The SRF Postbaccalaureate Fellowship Program offers recent graduates a gap year option where they can strengthen their research and communication skills in preparation for such opportunities as graduate programs, medical programs, and biotech positions. Like the SRF Summer Scholars Program, the goal of the Postbaccalaureate Fellowship Program includes assignments and training that hones writing and presentation skills. These training exercises are completed within the framework of a research project that the Fellow will be tasked with completing under the guidance of a scientific mentor.
SRF Education undergraduate programs primarily are designed to address two pressing needs in STEM education: the availability of novel, inquiry-based research opportunities and scientific communication skills. Whether a student plans to pursue postgraduate studies or apply for a research position at a pharmaceutical company, practical experience is key. However, research opportunities are limited at some colleges, and specific fields of research, such as tissue engineering, may be completely absent.
SRF Education sets itself apart from many other training programs with its focus on the development of scientific communication skills in addition to enhancing laboratory and critical thinking skills. Over the course of its educational programs, participants are guided through practical writing assignments that simulate documents scientists are often asked to produce, such as grant proposals. The communication training culminates in a formal presentation at a symposium where participants present the results of their work to their peers and mentors.
Review the following to confirm your eligibility to participate in the program:
If you have any questions regarding your eligibility for the program, you may contact SRF Director of Education Gregory Chin at [email protected].
Below is an alphabetical list of the Principal Investigators (PIs) and their 2019 Postbaccalaureate Fellowship research projects. Participating labs and specific research projects are similar but vary slightly from year to year. The 2020 Postbaccalaureate Fellowship research project options will be announced when the 2020 application period opens on November 1, 2019.
Neurofibrillary tangles are a defining hallmark of both Alzheimer’s and Parkinson’s disease and they or similar aggregates also appear in the neuronal cytoplasm in other neurodegenerative diseases of old age. One possibility for their formation is that these tangles arise from an autophagic “traffic jam” caused by lysosomal inactivation. Lysosomal autophagy is an important mechanism by which cells rid themselves of such proteotoxic aggregates. Restoration of lysosomal function therefore constitutes an attractive candidate target for these disorders. As part of funded research from the SENS Research Foundation, we have established human tau P30L mutant versus wildtype-expressing neurons as an in vitro model of disease to test whether restoration of lysosomal function can prevent or reverse the formation of toxic tau aggregates. We determined using this model that low-dose (0.1 microM) application of a pharmacological accelerator of autophagic flux, K604, decreases levels of phosphorylated tau and protects against neurite retraction associated with the P30L model, even following their formation. We now propose to use this model to test newly identified lysosomal rejuvenating factors recently identified by our laboratory as part of a compound library screen for such compounds. These could potentially serve as novel therapeutics for the treatment of Alzheimer’s and Parkinson’s disease.
Mitochondria are the power plants of the cell and are also the only cellular organelle that possess their own DNA in mammals. In humans, mitochondrial DNA (mtDNA) codes for 13 important proteins, which all assemble into the oxidative phosphorylation relay. Mutations in mtDNA occur as a consequence of constant exposure to reactive oxygen species produced by the mitochondrial energy generation process as well as mistakes in mtDNA replication. These mutations accumulate over time due to inefficient repair mechanisms and compromise respiratory chain function. Inherited and acquired mutations in mtDNA result in impaired energy generation and are the cause for several pathologies such as Leber’s hereditary optic neuropathy (LHON), Myoclonic Epilepsy with Ragged Red Fibers (MERRF), Kearns-Sayre syndrome and Leigh syndrome.
Using the allotopic approach, we have identified specific targeting elements/sequences that can improve expression of these essential genes from the nuclear DNA and their transport to the correct location in mitochondria. The Fellow selected will get the opportunity to design a library of constructs to attempt to rescue specific mtDNA mutations in model patient cell lines. The ability of re-engineered genes to rescue function will be evaluated through various techniques, such protein gels, qPCR and activity assays, with the potential of extending the studies to animal models. Time permitting, the Fellow will validate these constructs for expression from a safe harbor locus using the CRISPR/Cas9 and dual integrase mediated cassette exchange (DICE). Candidates with an interest in mitochondrial biology and with exposure to cell culture, molecular biology and protein biochemistry are encouraged to apply.
The potential project will involve modeling disease and aging in human induced pluripotent stem models. The Ellerby laboratory has established a number of disease models of Huntington’s disease, Parkinson’s disease and aging. We have developed different methods to identify novel therapeutic targets for HD and aging. The intern will generate models of disease and evaluate therapeutic targets to validate these for treatment of the disease.
The Loring lab is focused on harnessing the power of pluripotent stem cells for regenerative medicine. We believe that cells derived from pluripotent stem cells will revolutionize medicine and lead to longer and healthier lives. We are looking for an intern to work on our cell therapy project for Parkinson’s disease in which induced pluripotent stem cells from Parkinson’s patients are used to derive dopaminergic neurons, the same neurons which are lost in the brains of Parkinson’s patients. The aim of this Postbaccalaureate Fellow project is to evaluate whole-genome gene expression profiles from dopaminergic neurons derived from 10 different patient lines helping to build a model by which future cell lines can be evaluated prior to clinical use. The Fellow will generate the neurons from the patient stem cell lines and analyze the resulting gene expression data.
This research project is geared toward performing translational research studying aging as it relates to the immune system and senescent cells. More specifically, the Summer Scholar will study how the immune system interacts with senescent cells. Research will include testing of candidate signaling protein blockers to try to induce killing of senescent cells. Another aspect of this project will involve identifying and characterizing new types of senescent cells from among the many tissue and cell types in the body. This will involve high-throughput microscopy on our robotic microscope. The research project will be a collaborative effort between SRF and the Buck Institute for Research on Aging, located in Novato, CA.
We believe the study of stem cell biology will provide insights into many areas: developmental biology, homeostasis in the normal adult, and recovery from injury. Indeed, past and current research has already produced data in these areas that would have been difficult or impossible via any other vehicle. We have engaged in a multidisciplinary approach, simultaneously exploring the basic biology of stem cells, their role throughout the lifetime of an individual, as well as their therapeutic potential. Taken together, these bodies of knowledge will glean the greatest benefit for scientists and, most importantly, for patients. All of our research to date has been performed in animal models with the ultimate goal of bringing them to clinical trials as soon as possible.
Possible research project options include:
Below is an alphabetical list of the Principal Investigators (PIs) and their 2020 Postbaccalaureate Fellowship research projects.
Neurofibrillary tangles are a defining hallmark of both Alzheimer’s and Parkinson’s disease, and they or similar aggregates also appear in the neuronal cytoplasm in other neurodegenerative diseases of old age. One possibility for their formation is that these tangles arise from an autophagic “traffic jam” caused by lysosomal inactivation. Lysosomal autophagy is an important mechanism by which cells rid themselves of such proteotoxic aggregates. Restoration of lysosomal function therefore constitutes an attractive candidate target for these disorders. As part of funded research from the SENS Research Foundation, we have established human tau P30L mutant versus wildtype-expressing neurons as an in vitro model of disease to test whether restoration of lysosomal function can prevent or reverse the formation of toxic tau aggregates. We determined using this model that low-dose (0.1 microM) application of a pharmacological accelerator of autophagic flux, K604, decreases levels of phosphorylated tau and protects against neurite retraction associated with the P30L model, even following their formation. We now propose to use this model to test newly identified lysosomal rejuvenating factors recently identified by our laboratory as part of a compound library screen for such compounds. These could potentially serve as novel therapeutics for the treatment of Alzheimer’s and Parkinson’s disease.
Mitochondria are the power plants of the cell and are also the only cellular organelle that possess their own DNA in mammals. In humans, mitochondrial DNA (mtDNA) codes for 13 important proteins, which all assemble into the oxidative phosphorylation relay. Mutations in mtDNA occur as a consequence of constant exposure to reactive oxygen species produced by the mitochondrial energy generation process as well as mistakes in mtDNA replication. These mutations accumulate over time due to inefficient repair mechanisms and compromise respiratory chain function. Inherited and acquired mutations in mtDNA result in impaired energy generation and are the cause for several pathologies such as Leber’s hereditary optic neuropathy (LHON), Myoclonic Epilepsy with Ragged Red Fibers (MERRF), Kearns-Sayre syndrome and Leigh syndrome.
At SENS Research Foundation, we are in the early stages of creating an exciting and innovative system to repair mitochondrial mutations. Using the allotopic approach, we have identified specific targeting elements/ sequences that can improve expression of these essential genes from the nuclear DNA and their transport to the correct location in mitochondria. The Postbaccalaureate Fellow selected will use a computational approach to design and test a library of constructs in model patient cell lines with specific mutations to mtDNA. The ability of re-engineered genes to rescue function will be evaluated through various techniques, such as protein gels, qPCR, and activity assays, with the potential of extending the studies to animal models.
The human oocyte is the largest cell in multicellular organisms with mitochondria being the most abundant organelle. Mitochondria produce energy in the form of ATP through oxidative phosphorylation and are crucial for oogenesis, fertilization, and implantation of the embryo. Age-related infertility in women has been linked to depleted levels of mitochondria and accumulation of certain mutations in the mtDNA of oocytes. To date, there have been several assisted reproductive technologies (ART) that have been used to deliver exogenous mitochondria and/or replace damaged mtDNA in oocytes. Although there has been some success with mitochondria replacement therapy (MRT), there are still significant challenges. Our goal is to explore non-invasive strategies to improve mitochondrial health / numbers in oocytes. The selected candidate will develop novel tools to deliver exogenous mitochondria to cells through in vitro models and assess their viability in the recipient cell. The potential of these tools in the fertility space will also be explored. Candidates with some mouse experience especially are encouraged to apply.
The Postbaccalaureate Fellowship project will involve modeling disease and aging in human induced pluripotent stem models. The Ellerby laboratory has established a number of disease models of Huntington’s disease, Parkinson’s disease and aging. We have developed different methods to identify novel therapeutic targets for HD and aging. The candidate will generate models of disease and evaluate therapeutic targets to validate them for treatment of the disease.
Senescent cells are characterized by an irreversible arrest of the cell cycle and secrete a unique milieu of pro-inflammatory cytokines, chemokines, and growth factors collectively referred to as the senescence-associated secretory phenotype (SASP) due to which these cells have been implicated in a large number of age-related diseases, and recent efforts to develop therapeutic interventions are centered around selectively eliminating senescent cells (senolytics). While these approaches present two possible avenues for reducing the impact of senescent cells, they still lack specificity for their intended target.
We are focusing on developing therapeutic interventions to selectively eliminate senescent cells by utilizing innate immune cells like Natural Killer (NK) cells. These innate immune cells have evolved mechanisms to selectively induce apoptosis in target cells based on the expression of ligands on the target cells. In addition, recent publications suggest that (a) senescent cells have evolved mechanisms to escape NK cells or (b) NK cells lose their ability to eliminate senescent cells with aging. We will utilize approaches to isolate and enrich NK cells from human blood and investigate the mechanism by which they can selectively target and kill senescent cells. The main aim of the project is to test these hypotheses using in vitro and ex vivo cell co-culture experiments.
This approach will afford better understanding of mechanisms involved in NK cell interaction with senescent cells, which will be critical in designing targeted therapeutic approaches to age-related diseases caused by the accumulation of senescent cells.
We believe the study of stem cell biology will provide insights into many areas: developmental biology, homeostasis in the normal adult, and recovery from injury. Indeed, past and current research has already produced data in these areas that would have been difficult or impossible via any other vehicle. We have engaged in a multidisciplinary approach, simultaneously exploring the basic biology of stem cells, their role throughout the lifetime of an individual, as well as their therapeutic potential. Taken together, these bodies of knowledge will glean the greatest benefit for scientists and, most importantly, for patients. All of our research to date has been performed in animal models with the ultimate goal of bringing them to clinical trials as soon as possible.
Possible research project options include:
The Genotype-Tissue Expression (GTEx) project funded by NIH common fund has sequenced thousands of human tissue samples from around 1000 people and 56 different types of organs. One of the main aims is to understand the association of genetic variations to phenotypes. However, the massive data generated by GTEx not only can provide information to explain the variations but also can be used to study aging. The GTEx cohort contains all age groups, and the data provides molecular profiles from multi-omics. Most of the previous aging studies were done using animal models or with very limited clinic data. For a few large-scale studies, they are mainly based on genomic information in general. As part of the GTEx project, our lab has sequenced the proteome of multiple organs from many individuals. Compared to genomics, proteomics is closer to phenotype and can provide direct evidence. Integrating proteomics information with other omics can provide a more comprehensive molecular profile for the study of aging at organ level. However, integrating information from multi-omics is a daunting task. It requires knowledge from both domains and also needs sophisticated mathematical models. We believe results from this study will greatly advance the understanding of aging.
– The 2020 SRF Postbaccalaureate Fellowship Program application period will open on Friday, November 1, 2019. –
The 2020 SRF Postbaccalaureate Fellowship Program application period is now closed.
Offering undergraduate students the opportunity to conduct biomedical research to combat diseases of aging under the guidance of a scientific mentor and emphasizing the development of laboratory and communication skills to develop well-rounded future scientists.
Offering undergraduate students the opportunity to conduct biomedical research to combat diseases of aging under the guidance of a scientific mentor and emphasizing the development of laboratory and communication skills to develop well-rounded future scientists.
Funding PhD students at Oxford University in the field of healthcare translation to research international guidelines pertaining to digital health development and implementation, as well as healthcare regulation and standards world-wide.
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