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 Academic Affairs Dr. Lilli Fishman at [email protected].
Below is an alphabetical list of the Principal Investigators (PIs) who hosted 2021 Postbaccalaureate Fellowship research projects. Host labs and projects for the 2022 program will be confirmed soon.
Aß oligomers (AßO) are the toxic species thought by many to drive Alzheimer’s Disease. However, how AßO can drive neurodegeneration has been a long-standing debate that is as of yet unresolved. On the other hand, the study of senescence within the central nervous system (CNS) has recently began to emerge. Senescent cells can be deleterious by developing the senescence-associated secretory phenotype (SASP), which includes the release of inflammatory and oxidative factors. Senescence can also propagate autonomously by secondary senescence. Finally, outside of the brain, senescent cells can be cleared by natural killer cells, part of the innate immune system.
Our hypothesis is that AßO-induced senescence results in the SASP, causing inflammation, oxidative and proteotoxic stress conducive to cognitive impairment. Secondary senescence through neuronal projections can explain the spread of pathology. Finally, natural killer cell infiltration into the brain parenchyma amidst loss of blood brain barrier integrity can result in widespread senescent cell killing, potentially marking the onset of neuronal death in clinical AD. To test our hypotheses, we are assessing AßO-induced senescence in primary neuron cultures and natural killer cell co-cultures using histo-cytometry: which includes immunocytochemistry, spectral scanning plus linear unmixing confocal imaging, and image-data processing with IMARIS and FlowJo.
Mitochondria are the power plants of the cell and are also the only cellular organelle in mammals that possess their own DNA. 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 compromised 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 Summer Scholar 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 functions of the brain emerge from communication between neurons. The language of neuronal communication is mediated by chemicals that are released from one neuron and sensed by another. These chemical signals consistent of both “fast acting” neurotransmitters, as well as more than 200 neuromodulators that act on longer timescales. Neuropeptides are the largest and most diverse class of neuromodulators, and they control vital processes like energy homeostasis, as well as motivational and emotional states such as sleep, arousal, pain, stress, and mood. Yet, we still lack a clear understanding of how neuropeptides generate the diverse behavioral outputs of the brain. In particular, the molecular mechanisms by which neuropeptides are turned ‘off’ once they have been released from a neuron are not well understood. To address this challenge, we are systematically identifying neuropeptidases, the enzymes that turn off neuropeptide signaling, and mapping which neuropeptides they inactivate. We are seeking undergraduate student researchers to assist a postdoctoral scholar in the lab to characterize identified neuropeptidases and manipulate their expression within specific cell types to determine their role(s) in behavior and aging.
Desired Skills or Experience: Completed coursework in biology, biochemistry, chemistry, genetics, and neuroscience desired but not necessary. Familiarity and proficiency with the following techniques desirable: C. elegans maintenance, PCR, cloning, microscopy, mass spectrometry.
Senescent cells are characterized by an irreversible arrest of the cell cycle. They secrete a unique milieu of pro-inflammatory cytokines, chemokines, and growth factors collectively referred to as the senescence-associated secretory phenotype (SASP). These cells have been implicated in a large number of age-related diseases, and recent efforts to develop therapeutic interventions are centered around either selectively eliminating senescent cells (senolytics) or reducing SASP secretion (senomorphics). While these approaches present two possible avenues for reducing senescent cells’ impact, they still lack specificity for their intended target.
We focus 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 to selectively induce apoptosis in target cells that express ligands, such as senescent cells. However, recent studies have shown that some senescent cells employ mechanisms to escape NK-mediated clearance, while ‘aged’ NK cells become less efficient at eliminating target cells.
The laboratory focuses on enhancing the targeted elimination of senescent cells by NK cells. We are pursuing three main avenues of research:
These approaches will afford a better understanding of interactions between NK cells and senescent cells in the context of aging and help develop novel therapeutic interventions for enhanced elimination 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. We have taken two disparate organ systems, the brain and the lung, and are discovering parallels in their development, response to infections and molecular functions. 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 human stem cells and verified 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 2021 SRF Postbaccalaureate Fellowship Program application period will open on Monday, November 2, 2020. –
The Postbaccalaureate Fellowship Program application is currently closed.
Our next application window will open on October 15.
The 2023 SRF Postbaccalaureate Fellowship Program application is currently open.
Application Deadline: January 15th at midnight PST.
Selected applicants will be contacted for interviews in the late winter and decisions will be made by May 15th.
Please be sure to download the recommendation instructions and note that your application will not be processed until your letter(s) of recommendation have been received.
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.