Research

Bodmer Lab
The Bodmer Laboratory uses the Drosophila model system to investigate the molecular mechanisms that underlie heart formation during embryogenesis as well as adult heart function.

Current Researchers

Lab Head

Rolf BodmerProfessor, Program Director
E-mail: rolf@sbpdiscovery.org
Phone: (858) 795-5295

Biography
Rolf Bodmer earned his Ph.D. in Biochemistry and Neurobiology from the University of Basel, Basel, Switzerland in 1983. Dr. Bodmer trained as a postdoctoral fellow in Neurobiology at the Albert Einstein College of Medicine in New York, and also studied Molecular Genetics at the University of California, San Francisco. He was appointed Assistant Professor of Biology in 1990 at the University of Michigan. There he was promoted to Associate Professor of Biology in 1996, and then appointed to Associate Professor of Molecular, Cellular and Developmental Biology in 2001. Dr. Bodmer joined Sanford-Burnham Medical Research Institute in 2003, where he is Professor and Program Director of the Development and Aging Program in the Neuroscience, Aging and Stem Cell Research Center.

Research Assistant Professor

Karen OcorrResearch Assistant Professor
E-mail: kocorr@sbpdiscovery.org
Phone: (858) 795-5125

Biography
Karen Ocorr earned her Ph.D. in Neurobiology from Wesleyan University in 1982. She subsequently held postdoctoral fellowships at the University of Texas Medical School – Houston and Stanford Medical School. In 1991 she moved to the University of Michigan where she taught Introductory Biology, Cell Biology, Animal Physiology and Biochemistry. Based on her teaching experience she co-wrote the “Absolute Ultimate Guide to Lehninger’s Biochemistry” now in its 6th edition. She returned to research in 2004 when she joined the Sanford-Burnham Medical Research Institute where she is currently a Research Assistant Professor in the Development & Aging Program.

Lab Managers

Staff Scientist

Ryan BirseStaff Scientist 
E-mail: rbirse@sbpdiscovery.org
Phone: (858) 646-3100 x3801

Biography
Ryan Birse received his Ph.D. from Stockholm University with his research focusing on the genetics involved in neuropeptide regulation of lipid metabolism and nutritional stress responses. Currently, Ryan is working on understanding the regulation of metabolism through dietary modification (high fat diet) and how over-nutrition disrupts normal cardiac function and lipid metabolism.

Ryan’s recent work focuses on the fundamental genetic relationships between obesity and heart dysfunction in a simplified system. He has recently established that in the Drosophila high caloric diets cause excessive fat accumulation, which leads to metabolic syndrome-like symptoms eventually leading to severe cardiac dysfunction. To further expand this model Ryan is working to elucidate the novel, multigenerational tissue specific mechanisms that modulate lipolytic activity, which mediates the adverse effects of high caloric parental diet to the progeny. With the use of these models we the have the potential to greatly enhances our genetic/molecular understanding of trans-generational cardiac lipotoxicity and the effects of diet induced cardiac dysfunction. These findings will only help to enhance the fields understanding the influence of parental and acute metabolic (lipid) imbalance on heart dysfunction.

Georg VoglerStaff Scientist 
E-mail: gvogler@sbpdiscovery.org
Phone: (858) 646-3100 x3801

Biography
Georg Vogler Ph.D. obtained his Ph.D. in the Technau lab at the University of Mainz, Germany where he was working on Drosophila nervous system development. Along with his Ph.D. supervisor, Joe Urban, Geo analyzed the function of the zinc-finger transcription factor Zfh1 on motoneuron development. Back then, he became interested in tissue morphogenesis and joined Rolf's lab to study the orphogenesis of the embryonic Drosophila heart. Currently, Geo is investigating how cardiac specification is integrated within the cardiac cells to cause the cell shape changes necessary to form the heart tube.

Postdoctoral Fellows

Leah CannonPostdoctoral Fellow 
E-mail: lcannon@sbpdiscovery.org
Phone: (858) 646-3100 x3237

Biography
Leah trained and practiced as an emergency veterinarian in Australia before completing a Ph.D. in molecular cardiology at the Victor Chang Cardiac Research Institute. During her Ph.D., she investigated the molecular causes of Hypertrophic Cardiomyopathy. In 2011, Leah moved to San Diego to join the Bodmer Lab. Here she is using the power of Drosophila genetics to uncover the causes of cardiac aging.

Soda DiopPostdoctoral Fellow 
E-mail: sdiop@sbpdiscovery.org
Phone: (858) 646-3100 x3801

Biography
Leah trained and practiced as an emergency veterinarian in Australia before completing a Ph.D. in molecular cardiology at the Victor Chang Cardiac Research Institute. During her Ph.D., she investigated the molecular causes of Hypertrophic Cardiomyopathy. In 2011, Leah moved to San Diego to join the Bodmer Lab. Here she is using the power of Drosophila genetics to uncover the causes of cardiac aging.

Sreehari KalvakuriPostdoctoral Fellow 
E-mail: skalvakuri@sbpdiscovery.org
Phone: (858) 646-3100 x3801

Biography
Sreehari earned his Ph.D in Molecular Genetics and Developmental Biology in Markus Noll's lab at University of Zürich, Switzerland. As a graduate student, Sreehari has analyzed the cis-regulatory elements of Drosophila Paired gene in great detail, which helped him to uncover novel functions of Paired gene in larval development and male fertility. After completion of his graduate studies, he has developed interest in disease models particularly in Parkinson's disease (PD) models.

In Bodmer lab, he has been screening for genes that would genetically interact with PINK1/Parkin in an effort to find alternative targets for treating PD patients. In addition to his PD model work, Sreehari is also interested in understanding the roles of PINK1/Parkin in cardiac function especially the protective role of Parkin against Ischemic injury and age induced decline in cardiac function.

Stan WallsPostdoctoral Fellow 
E-mail: swalls@sbpdiscovery.org
Phone: (858) 646-3100 x4314

Biographic
Stan Walls obtained his PhD from the University of California San Diego in Molecular Biology, where he studied under Dr. Greg L. Harris at SDSU. As a Rees-Stealy and American Heart Association Predoctoral Fellow, his primary focus was on the role of bioactive sphingolipids in the etiology of obesity, where his research elucidated novel regulatory control of distinct metabolic pathways by both ceramide and sphingosine 1-phosphate.
As an NIH Ruth L. Kirschstein Postdoctoral Fellow under the NHLBI, Stan is currently working towards elucidating the role of ceramide in the pathogenesis of diabetic cardiomyopathy. His current approach involves using proteomic screening of ceramide-interacting proteins in search of novel regulatory mechanisms through which ceramide exerts its cardiotoxic effects.

Graduate Students

Katja BirkerGraduate Student 
E-mail: kbirker@sbpdiscovery.org
Phone: (858) 646-3100 x3801

Biography
Katja earned her degree in honors biology at the University of British Columbia in Canada. There, her thesis work focused on examining cation secretion in the renal tubules of Drosophila. Katja was intrigued by the power this organism held in the research community. With her passions set on biomedical research, she set her sights on Rolf Bodmer’s lab where she would be able to use this simple genetic organism in biomedically-relevant research.

Currently, Katja focuses on understanding the potential genetic mechanisms behind a congenital heart disease, Hypoplastic Left Heart Syndrome (HLHS), using the fly heart model. She is screening multiple candidate genes and selecting those that have strong phenotypes to further analyze in depth. She is interested in finding genes and mechanisms that are important in heart development and function and possibly involved in HLHS.

Rachel Zarndt EllisonGraduate Student 
E-mail: rellison@sbpdiscovery.org
Phone: (858) 646-3100 x3237

Biography
As a scientist and mountaineer, I have long been interested in the adaptations animals make to high altitude environments where the levels of oxygen are often too low to support normal life. Recently, human populations living for multiple generations at high altitude were shown to have a strong genetic selection for certain genes with known involvement in hypoxia pathways (specifically, members of the HIF pathway).

Using a unique population of Drosophila selected over multiple generations for tolerance to extreme hypoxia, we investigate novel genetic changes underlying physiological adaptations to hypoxia through an interdisciplinary, collaborative approach. By investigating key genetic pathways shown to be altered in multiple species adapted to high altitude environments and in our unique Drosophila populations, I aim to demonstrate a clear link between genetic mutations and cardiac function under hypoxia. These findings may reveal completely novel pathways related to the hypoxia response, and are of benefit to those seeking new treatments for hypoxic illnesses (e.g., cardiovascular disease, pulmonary hypertension, stroke).

Research Technicians

Visiting Scientists

Tony CammaratoVisiting Scientist
Assistant Professor of Cardiology at John Hopkins
E-mail: acammar3@jhmi.edu
Phone: (858) 646-3100 x3801

Hua BaiVisiting Scientist
Investigator at Brown University
E-mail: hua_bai@brown.edu

Biography
I am interested in understanding the molecular mechanism of muscle aging, with an emphasis on autophagy and TGF-beta signaling. My recent studies revealed an interesting link between Activin signaling (a member of the TGF-beta superfamily) and muscle autophagy and proteostasis. I also showed that muscle-specific inhibition of Activin signaling prolonged lifespan of Drosophila, the fruit flies. Although it is known that many members of the TGF-beta superfamily play important roles in various muscle pathology, the role of Activin in age-associated cardiomyopathy and functional decline is not well understood. Therefore, my future research aims to address two fundamental questions: 1). Whether and how Activin regulates tissue homeostasis and tissue functions in aging heart? 2). Can enhanced autophagy prevent the cardiomyopathy and the decline of heart functions with age?

Girish MelkaniVisiting Scientist
Research Assistant Professor at San Diego State University 
E-mail: gmelkani@sbpdiscovery.org
Phone: (858) 646-3100 x3801

Biography
We are using multidisciplinary integrative approaches to investigate the mechanism of amyloid‐induced protein‐unfolding, aggregation and metabolic defects that lead to cardiomyopathies, diabetes mellitus, muscle atrophy and inclusion body myopathy in a Drosophila melanogaster (fruit fly) model. Amyloid precursor proteins are prone to misfolding and are involved in cardiac amyloidosis. Amyloidosis constitutes a large group of proteinopathies characterized by the accumulation of misfolded proteins into aggregates in various tissues.

Several amyloid‐linked neurodegenerative and metabolic diseases, including Huntington's disease, Alzheimer's disease, tauopathy, Parkinson's disease, amyotrophic lateral sclerosis, and diabetes mellitus exhibit pathological protein aggregates and are often associated with striated muscle defects. Amyloidosis' relationship with striated muscle defects and metabolic disorders has been largely overlooked and the mechanisms of amyloid‐related striated muscle and metabolic disorders are poorly understood.

Former Researchers

Director of Cardiology & Catheterization Lab, Shonan Kamakua General Hospital 
E-mail: akasaka-cba@umin.net

Principal Investigator at University of Edinburgh, Heart Foundation
E-mail: P.S.Hartley@ed.ac.u

Graduate Student

Staff Scientist at Inserm, France