Payea and Mishra are Inaugural Recipients of the Sayeeda Zain Travel Award
Friday, July 14, 2017
The department of Biochemistry and Biophysics recently presented to the inaugural Sayeeda Zain Travel Award to Mathew Payea and Laxmi Narayan Mishra.
Matthew Payea is a 6th year graduate student in the Biochemistry Ph.D. program studying tRNA biology in laboratory of Eric Phizicky. Matthew received his Bachelors in Science from Eastern Illinois University, majoring in Biochemistry. Matthew used the funding provided by the Sayeeda Zain Travel Award to attend the 22nd annual meeting of the RNA Society in Prague, Czech Republic this past June. There, he gave a talk on his research defining an RNA decay pathway in yeast that destroys mutant tRNAs.
Laxmi Narayan Mishra is a postdoctoral associate working in Dr. Jeffrey J Hayes’ Lab in the Department of Biochemistry and Biophysics, University of Rochester Medical Center. He has a Masters degree from University of North Bengal, Darjeeling, India and a Ph.D. in Biochemistry from Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, India. His research is focused on how epigenetic modifications alter chromosome structure to facilitate gene expression. His Dr. Mishra will use the Sayeeda Zain Travel Award to attend and present his research findings at the international EMBO conference on “The Nucleosomes: From Atoms to Genomes” at Heidelberg, Germany, in August 2017.
The Sayeeda Zain Travel Award is given semi-annually to one or more graduate students and postdoctoral fellows in the Department of Biochemistry and Biophysics at the University of Rochester School of Medicine and Dentistry. The award honors the life and achievements of Professor Sayeed Zain, Ph.D., a longtime faculty member in the Department of Biochemistry and Biophysics. Learn more about the award and Dr. Zain.
Matthew Payea (left) with Dr. Jeffrey Hayes
Laxmi Narayan Mishra (left) with Dr. Jeffrey Hayes
Thursday, July 13, 2017
Emily Boynton and Molly Miles from URMC’s Department of Public Relations and Communications met with a small group of URBEST trainees to discuss how the Medical Center and other academic institutions are sharing science in the social world we live in. They provided some examples of different types of visuals and videos that get great engagement on Facebook, Twitter and other social media sites. The goal? URBEST and The Public Relations and Communications team wanted to find and offer prizes for three original visuals or videos from students and trainees that highlight UR innovation and research. Money, video packs and fame!
First prize was awarded to a team of scientists: Chris Goodwin and Sierra Fox from Biochemistry and Molecular Biology and their camera man Nicholas Nobiletti from Pharmacology and Physiology for What Is CRISPR? They split $750 of prize money.
Read More: Budding UR Scientists and Science Communicators
Thursday, June 29, 2017
Scientists are a step closer to understanding how DNA, the molecules that carry all of our genetic information, is squeezed into every cell in the body. How DNA is “packaged” in cells influences the activity of our genes and our risk for disease. Elucidating this process will help researchers in all areas of health care, from cancer and heart disease, to muscular dystrophy and osteoarthritis.
DNA is a long, floppy molecule, and there’s more than three feet of it in every cell. Our DNA is housed in structures called chromosomes, which condense the DNA to fit into the cell’s tight quarters.
Scientists from the department of Biochemistry and Biophysics at the University of Rochester School of Medicine and Dentistry worked with colleagues in France and Japan to describe the first step of DNA packing in a cell. They provided the first-ever detailed picture of the most basic building block of chromosomes, known as the nucleosome, and found that a protein known as H1 (for linker histone H1) helps DNA become more compact and rigid within the nucleosome. In contrast, when H1 isn’t present, the DNA is loose and flexible.
The tight structure that H1 creates helps shield our DNA from various factors that can activate or “turn on” certain genes. Without H1, DNA is more accessible to factors that could trigger disease-causing genes.
Published in the journal Molecular Cell, this finding will inform research on all processes that involve chromosomes, such as gene expression and DNA repair, which are critical to the understanding of diseases such as cancer, according to Jeffrey J. Hayes, Ph.D., senior study author and the Shohei Koide Professor and chair of the department of Biochemistry and Biophysics.
The teams in France and Japan used specialized microscopes and X-rays to capture pictures of DNA molecules interacting with H1 and other key proteins. Because of the size of the DNA and protein molecules, the pictures generated by these techniques were fuzzy and difficult to analyze.
Lead study author Amber Cutter, a graduate student in Hayes’ lab, put all of the components – DNA, H1, and other proteins – together in tiny test tubes and conducted various biochemical experiments. Her tests, coupled with the X-ray images, confirmed H1’s role.
Cutter (pictured at right), who is entering her fifth year in Hayes’ lab, admits that the science is complex and that a lot more research needs to be done before this work can inform clinical treatment. But, the importance of understanding the most basic biological processes should not be underestimated. “In order to determine what happens when things go wrong in diseases like cancer, we need to know what happens when things go right.”
Hayes and Cutters' work was supported by the National Institutes of Health.
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The University of Rochester Medical Center is home to approximately 3,000 individuals who conduct research on everything from cancer and heart disease to Parkinson’s, pandemic influenza and autism. Spread across many centers, institutes and labs, our scientists have developed therapies that have improved human health locally, in the region and across the globe. To learn more, visit www.urmc.rochester.edu/research.
Read More: Jeffrey Hayes Helps Increase Our Understanding of DNA's Path Into Cells
Friday, May 26, 2017
Cells grow and divide during the cell cycle
Cancer is an extremely complex disease, but its definition is quite simple: the abnormal and uncontrollable growth of cells. Researchers from the University of Rochester’s Center for RNA Biology have identified a new way to potentially slow the fast-growing cells that characterize all types of cancer. The findings, reported today in the journal Science and funded by the National Institutes of Health, were made in kidney and cervical cancer cells in the laboratory and are a long way from being applied in people. But, they could be the basis of a treatment option in the future, the authors said.
Cancer: The Cell Cycle Gone Wrong
All cells go through the “cell cycle,” a series of events that culminate in orderly cell growth and division. In cancer, the cell cycle is out of whack; cells divide without stopping and invade surrounding tissues.
Lynne Maquat, Ph.D.
Researchers identified a protein called Tudor-SN that is important in the “preparatory” phase of the cell cycle – the period when the cell gets ready to divide. When scientists eliminated this protein from cells, using the gene editing technology CRISPR-Cas9, cells took longer to gear up for division. The loss of Tudor-SN slowed the cell cycle.
“We know that Tudor-SN is more abundant in cancer cells than healthy cells, and our study suggests that targeting this protein could inhibit fast-growing cancer cells,” said Reyad A. Elbarbary, Ph.D., lead study author and research assistant professor in the Center for RNA Biology and the department of Biochemistry and Biophysics at the University of Rochester School of Medicine and Dentistry.
Elbarbary, who works in the laboratory of senior study author Lynne E. Maquat, Ph.D., a world-renowned expert in RNA biology, adds that there are existing compounds that block Tudor-SN that could be good candidates for a possible therapy.
Putting the Brakes on Cell Growth
Maquat’s team discovered that Tudor-SN influences the cell cycle by controlling microRNAs, molecules that fine tune the expression of thousands of human genes.
When Tudor-SN is removed from human cells, the levels of dozens of microRNAs go up. Boosting the presence of microRNAs puts the brakes on genes that encourage cell growth. With these genes in the “off” position, the cell moves more slowly from the preparatory phase to the cell division phase.
“Because cancer cells have a faulty cell cycle, pursuing factors involved in the cell cycle is a promising avenue for cancer treatment,” noted Maquat, director of the Center for RNA Biology and the J. Lowell Orbison Endowed Chair and professor of Biochemistry and Biophysics.
Maquat, who also holds an appointment in the Wilmot Cancer Institute, and Elbarbary have filed a patent application for methods targeting Tudor-SN for the treatment and prevention of cancer. Research next steps include understanding how Tudor-SN works in concert with other molecules and proteins so that scientists can identify the most appropriate drugs to target it.
Keita Miyoshi, Ph.D., staff scientist in Maquat’s lab, served as lead study author with Elbarbary. Jason R. Myers and John M. Ashton, Ph.D. from the UR Genomics Research Center played an instrumental role in the study analysis.
Read More: Study: A New Way to Slow Cancer Cell Growth
Thursday, April 27, 2017
Researchers from the University of Rochester Center for RNA Biology: From Genome to Therapeutics examined the role of piRNA in safeguarding the integrity of the genetic information in germ cells. It's known that piRNA -- a type of ribonucleic acid (RNA) that's found most readily in the testes and ovaries -- shields germ cells by silencing the genetic sequences of viral intruders. It's also known that defects or mutations in piRNA lead to infertility in humans and other animals. What's not known is how piRNAs are generated in the first place.
A team led by Xin Li, Ph.D., assistant professor in the departments of Biochemistry and Biophysics and Urology at the University of Rochester School of Medicine and Dentistry, analyzed rooster testes to find out.Read More: Using rooster testes to learn how the body fights viruses
BMB, BSCB Students Win 2017 Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student
Saturday, April 1, 2017
BMB and BSCB graduate students, Lauren Benoodt, Tyler Couch, and Lisa Houston have been selected as joint winners of the 2017 Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student. The students will be presented with a certificate, as well as checks of $700 for each. The three of them were TA’s for IND 408 (Advanced Biochemistry) in the Fall of 2016.
The Edward Peck Curtis Award for Excellence in Teaching by a Graduate Student was established to recognize graduate students who advance the teaching mission of the University by providing highly skilled and innovative undergraduate instruction.
The strongest nominations show innovation in teaching and a positive impact on the learning of undergraduates.
Congratulations Lauren, Tyler, and Lisa!
Tuesday, February 7, 2017
Lynne E. Maquat, Ph.D. has spent her career unraveling what happens in our cells during disease, making seminal contributions to our understanding of RNA’s role in sickness and in health. She’s also committed countless hours to mentoring the next generation of researchers and advocating for young women in the sciences. For these exceptional efforts, she’s receiving the 2017 Lifetime Achievement Award in Science from the international RNA Society.
The J. Lowell Orbison Endowed Chair and Professor in the Department of Biochemistry and Biophysics at the University of Rochester School of Medicine and Dentistry, Maquat began her professional career studying inherited anemias. She discovered a quality control process that blocks the creation of toxic proteins that cause disease. Known as nonsense-mediated mRNA decay or NMD, this process plays a part in one third of all inherited diseases, such as cystic fibrosis and muscular dystrophy, and one third of all acquired diseases, including a number of cancers.
“This award recognizes Lynne’s pioneering contributions to understanding the mechanisms of RNA, as well as her outstanding leadership, support and commitment to our field, including her role as a model for new generations of scientists,” said Juan Valcarcel Juarez, current president of the RNA Society, who works at the Centre for Genomic Regulation in Barcelona, Spain.
James McSwiggen, CEO of the RNA Society, added, “I can’t imagine a more appropriate choice of awardee.”Read More: Maquat Receives Lifetime Achievement Award in Science from International RNA Society