Genetics, Development, and Stem Cells
Students entering graduate school through the program of Genetics, Development, and Stem Cells will perform cutting-edge research on topics including organism function and development, disease models, stem cell biology. Advanced cutting-edge experimental systems in genetics, molecular biology, genomics, proteomics and computational biology are used and taught. This training will lead to a Ph.D. degree in Genetics and will qualify students for high level research careers in academia and in the burgeoning biotech industry.
Monday, August 14, 2017
If you head to your doctor with a fever and cough or other signs you’re getting sick, there’s a good chance your doctor won’t know what’s behind it. It’s hard to test for certain diseases, like bacterial pneumonia.
When patients come in with respiratory viruses like the common cold and sinus infections, doctors often send them home with an antibiotic prescription. The problem is, antibiotics only target bacteria and won’t do anything to fight a virus. Still, about 30 percent of antibiotics prescriptions are for viral infections, according to the CDC. (Make sure to ask these essential questions before taking antibiotics.)
Not only is an antibiotic completely unhelpful against a virus, but it could have major consequences. Antibiotics kill most of the bacteria behind your infection—but not all of them. The bacteria that are strong enough to survive will multiply to create more bacteria that are resistant to treatment, too. Over time, this means there will be more resistant bacteria than ones that antibiotics can kill, so the infections will be harder to treat.
And if you take antibiotics when you don’t need to, or use antibacterial soap, you’re speeding that process along. Eventually, diseases that used to be easy to treat with antibiotics could become dangerous again.
Luckily, researchers might have found a way to tell the difference between bacterial and viral infections, so you won’t get a useless antibiotic. In a study in the journal Scientific Reports, researchers took blood from 94 patients who had lower respiratory tract infections. Lab tests found genetic markers in the blood that could correctly figure out if an infection was viral or bacterial 80 to 90 percent of the time. (Find out how genetic tests could help you lose weight, too.)
Because the sample size was so small, more tests will be needed before doctors can start using this diagnosis method in their offices. But if it does take off, it will be a lot easier than testing for specific diseases.
“Our genes react differently to a virus than they do to bacteria,” says study co-author Thomas Mariani, PhD, pediatrics, environmental medicine, and biomedical genetics professor at University of Rochester Medical Center, in a statement. “Rather than trying to detect the specific organism that’s making an individual sick, we’re using genetic data to help us determine what’s affecting the patient and when an antibiotic is appropriate or not.”
In the meantime, if you think you’re not feeling well, use these natural remedies for cold and flu.Read More: Doctors Might FINALLY Be Able to Tell If Your Infection Is Bacterial or Viral
Wednesday, July 26, 2017
On Monday PhD candidate Margaret Hill presented her work investigating intrahepatic cholangiocarcinoma (iCCA), a form of liver cancer which morphologically resembles the biliary tract. Margaret completed her work under guidance of Dr. Aram Hezel. Her work helps us to understand the interplay between chronic liver injury, a common risk factor for this cancer and the cell of origin as she proved that hepatocytes, as opposed to biliary cells, may serve as a cell of origin for this cancer. Further investigation into important pathways known to be activated in biliary-derived iCCA showed hepatocyte-derived iCCA similarly up-regulates the Wnt and Notch pathways and thus could be targeted for treatment. Margaret went on to probe the importance of MCL-1, the most commonly amplified gene in iCCA, and identified a genetic subset of iCCA cancers which appear to depend on MCL-1 expression. Together, Margaret's work may have important therapeutic implications for iCCA. Well done Margaret and congratulations to Aram!
Monday, July 10, 2017
The ubiquitous human herpesvirus 6 (HHV-6) may play a critical role in impeding the brain’s ability to repair itself in diseases like multiple sclerosis. The findings, which appear in the journal Scientific Reports, may help explain the differences in severity in symptoms that many people with the disease experience.
“While latent HHV-6 – which can be found in cells throughout the brain – has been associated with demyelinating disorders like multiple sclerosis it has not been clear what role, if any, it plays in these diseases,” said Margot Mayer-Proschel, Ph.D., an associate professor at the University of Rochester Medical Center Department of Biomedical Genetics and co-author of the study. “These findings show that, while in the process of hiding from the immune system, the virus produces a protein that has the potential to impair the normal ability of cells in the brain to repair damaged myelin.”
"Read More: Hidden Herpes Virus May Play Key Role in MS, Other Brain Disorders
Tuesday, June 13, 2017
University of Rochester Medical Center researchers have discovered that loss of muscle stem cells is the main driving force behind muscle decline in old age in mice. Their finding challenges the current prevailing theory that age-related muscle decline is primarily caused by loss of motor neurons. Study authors hope to develop a drug or therapy that can slow muscle stem cell loss and muscle decline in the future.
"Read More: Stem Cells May Be the Key to Staying Strong in Old Age
Video of 3 Minute Thesis Event
Thursday, June 8, 2017
We have the video of the full event with all presentations fully captions and with the slides running in time with the videos.
3MT Presenters, Programs & Topics
Thesis presentations in order
- Stephanie Carpenter (Chemistry) - Solving the Mystery of Iron Chemistry
- Sarah Catheline (Pathways of Human Disease) - Inhibiting Inflammaging to Treat Osteoarthritis(OA)
- Scott Friedland (Genetics, Development & Stem Cells) - Pancreatic Cancer and the Tale of the Broken Librarian
- Claire McCarthy (Toxicology) - Investigating the Toxicological Effects of Dung Biomass Smoke Exposure
- Taylor Moon (Immunology, Microbiology and Virology) - The New Epidemic
- Thuy-Vy Nguyen (Social-Personality Psychology) - Solitude *Winner*
- Manisha Taya (Cellular & Molecular Pharmacology and Physiology) - Understanding Lymphangioleiomyomatosis (LAM): The “Other” Steroid-Dependent Cancer From Bed-Side to Bench and Back Again
- Janelle Veazey (Immunology, Microbiology and Virology) - Role of Protein Kinase D in Epithelial Cells During Respiratory Infection
Full 3MT 2017 Event Video (CC)
Monday, May 15, 2017
On May 11th, 2017, Scott Friedland took 2nd place in the Three Minute Thesis (3MT) competition with his talk entitled, “Pancreatic Cancer and the Tale of the Broken Librarian. 3MT, created at The University of Queensland in Australia, is an effort to bring awareness to research and scientific communication, in which competitors have 3 minutes to get across the thrust of their thesis to a general audience. Scott is an MD/PhD student currently working in the lab of Dr. Aram Hezel in the Genetics, Development, and Stem Cells program. His research focuses on defining the role of ARID1A and the SWI/SNF complex in pancreatic cancer and development.Read More: Scott Friedland takes 2nd place in the Three Minute Thesis (3MT) competition
29th Annual Genetics Day Symposium
Thursday, May 4, 2017
This year's Genetics Day provided another opportunity to celebrate the impact of Genetics on science and medicine. The program consisted of four short talks by U of R scientists, a poster session and the Keynote event, the Fred Sherman Lecture, delivered this year by Dr. David Sabatini from the Whitehead Institute for Biomedical Research at MIT. Dr. Sabatini talked about “Growth Regulation by the mTOR Pathway”.
This year’s Genetics Day Poster Session included posters from research laboratories across the University. Three graduate students and one post-doctoral associate were awarded poster prizes:
Andrew Allbee – Biteau Lab
dLMX1A is Required for Drosophila Ovary Stem Cell-Niche Unit Establishment
Amber Cutter – Hayes Lab
Molecular Characterization of Nucleosome Recognition by Linker Histone H1.0
Browyn Lucas – Maquat Lab
Evidence for Convergent Evolution of Sines for Staufen-Mediated Control of MRNA Decay
Janet Lighthouse – Small Lab
Expression Profiling Reveals the Cardioprototective Role of Metallothioneins in Exercise
Genetics Day has been a long-standing tradition at the University of Rochester and more recently includes the Fred Sherman lecture in memory of Fred Sherman a renowned biochemist and geneticist, who led international efforts to establish the yeast Saccharomyces cerevisiae as the premier genetic eukaryotic model system. The lecture is made possible by a generous fund endowed by Fred Sherman's wife, Elena Rustchenko-Bulgac, herself a research professor at the URMC.
GDSC Graduate Justin Komisarof successfully defends
Friday April 28
Tuesday, May 2, 2017
MD/PhD candidate Justin Komisarof presented his work on the hunt for a common cancer gene signature. Building on prior work by the Land and McMurray labs, Justin used bioinformatic approaches to search for the presence of a ‘cooperation response gene’ (CRG) cancer gene expression signature a broad panel of different tumors. Using microarray gene expression datasets from GEO in colon, pancreatic, prostate, and head and neck cancers, Justin found a core set of consistently disregulated CRGs. A more in-depth study of genotype-phenotype correlation in colon cancer samples revealed that this CRG dysregulation did not track with p53 or Ras mutations, suggesting that CRG dysregulation occurs in multiple human cancers, and that the CRG expression pattern is independent of mutational status and may emerges as a function of the malignant state. Justin also applied this CRG-based analysis to prostate cancer samples and identified a core set of CRGs that when combined with clinical staging predicts recurrent outcomes with greater than 80% accuracy – a highly significant improvement over current methods. Justin’s work provides an important step forward for both diagnostic and future therapeutic approaches.
A four gene signature predictive of recurrent prostate cancer.
Komisarof JMcCall M, Newman L, Bshara W, Mohler JL, Morrison C, Land H.
Oncotarget. 2017 Jan 10;8(2):3430-3440.
GDSC Students attend the March for Science
Tuesday, April 25, 2017
Students from the Genetics Program attended The Rochester March for Science on Saturday April 22
Fanju Meng (Biteau Lab), Sreejith (Biteau Lab), Emily Wexler (Portman Lab),
Sebastian Rojas Villa (Biteau Lab), Robert Hoff (Bohmann Lab), Andrew Allbee (Biteau Lab)
Michael John Beltejar awarded CTSI Pilot Trainee Grant
Thursday, April 13, 2017
Michael John Beltejar, a 4th year student in the Genetics, Development, and Stem Cells PhD program with a research focus in Genetic contributions to bone strength has been awarded CTSI Pilot Training Grant.
CTSI Pilot Trainee Grant RFA
A major priority for the CTSI is the active support of research collaborations via cross-disciplinary collaboration, and the support of research that addresses significant problems related to population health. Thus, applications directly addressing these areas are strongly encouraged. Trainee awards help awardees obtain the most prestigious fellowship possible following the project. The project should be part of a long-term plan to become an independent investigator. The award provides a maximum of $25,000 for a period of one year.
Osteoporosis remains a significant concern. By 2025, osteoporotic fractures are expected to increase to 3 million with an estimated cost of $25.3 billion. Morbidity and mortality increases following all major fractures in patients over 55 years of age. It is widely understood that compromised bone strength is the underlying pathophysiology of osteoporosis. Currently, bone mineral density (BMD), is the basis for diagnosis and the main target for osteoporosis therapy. BMD is an important clinical tool, but explains only 55 % of fractures, leaving the needs of 45% of patients unaddressed. Fundamentally, bone strength has two interconnected but distinct components: quantity and quality. While BMD reflects quantity, bone quality (BQ) reflects morphologic and compositional properties. However, developing therapies based on BQ is limited by two major gaps in knowledge: 1) Which genes regulate BQ and 2) Does estrogen deficiency modify the genetic regulation of BQ? Therefore, the objective of the work proposed is to construct a genetic network to identify candidate genes regulating bone composition(SA1) and determine if estrogen deficiency interacts with these genes(SA2).
The rationale for the proposed work is that bridging these gaps in knowledge is a crucial first step in the identification of novel therapeutics. The results produced from SA1 will inform ongoing research in the lab--in particular, a genome-wide association study identifying locations in the genome that are responsible for bone quality. Secondly, the results of SA2 have a strong potential to unlock research on multiple levels osteoporosis management. Identification of novel genes could be used as a new biomarker to identify at risk individuals earlier. Downstream activity of these genes could become additional metrics to monitor disease progression. Finally, these genes become putative targets for novel therapies. The research in this application is innovative because it is a significant departure which shifts focus from BMD to BQ as an equally important contributor of fracture resistance.
GDSC Student to join the Steven’s Laboratory at Harvard Medical
Tuesday, December 27, 2016
Nicole Scott-Hewett, a recent graduate of the GDSC program will be joining Beth Steven’s laboratory at the Boston Children's Hospital F.M. Kirby Neurobiology Center. There Nicole will be involved in projects related to understanding mechanisms of complement and microglia-mediated pruning in development and in disease models. With her paper in this month’s issue of PLoS Biology on lysosomal dysfunction, Nicole leaves us with a fanfare. We wish her all the best for her new beginnings in Boston!
Wednesday, December 21, 2016
Department of Biomedical Genetics researchers believe they have identified a new means of treating some of the most severe genetic diseases of childhood, according to a new study in PLOS Biology. The diseases, called lysosomal storage disorders (LSDs), are caused by disruptions in the functioning of the stomach of the cell, known as the lysosome. LSDs include Krabbe disease, Gaucher disease , metachromatic leukodystrophy and about 40 related conditions. In their most aggressive forms, they cause death of affected children within a few years after birth.
The research was spear-headed by Nicole Scott-Hewett and Chris Folts, two recent graduates of the program in Genetics, Development and Stem Cells. Led by the article's corresponding author Mark Noble, Ph.D., the team discovered for the first time how specific toxic waste products that accumulate in LSDs cause multiple dysfunctions in affected cells. They also found that several drugs already approved for other uses have the unexpected ability of overcoming the cellular toxic build-up, providing new opportunities for treatment. Key to this discovery was the finding that these drugs can help restore normal acidification of the lysosome.
In a mouse model of Krabbe disease (one of the most severe LSDs), Drs. Folts and Scott-Hewett found that their lead study drug, colforsin, increased survival as effectively as in studies where disease-causing mutations were corrected by gene therapy. Colforsin is approved in Japan to treat cardiac disease, which provides information to investigators about its use in humans.
Increased survival in mice occurred even though treatment was started later than is necessary for gene therapy. The research treatment also decreased damage to the brain and improved the quality of life in the diseased mice. All of these outcomes are critical goals in the treatment of children with Krabbe disease or related illnesses, said Noble, who is the Martha M. Freeman, M.D., Professor in Biomedical Genetics at URMC.
"One of the great challenges in these diseases is that they are both rare and come in many different varieties, and advances have tended to focus on single diseases," Noble said. "In contrast, our findings suggest our treatments will be relevant to multiple disorders. Also, we saw benefits of our treatment even without needing to correct the underlying genetic defects. That gives us great hope that we could combine our treatments with other candidate approaches to gain additional benefits."
If the results can be translated into humans, Noble said, the repurposed drugs might improve the quality of life for afflicted children while more difficult experimental genetic treatments are pursued. The complete study can be found at: PLoS Biology
Read More: Repurposed drugs may offer improved treatments for fatal genetic disorders
Meng Wang, a former graduate student in the laboratory of Dr. Bohmann, has been named a Howard Hughes Medical Institute (HHMI) Faculty Scholar
Tuesday, December 20, 2016
Meng Weng, PhD
Dr. Meng Wang a former graduate student in the laboratory of Dr. Bohmann, has been named a Howard Hughes Medical Institute (HHMI) Faculty Scholar, a grant awarded to outstanding young scientists and researchers who have made impressive accomplishments and have a bright future in making groundbreaking contributions.
Dr. Wang is currently an associate professor at Baylor College of Medicine, where she studies the influence of endocrine and metabolic functions on aging, using C. elegans as a model system.
Tuesday, December 20, 2016
Researchers from Wilmot Cancer Institute and Roswell Park Cancer Institute in Buffalo reported in the journal Oncotarget that they have discovered a possible new tool for predicting whether prostate cancer will reoccur following surgery based on the expression patterns of four genes.
The Wilmot/Roswell Park tool was able to predict recurrence, based on human tissue samples and known patient outcomes, with 83 percent accuracy. Currently the only other way to estimate tumor aggressiveness is with a Gleason score, a grading system for prostate tumors that has limited power in most cases, researchers said.
Some prostate cancers grow very slowly, and when the disease is detected early, the five-year survival rates are nearly 100 percent. However, some men are diagnosed with more aggressive localized disease and, even after having a radical prostatectomy, cancer will return in one-third of patients.
“Our study sought to improve upon the prediction tools used in these types of cases so that oncologists would know with more certainty when to recommend additional treatment, such as radiotherapy, immediately after surgery,” said Hucky Land, Ph.D., director of research at Wilmot and the Robert and Dorothy Markin Chair of the Department of Biomedical Genetics, who led the research. (Most patients receive no further treatment after surgery.)
Earlier, Land’s lab discovered a large group of non-mutated genes that are actively involved in cancer development. After analyzing expression of this gene set in frozen prostate cancer tissue samples, researchers discovered the four-gene signature, which was expressed differently in prostate cancer that later returned. Justin Komisarof, an M.D./Ph.D. student in the Land lab, developed the various algorithms and methods to evaluate the gene signature. The research team concluded that their tool outperformed other scientific methods, and they have applied for a U.S. patent.
The National Institutes of Health and Wilmot Cancer Institute/Roswell Park Cancer Institute Collaboration Pilot Funds supported the research. Chief collaborators from Roswell Park include Carl Morrison, M.D., executive director of the Center for Personalized Medicine, and James Mohler, M.D., associate director and senior vice president for translational research at Roswell.
Read More: Research Led by Hucky Land Points to Prostate Cancer Tool
Wilmot Co-directors Honored with Davey Award
Tuesday, November 15, 2016
Hartmut “Hucky” Land, Ph.D. (left) and David C. Linehan, M.D.
Wilmot Cancer Institute’s co-directors Hartmut “Hucky” Land, Ph.D., and David C. Linehan, M.D., were recognized recently with the Davey Award, an honor bestowed on University of Rochester faculty members who have made outstanding contributions to cancer research.
They received their awards at the 21st annual Wilmot Scientific Symposium Nov. 10. The award for Land, who organizes the annual symposium, was a surprise orchestrated by Jonathan W. Friedberg, M.D., M.M.Sc., director of Wilmot Cancer Institute.
At the symposium, Land presented the planned Davey Award to Linehan, who is also Wilmot’s director of clinical operations and the Seymour I. Schwartz Professor and Chairman of Surgery. Linehan was recognized for his work studying the role of the tumor microenvironment in promoting treatment resistance in pancreatic cancer.
Before his lecture, Linehan presented Land the surprise award with a recorded video message from Friedberg. Land, who is also Wilmot’s director of research and the Robert and Dorothy Markin Professor of Biomedical Genetics, was recognized for his body of work and for his work studying the genetic programs that control all of cancer’s worst shared features — such as a cancer cell’s ability to quickly divide and survive despite aggressive treatment.
Monday, November 14, 2016
Researchers at the University of Rochester Medical Center believe they have identified a new means of enhancing the body’s ability to repair its own cells, which they hope will lead to better diagnosis and treatment of traumatic nerve injuries, like those sustained in car accidents, sports injuries, or in combat. In a study published today, the team showed that a drug previously approved for other purposes can ‘wake up’ damaged peripheral nerves and speed repair and functional recovery after injury.
The study appearing in EMBO Molecular Medicine, demonstrates for the first time that 4-aminopyridine (4AP), a drug currently used to treat patients with the chronic nerve disease, multiple sclerosis, has the unexpected property of promoting recovery from acute nerve damage. Although this drug has been studied for over 30 years for its ability to treat chronic diseases, this is the first demonstration of 4AP’s benefit in treating acute nerve injury and the first time those benefits were shown to persist after treatment was stopped.
Study authors, John Elfar, M.D., associate professor of Orthopaedics, and Mark Noble, Ph.D., Martha M. Freeman, M.D., Professor in Biomedical Genetics, and their laboratory team, found that daily treatment with 4AP promotes repair of myelin, the insulating material that normally surrounds nerve fibers, in mice. When this insulation is damaged, as occurs in traumatic peripheral nerve injury, nerve cell function is impaired. These researchers found that 4AP treatment accelerates repair of myelin damage and improvement in nerve function. Read More: Repurposed Drug May Offer Diagnosis, Treatment for Traumatic Nerve Damage
Sunday, November 13, 2016
Dr. Catherine Ovitt
Salivary glands, which make as much as a quart of saliva each day, don’t pose a life-threatening risk if they stop working properly. But given their roles — they are important for swallowing, keep the inside of your mouth moist so your cheeks can move around, and have both anti-fungal and anti-bacterial properties — a malfunction would greatly impact quality of life.
Medical scientist Catherine Ovitt has dedicated her career to the study of salivary glands, in particular to establishing therapeutic strategies for their repair or regeneration after damage from radiation treatment due to head and neck cancers, or because of cellular damage from autoimmune diseases.
“A long-term goal would be to develop some sort of cell therapy treatment, some kind of transplantation or artificial salivary gland,” said Ovitt, who lives in Pittsford and is an associate professor in the Center for Oral Biology, part of UR Medicine’s Eastman Institute for Oral Health. Without the glands, she added, “you end up losing all your teeth.”Read More: Catherine Ovitt Featured in D&C's Hot Jobs
Wednesday, October 12, 2016
Cancer cells have their own unique ways of reproducing, involving a shrewd metabolic reprograming that has been observed in virtually all types of cancer but not in normal cells. Now, University of Rochester Medical Center scientists have pinpointed one key source of the problem, which could lead to new treatment opportunities.
In an article published by Cell Reports, the scientific team shows for the first time how cancer-causing mutations control and alter the way cancer cells biosynthesize and replicate.
The discovery is the result of a close collaboration between the laboratories of Joshua Munger, Ph.D., associate professor of Biochemistry and Biophysics, and Hucky Land, Ph.D., the Robert and Dorothy Markin Professor and Chair of Biomedical Genetics and director of research at the URMC’s Wilmot Cancer Institute.
“Every tissue or cell type in the body has different metabolic needs but as cells become cancerous their metabolism shifts in ways that are very different from normal cells,” Munger said. “Being able to identify those differences is critical for developing treatment targets.”Read More: Wilmot Scientists Exploit Cell Metabolism to Attack Cancer
6th Annual Stem Cell and Regenerative Medicine Symposium
Monday, June 27, 2016
Dr. Jack Kessler
In celebration of the NYSTEM-funded training program in stem cell biology at the University of Rochester, researchers convened for a day of presentations and discussions on advances in stem cell biology. To emphasize the excellence of our junior scientists, five NYSTEM trainees (both pre- and post-doctoral, took turns with leaders in the field of stem cell medicine to present their work. The meeting kicked off with a presentation by Dr. Jack Kessler, Northwestern University Feinberg School of Medicine) describing the factors controlling adult neural stem cell maintenance – a key determinant of cognitive health.
Dr. Kunle Odusi
Dr. Angela Christiano (center)
Dr. Kunle Odunsi (Roswell Park Cancer Institute) spoke in his role as director of the immune-therapy program on the importance of gene-engineered, tumor recognizing CD4 T-cells in anti-tumor therapy.
Dr. Angela Christiano (Columbia University) provided an impressive example of the power of iPSC technology with the development of 3D-skin tissue for treatment of such devastating skin diseases as epidermolysis bulbosa.
Presentations by NYSTEM trainees Fanju Meng (Biteau lab), Wenxuan Liu (Chakkalakal Lab), Michael Rudy (Mayer-Proschel Lab), Dr. Andrew Campbell (Proschel Labs), and Dr. Nicole Scott (Noble Lab) rounded out a day full of exciting new work that highlights the broad impact of stem cell biology on medicine today – and the success of the SCRMI training program. The meeting was buoyed by good vibes and food provided by the backdrop of the Rochester International Jazz Festival.
Congratulations To This Year’s Poster Prize Winners
Graduate Student Category
Zhonghe Ke, High Levels of Niche Ha of the NMR Mediates the Maintenance of LT-HSC by reducing ROS Levels, Gorbunova Lab
Jayme Olsen, Generation of Human Erythroblasts with Increased EX Vivo Self-Renewal, Palis Lab
Michael Trembley, Novel Mechanisms of the Epicardial-Derived Cell Mobilization, Small Lab
Pearl Quijada, Novel Mechanisms of Epicardium Dependent Cardiac Repair, Small Lab
Thank you to all participants for a great event. See you again in 2017!
Wednesday, June 22, 2016
Catherine Ovitt is one of this year’s three recipients of the 2016 IADR Innovation in Oral Care Awards. She accepted the award from IADR President Dr. Marc Heft at the IADR/APR General Session & Exhibition in Seoul, Republic of Korea. The three prestigious awards recognize research in innovative oral care technologies that may maintain and improve oral health, and are supported by GlaxoSmithKline.Read More: Catherine Ovitt receives 2016 IADR Innovation in Oral Care Award
Post-doctoral Fellow wins the 2016 Weiss Toxicology Scholar Award
Wednesday, June 1, 2016
Dr. Luisa Caetano-Davies (Biomedical Genetics) was the postdoctoral winner of the third annual Weiss Toxicology Award. The award was created to strengthen training and research in the Toxicology Training Program by enhancing support of talented future leaders in the field of toxicology, particularly those with an interest in neurotoxicology. The award is presented annually to a meritorious trainee with an interest in Neurotoxicology. Dr. Caetano-Davies is member of the Proschel lab and is studying the effects of environmental toxicants on early stages of Parkinson Disease pathology, in particular with a focus on astrocyte dysfunction. Carolyn Klocke (Cory-Schlechta Lab) was the winner of the graduate student category. Congratulations!
GDSC Graduate Nirmalya Chatterjee reports a novel role of Bet proteins in the control of the oxidative stress response pathway.
Friday, May 27, 2016
Bet proteins are a subclass of bromodomain containing epigenetic “readers”. These proteins have complex and incompletely understood functions in the control of gene expression and chromatin organization. The human Bet proteins Brd3 and Brd4 have been implicated in cancer and thanks to the availability of specific inhibitors, have emerged as promising drug targets. The paper by Nirmalya Chatterjee, Min Tian and others describes experiments in Drosophila that discovered a novel function for Bet proteins: the regulation of the transcription factor Nrf2. The reported data show that a Drosophila Bet protein is part of a previously unknown pathway that can control Nrf2 activity. This is of interest as Nrf2 plays a prominent role in the defense against oxidative stress, protection against various diseases, and aging. Nirmalya Chatterjee, a recent member of the Bohmann Lab, received the PhD last September and is currently working as a postdoc in the group of Norbert Perrimon at Harvard Medical School.
Nirmalya Chatterjee2, Min Tian3, M., Kerstin Spirohn, Michael Boutros & Dirk Bohmann (2016) Keap1-Independent Regulation of Nrf2 Activity by Protein Acetylation and a BET Bromodomain Protein, PLoS Genetics, will go to press 5/27/2016. PMID: 27233051
Luisa Caetano-Davies wins “Best Oral Presentation” Award.
Thursday, May 26, 2016
Luisa, a post-doctoral fellow in the Proschel Lab
, received the award for her presentation on “Astrocyte dysfunction in Parkinson Disease” at the 2016 Environmental Medicine and Toxicology Training Program retreat. Her presentation described the use of both iPSC-based disease-in-a-dish and in vivo animal models to identify early astrocyte defects in PD disease etiology. Congratulations, Luisa!
GDSC Student Xuan Li publishes on the role of Cdk12 in response to stress.
Monday, May 23, 2016
The phosphorylation of RNA polymerase II in the C-terminal domain, or CTD, is an essential step for the transcription of all eukaryotic protein coding genes. The paper be Xuan Li and colleagues describes the unexpected discovery that a certain CTD kinase, called CDK12, is not universally required, but is only needed for the transcription of genes that are inducible by stress, such as heat, DNA damage or reactive oxygen species. This finding suggests that CTD phosphorylation plays a role in the regulation of specific gene expression programs, rather than being a generic step of transcription. This work involved a large-scale robotic RNAi screen in collaboration with the Boutros lab in Heidelberg, as well as genetic and biochemical experiments in the Drosophila model system. Xuan Li, a graduate student in the Bohmann Lab is currently doing an internship at Takeda Pharmaceuticals in Boston and will defend her PhD in November.
Xuan Li1, Nirmalya Chatterjee2,, Kerstin Spirohn, Michael Boutros & Dirk Bohmann (2016) Cdk12 Is A Gene-Selective RNA Polymerase II Kinase That Regulates a Subset of the Transcriptome, Including Nrf2 Target Genes. Scientific Reports, 6:21455. PMID: 26911346
Cindy (Xiaowen) Wang in the Noble Lab wins 2016 GSS Poster Prize
Tuesday, May 17, 2016
Cindy (Xiaowen) Wang in the Noble Lab wins 2016 GSS Poster Prize with her work on:
Identifying c-Cbl as a critical point of intervention in acquired tamoxifen resistant breast cancer.
(Co-authors Jennifer L Stripay, Hsing-Yu Chen and Mark D Noble).
Garry Coles wins 2016 Vincent du Vigneaud Award For Excellence in Graduate Research
Tuesday, May 17, 2016
Garry Coles, graduate of the Genetics, Development and Stem Cell program received this years du Vigneaud commencement award. The University of Rochester School of Medicine and Dentistry recognizes outstanding post-baccalaureate research efforts and promising PhD candidates through the Vincent du Vigneaud Award, in honor of Vincent du Vigneaud, himself a PhD graduate of the University of Rochester and recipient of the 1955 Nobel Prize in Chemistry.
Gary's PhD thesis, entitled "KIF7 and microtubule dynamics function to regulate cellular proliferation and cell cycle progression" focuses on deciphering the role of Kinesin family member 7 (Kif7) on cell cycle control during mammalian development. The work was conducted in Dr. Kate Ackerman's laboratory and has been published in the Proceedings of National Academy of Sciences (PNAS), PLoS Genetics and Developmental Biology.
Dr. Wellington Cardoso, Director for the Center for Human Development at Columbia University Medical Center, comments: "I have been closely following the work of Dr. Coles and his mentor Dr. Kate Ackerman, since we share a similar research interest. Dr. Coles has made important contributions to our understanding of the mechanisms regulating diaphragm and lung morphogenesis… I am confident that he will continue to make great contributions to the field in his future career."
This outlook is also shared by Dr. Hartmut Land, Chair of the Department for Biomedical Genetics and Director of Research at the Wilmot Cancer Center: "Garry is an incredibly driven and inquisitive scientist, and he has a fabulous enthusiasm for his work…(He) has grown tremendously during his time in graduate school. His maturity and independence are ahead of the curve for most post-doctoral fellows." Dr. Land concludes, "Given (Garry's) exceptional talent to make things work, his curiosity and great persistence, I am certain that he will contribute significantly to any scientific environment... (and)… become a leader in his field".
Class of 2014 Prelim season begins
Thursday, May 12, 2016
On Friday, May 6th, Andrew Albee opened the 2016 season of Prelim Exams. According to his committee, Andrew passed his qualifying exam with flying colors, and the committee looks forward to the outcome of his work. His studies on the function of Lmx Homeobox transcription factors in early somatic progenitors of the Drosophila ovary are also the basis of an F31 application submitted in February of this year. Congratulations, Andrew!
28th Annual Genetics Day Meeting
Wednesday, May 11, 2016
Dr. Michael Levine
This year's Genetics Day provided another opportunity to celebrate the impact of Genetics on science and medicine. An excellent selection of speakers from the University of Rochester Medical Center highlighted the importance of diverse genetic mechanisms ranging from chromatin remodeling in erythropoesis (Laurie Steiner) and DNA damage repair (Xi Bin) to translational control by riboswitches (Joe Wedekind) and di-codon usage (Elizbeth Grayhack). Genetics Day concluded with the Fred Sherman lecture by Dr. Michael Levine (Princeton University). His presentation on visualizing the mechanisms of transcriptional enhancers was equally entertaining and insightful. Originally from the Hollywood area, and by his own admission a closet movie producer, Dr. Levine wowed audiences with in vivo movies of enhancer reporters, shedding new light on what we all thought was an established principle of molecular genetics.
Manisha Taya – Hammes Lab
The Role of Estrogen Signaling in a Mouse Model for Lymphangioleiomyomatosis (Lam)
Sam Carrell – Thornton Lab
Silencing of Myotonic Dystrophy Protein Kinase (Dmpk) Does Not Affect Cardiac or Muscle Function In Mice
Walter Knight – Yan Lab
The Role and Mechanism of Cyclic Nucleotide Phosphodiesterase 1c in Regulating Pathological Cardiac Remodeling and Dysfunction
Vincent Martinson - Jaenike lab
Gut Microbiota of Distantly Related Drosophila Species Share Similar Bacterial Diversity
Genetics Day has been a long standing tradition at the University of Rochester And more recently includes the Fred Sherman lecture in memory of Fred Sherman a renowned biochemist and geneticist, who led international efforts to establish the yeast Saccharomyces cerevisiae as the premier genetic eukaryotic model system. The lecture is made possible by a generous fund endowed by Fred Sherman's wife, Elena Rustchenko-Bulgac, herself a research professor at the URMC.
Heather Natola Wins 2016 Edward Peck Curtis Award for Excellence in Undergraduate Teaching
Thursday, April 28, 2016
We are proud to announce that Heather Natola has been selected to receive the 2016 Edward Peck Curtis Awards for Excellence in Undergraduate Teaching. Ms. Natola received high praise from her students, faculty in the Department of Biomedical Genetics and Rochester Museum and Science Center.
Ms. Natola is a graduate student researcher in the Pröschel Lab, where she investigates new therapeutic approaches to spinal cord injury as part of the UR Stem Cell and Regenerative Medicine Institute.
"Ms. Natola was particularly instrumental in providing students with in-depth and detailed training, which had a significant positive impact on the student’s engagement and learning"
-Hartmut Land, Ph.D., Chair, Department of Biomedical Genetics
"Despite her ambitious and demanding research work, Heather has volunteered for all of these teaching activities. Clearly she has not only become an ambassador for science as a whole, but has helped fulfill the mission of our school. What more can we ask of a graduate student?"
Christoph Proschel, Ph.D., Program Director - Genetics Development & Stem Cells Ph.D. Program
Heather is enthusiastic and committed to promoting interest in science and an attitude of life-long learning
-Kara Verno, Program Supervisor - Rochester Museum and Science Center
You can read more about Heather’s commitment and passion for teaching by reading her statement to the Curtis Award Committee.
Wednesday, February 17, 2016
A Wilmot Cancer Institute investigator discovered a gene that’s required for the initiation of melanoma and the growth of disseminated melanoma cancer cells in the lungs.
The findings suggest that the gene’s signaling pathway may be proof that melanoma stem cells exist, a question that’s being debated by scientists.
Lei Xu, Ph.D., associate professor of Biomedical Genetics at the University of Rochester Medical Center, is lead author of the study, which was recently published in PLOS ONE and funded by a Wilmot Cancer Institute pilot grant. The Xu lab investigates the multiple, complex steps that occur as cancer cells spread from the original tumor to other parts of the body.
Read More: Tracking Melanoma Metastasis Leads to Key Gene Discovery
Monday, February 1, 2016
The photo shows a blue-stained stem cell and a red-stained stem cell that each generated new bones cells after transplantation.
A team of Rochester scientists has, for the first time, identified and isolated a stem cell population capable of skull formation and craniofacial bone repair in mice—achieving an important step toward using stem cells for bone reconstruction of the face and head in the future, according to a new paper in Nature Communications.
Senior author Wei Hsu, Ph.D., dean’s professor of Biomedical Genetics and a scientist at the Eastman Institute for Oral Health at theUniversity of Rochester Medical Center, said the goal is to better understand and find stem-cell therapy for a condition known as craniosynostosis, a skull deformity in infants. Craniosynostosis often leads to developmental delays and life-threatening elevated pressure in the brain.
Hsu believes his findings contribute to an emerging field involving tissue engineering that uses stem cells and other materials to invent superior ways to replace damaged craniofacial bones in humans due to congenital disease, trauma, or cancer surgery.
For years Hsu’s lab, including the study’s lead author, Takamitsu Maruyama, Ph.D., focused on the function of the Axin2 gene and a mutation that causes craniosynostosis in mice. Because of a unique expression pattern of the Axin2 gene in the skull, the lab then began investigating the activity of Axin2-expressing cells and their role in bone formation, repair and regeneration. Their latest evidence shows that stem cells central to skull formation are contained within Axin2 cell populations, comprising about 1 percent—and that the lab tests used to uncover the skeletal stem cells might also be useful to find bone diseases caused by stem cell abnormalities.
The team also confirmed that this population of stem cells is unique to bones of the head, and that separate and distinct stem cells are responsible for formation of long bones in the legs and other parts of the body, for example.
The National Institutes of Health and NYSTEM funded the research.
Read More: Scientists Discover Stem Cells Capable of Repairing Skull, Face Bones
Tuesday, December 1, 2015
Researchers in the Department of Biomedical Genetics have unraveled one of the key molecular mechanisms that regulate stem cell behavior, a discovery that could provide important insight into regenerative medicine and certain forms of cancer.
The study – led by Benoit Biteau, Ph.D. – appears in the journal Cell Reports, and was conducted in fruit flies, or drosophila. While diminutive in stature, fruit flies have proven to be an invaluable research tool and have made oversized contributions to medicine, particularly in the fields of molecular biology and genetics.
Benoit and his colleagues focused on a transcription factor called Sox21a which is uniquely found in the stem cells of the drosophila intestine. Transcription factors are proteins that control the expression of genes and, subsequently, help regulate cellular activity. Sox21a is the equivalent of Sox2, a transcription factor found in humans that is known to play an important role in the function of stem cells and cell reprogramming.
Read More: Study Provides New Insight on Stem Cell Function