, all Duke undergraduates are eligible to apply. Prior research experience is not required, since a goal of the program is to immerse students in cutting-edge research labs where they can acquire skills in experimental practices, data analysis and interpretation, and effective science communication. Those undergraduates currently involved in research in MGM labs are also eligible to apply. Candidates not currently working in MGM labs are encouraged to contact faculty of interest prior to submitting an application to discuss the possibility of doing summer research in a particular lab.
We encourage women and individuals from underrepresented groups to apply. Students will be selected based on academic record, letters of recommendation, and descriptions of research interests and goals.
The research engagement will run from June 3, 2019 – August 2, 2019. Students should be present full-time for the entire summer program, and ought not be enrolled in courses during the research engagement period.
Number of Awards
In Summer 2019, MGM SURE will grant 4-6 awards to support summer research projects of ~10 weeks in duration. Each award includes a $4000 stipend (to help cover accommodation and living expenses for 10 weeks) and $1000 in project expenses to be paid to the host lab. Note that housing/accommodation is not provided or coordinated by the program.
Projects involving human subjects, either in-person or online, may need approval from the Duke Institutional Review Board. All MGM SURE fellows will be required to complete the necessary online safety training offered through the Duke Safety Office
2019 MGM Sure Students
When a rabbit gives birth, its pups ascend towards the nipples of the doe and elicits a well-characterized head-searching pattern followed by the grasping of the doe’s nipple. This behavior has been linked to 2-methylbut-2-enal (2MB2), a volatile compound found in rabbit milk. In Dr. Matsunami’s lab, I am currently responsible for cloning and testing candidate receptors for 2MB2 in order to isolate the receptors that drive this head-searching, nipple-grasping behavior.
Previous work done by Dr. Silver’s lab has shown that the exon junction complex (EJC), an RNA binding protein important in splicing, translation, and other stages of RNA’s life cycle, has a significant role in the proper regulation of neural stem cells (NSCs). Mutations resulting in haploinsufficiency in any one of three core protein components of the EJC—Magoh, Rbm8a, or Eif4a3— were shown to produce similar NSC impairment phenotypes that cause microcephaly in mice. I have been involved in a research project investigating the function of a human-specific iso-form of the EJC component protein Magoh and its role in brain development. We are currently investigating its binding partners, particularly, its interaction with another core EJC protein, Rbm8a. Our goal is to determine if this Magoh iso-form, which is missing its third exon, has a different function than the full-length iso-form.
Michelle Kim Boyoung
The hepatitis C virus (HCV) NS3-NS4A protease complex is required for viral replication and is the major viral innate immune evasion protein. NS3-NS4A evades antiviral innate immunity by inactivating several proteins, including MAVS, an innate immune signaling protein, and Riplet, an E3 ubiquitin ligase that activates innate immune signaling. We have found that phosphorylation of NS4A, the cofactor for NS3, plays an important role in the inactivation of Riplet. My research will focus on identifying the cellular kinase that phosphorylates NS4A to regulate Riplet inactivation during HCV infection.
Anorexia is part of the behavioral response to infection that facilitates host survival – depriving pathogens of essential nutrients and reducing energy spent on food-seeking to better mount an immune response. Enteroendocrine cells (EEC) make up 1% of the intestinal epithelium and constitute the body’s largest endocrine organ. EEC release appetite-regulating hormones such as cholecystokinin, polypeptide YY, and ghrelin in response to luminal contents. EEC express functional Toll-like receptors, but their role in controlling food intake during infection is not well understood. My research focuses on characterizing the role of EEC hormone production in infection-induced anorexia using the zebrafish model organism.
The trehalose pathway has been identified as an attractive antifungal target because it is essential to the virulence and/or fitness of the pathogenic fungus Cryptococcus neoformans. The Tps1 enzyme is critical to the pathway because it is responsible for the first step in the production of trehalose; among others, eleven different proteins are predicted to interact with Tps1 based on yeast two-hybrid experiments performed in the Perfect laboratory. By indirectly measuring trehalose levels, I have identified two genes that were significantly altered in trehalose levels compared to wild-type strain (H99) when grown at 37 degrees Celsius. I will be conducting further tests to confirm that the observed phenotype is causal to the reduction in trehalose and allow me to characterize the interaction of the two genes with Tps1 and the trehalose pathway.
2018 MGM Sure Students
Organisms of the Leishmania genus are directly responsible for approximately 2 million new cases of infectious disease each year. The intracellular lifestyle employed by these pathogens is contingent upon the protease GP63. GP63, despite often being erroneously referred to as a single protease, is present in multiple forms with 7 copies of GP63 on chromosome 10 of Leishmania major and more divergent copies on chromosomes 28 and 31. However, it is unknown how these different copies of GP63 vary in their enzymatic properties and expression during infection. I hypothesize that different copies of GP63 cleave different substrates during infection. Therefore, I will be testing and comparing the substrate-specificities and kinetic properties of divergent copies of GP63.
I am a rising senior studying Biology & Global Health and I am involved with research at the Duke Human Vaccine Institute in the laboratory of Dr. Sallie Permar. Our lab investigates maternal and infant immune responses that contribute to impeding transmission of vertically transmitted neonatal viral pathogens (HIV, CMV, ZIKV), and how these immune responses can best be targeted by vaccine approaches. In the lab, I am involved with a project aiming to define the pressures that select infant transmitted/founder (T/F) viruses from the circulating virus pool in HIV-1 infected mothers. We have isolated and produced 47 HIV Env-specific IgG monoclonal antibodies (mAbs) from four HIV-infected transmitting women and 45 HIV Env-specific IgG mAbs from three HIV-infected non-transmitting women. We have defined the autologous HIV virus populations in these HIV-infected women and the Env sequences of HIV viruses that initiated infection in their matched infants. We will define the fine-epitope specificity and neutralization activity of these Env-specific mAbs against their paired maternal autologous viruses to test if infant T/F viruses are defined by their neutralization resistance to maternal neutralizing antibodies. Our findings will help inform the development of maternal vaccination strategies aimed at preventing mother-to-child transmission of HIV to help achieve an HIV-free generation.
An animal’s sense of smell is dependent on odorants binding to olfactory receptors in the nose. Different odorants bind different olfactory receptors, and the combination of receptors that an odorant binds to determines what smell is perceived by the organism. Enantiomers are molecules that are mirror images of each other. Although enantiomers have the same physical properties, some are known to smell different. For example, humans perceive (+)-carvone as caraway and perceive (-)-carvone as spearmint. Behavioral studies also suggest that mice have the ability to discriminate between enantiomeric pairs like (+)-carvone and (-)-carvone. On a similar note, previous studies suggest that animals have the ability to differentiate between deuterated odorants and undeteurated odorants. The goals of my project are in two parts: 1) to provide molecular evidence of a mouse’s ability to discriminate between enantiomeric pairs and 2) to provide molecular evidence that a mouse can differentiate between deuterated and undeteurated odorants.
I’m currently working on one of Dr. Chi’s research projects regarding the nutrient-sensing regulation of gigaxonin protein encoded by GAN gene. Gigaxonin is critical for the degradation and turnover of cytoskeleton proteins in axonal cells. I will be working with new methods in biotechnology to identify the intricacies of functional role of this protein and how its dysfunction contributes to human genetic disorder.
One system and phenotype of Epstein-Barr virus (EBV) infection under study is the latent/lytic switch in Burkitt lymphoma (BL) cells. Though much is known about the specific viral promoter controlling this (BZLF1), the effect of normal viral variation on lytic reactivation in latently infected cells has not been studied. In comparing the sequence variation in several lytic genes, we have found polymorphisms in the 3’UTR of the BALF5 gene (DNA polymerase) that could explain increased rates of lytic reactivation. Our hypothesis is that the different 3’UTRs among viral strains may lead to increased expression of the polymerase, increased DNA replication, and higher viral titers. Our goal is to probe in silico the targeting/lack of targeting of the BALF5 3’UTR by the EBV BART and other miRNAs, and to functionally characterize the BALF5 3’UTR from BL strains relative to B95-8 and M81 EBV strains.
Influenza A virus (IAV) has a segmented, negative-sense RNA genome. The mechanism through which IAV selectively packages its genome is not well understood, but it has been suggested that vRNA-vRNA interactions between the segments facilitate incorporation of each segment into progeny virions. My research focuses on achieving a better understanding of IAV packaging, particularly by using the reverse genetics system for IAV to perturb its terminal-end packaging signals and observing how such changes affect the virus.
A family of NSUN genes are writers for 5-methyl C (m5C). Methylation of cytosine to m5C is known to be necessary for cell function, but its role in viral pathogenesis remain unclear. Our research aims to study the effects of the NSUN2 gene and cytosine methylation on Murine Leukaemia Virus using both knockout and over expression NSUN2 cell lines. Mapping of NSUN2 RNA binding sites will also be performed to pinpoint the exact location of m5C on the viral RNA transcripts. Through the use of these tools we should be able to develop a better understanding of the role the epitranscriptome in MLV pathogenesis.