Eric S. Lander

Education

  • PhD, 1981, Oxford University
  • AB, 1978, Mathematics, Princeton University

Research Summary

Following the successful completion of the Human Genome Project, the challenge now is to decipher the information encoded within the human genetic code — including genes, regulatory controls and cellular circuitry. Such understanding is fundamental to the study of physiology in both health and disease. At the Broad Institute, my lab collaborates with other to discover and understand the genes responsible for rare genetic diseases, common diseases, and cancer; the genetic variation and evolution of the human genome; the basis of gene regulation via enhancers, long non-coding RNAs, and three-dimensional folding of the genome; the developmental trajectories of cellular differentiation; and the history of the human population.

Awards

  • William Allan Award, American Society of Human Genetics, 2018
  • James R. Killian Jr. Faculty Achievement Award, MIT, 2016
  • Block Memorial Award for Distinguished Achievement in Cancer Research, Ohio State University, 2013
  • AAAS Philip Hauge Abelson Prize, 2015
  • Breakthrough Prize in Life Sciences, 2013
  • Harvey Prize for Human Health, Technion University, Israel, 2012
  • Dan David Prize, 2012
  • Albany Prize in Medicine and Biomedical Research, Albany Medical College, 2010
  • Gairdner Foundation International Award, Canada, 2002
  • Max Delbruck Medal, Berlin, 2001
  • MacArthur Foundation, MacArthur Fellowship, 1987
Retinoic acid regulates transitions in mouse sperm production
November 7, 2017

CAMBRIDGE, MA – Sperm production requires progression through a well-orchestrated series of transitions in the testes that move diploid spermatogonia cells, with two complete sets of chromosomes, through a series of transitions to produce haploid sperm, with one copy of each chromosome, poised to swim and fertilize an available egg. There are four major transitions in sperm production, or spermatogenesis. The first is spermatogonial differentiation, during which spermatogonia differentiate, losing their stem-cell like qualities. The resulting spermatocytes then initiate meiosis and undergo two rounds of cell division to generate haploid spermatids. The spermatids undergo elongation and then the resulting sperm are released.

The signals that control progression through these transitions were poorly understood until 2015, when David Page, Member and Director of Whitehead Institute, professor of biology at Massachusetts Institute of Technology, and investigator with Howard Hughes Medical Institute and colleagues determined that retinoic acid (RA), a derivative of vitamin A that has been shown to play a key role in a number of developmental processes, was responsible for coordinating the first two stages of spermatogenesis-differentiation and meiosis. Now, in a paper published this week in the journal Proceedings of the National Academy of Sciences, Page, first author Tsutomu Endo, and colleagues extend those findings to show that RA signaling in mice coordinates the second two transitions as well.

Diagram of model by which retinoic acid coordinates spermatogenesisThe researchers used chemical manipulation of RA levels to determine that RA controlled the second two transitions, spermatid elongation and sperm release, in addition to the first two. With this knowledge in hand, the researchers were then able to drill down and get a better picture of how RA regulates male gamete production. One outstanding question has been how males are able to continually produce sperm throughout their lifetime, in contrast with females whose egg production and maturation is limited. Page and colleagues measured RA levels in the testes and discovered that it is cyclically produced, driving production of sperm during the male lifetime. In addition to the timing of RA production, the researchers also examined its source. From which cells was the RA signal coming? During the first two transitions, they determined that the RA was coming from the somatic Sertoli cells, the support cells of the testes, and in the second two transitions they determined that it was being released by the germ cells themselves-the meiotic (pachytene-stage) spermatocytes were found to be secreting RA to other germ cells in the testes.

These findings not only contribute to our fundamental understanding of male gamete formation, they also provide important clues for the field of reproductive technology. For years, scientists have been working on making gametes in the laboratory, but have had difficulty making functional sperm. This discovery of the role of RA in spermatogenesis adds important tools to the toolbox of assisted reproduction. The work shows that RA is required in both the early and late transitions of spermatogenesis and sheds light on an important component of laboratory efforts for sperm production.

Other researchers involved include Elizaveta Freinkman and Dirk G. de Rooij.

This research was supported by Howard Hughes Medical Institute (HHMI) and the United States Department of Defense (DoD W81XWH-15-1-0337)

Written by Lisa Girard
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David Page’s primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. He is also a Howard Hughes Medical Institute Investigator and a Professor of Biology at the Massachusetts Institute of Technology.
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Paper cited: Endo, T et al.  Periodic production of retinoic acid by meiotic and somatic cells coordinates four transitions in mouse spermatogenesis. Proc Natl Acad Sci. DOI: 10.1073/pnas.1710837114. Epub 2017 Nov 6.
Other work cited: Endo T et al. Periodic retinoic acid-STRA8 signaling intersects with periodic germ-cell competencies to regulate spermatogenesis. Proc Natl Acad Sci. DOI: 10.1073/pnas.1505683112. Epub 2015 Apr 20.
Stuck on the membrane

A pro-metastatic transcription factor’s journey from anonymity to a promising target for breast cancer therapy

October 20, 2017

An overwhelming majority of deaths from cancer are associated not with the primary tumor, but instead with its metastases to other sites in the body. For this reason, understanding the properties of cancer cells that give them a high metastatic potential, and identifying molecular strategies to intervene, is critical for improving clinical outcomes.

One of the hallmarks of cancer cells with high metastatic potential is an epithelial to mesenchymal transition (EMT). This shift in their gene expression landscape is a harbinger for both invasive behavior and anti-cancer drug resistance. One signaling pathway active in cells that have undergone EMT transition, the PERK pathway, has been of particular interest to Whitehead Institute Member and Massachusetts Institute of Technology associate professor of biology Piyush Gupta and postdoctoral researchers in Gupta’s lab, Yu-Xiong Feng and Dexter Jin. The PERK signaling pathway has been a sought-after target for a number of types of cancer, including breast cancer. Drug companies had largely given up on the PERK signaling pathway as a target, however, because when it is inhibited, it also has the unintended consequence of affecting glucose regulation to the degree that mice given PERK inhibitors typically develop diabetes within a few weeks. Gupta and colleagues hypothesized that downstream elements of the pathway could include targets with more specific effects on metastatic behavior, potentially enabling the development of therapies that do not result in the unintended consequences associated with inhibiting PERK. 

In a recent article in Nature Communications, Gupta, Feng, Jin, and colleagues describe CREB3L1, a factor downstream of the PERK pathway that is active in the subset of triple negative breast cancer cells and tumor cells that have undergone an EMT transition. CREB3L1 expression is associated with distant metastasis and is important for the transformed cell’s invasive and drug resistant properties. While factors like CREB3L1, called transcription factors, are usually difficult to target with small molecules, Gupta and his team zeroed in on a unique property it shares with only a small handful of other factors-it is normally stuck to the membrane of a cellular compartment called the endoplasmic reticulum and, in order for it to be active, it need to be cut free by factors called proteases. Gupta and colleagues show that certain protease inhibitors can actually stop the activation of CREB3L1 in its tracks, along with the invasive and drug resistance properties its activation confers. 

While the PERK signaling pathway has been an attractive target for anticancer therapy, its more general cellular role made it an intractable target. The downstream factor of the pathway  CREB3L1 is a potential new target for breast cancer therapy whose specificity of action makes it an attractive option for targeting metastatic behavior.

By Lisa Girard
Citation:
Feng Y-X, Jin DX, et al. “Cancer-specific PERK signaling drives invasion and metastasis through CREB3L1.” Nature Communications DOI:10.1038/s41467-017-01052-y
Department of Biology hosts its first Science Slam

Eight biology trainees had just three minutes to explain their research and earn favor with the judges and audience in new yearly event.

Raleigh McElvery | Department of Biology
October 5, 2017

Nearly 300 spectators crowded into a lecture hall at the Ray and Maria Stata Center on a recent Tuesday to witness the first annual Science Slam, hosted by MIT’s Department of Biology.

A science slam features a series of short presentations where researchers explain their work in a compelling manner and — as the name suggests — make an impact. The presentations aren’t just talks, they’re performances geared towards a science-literate but non-specialized public audience. In this case, competitors were each given one slide and three minutes to tell their scientific tales and earn votes from audience members and judges.

The jury included Ellen Clegg, editorial page editor of The Boston Globe and co-author of two award-winning books, “ChemoBrain” and “The Alzheimer’s Solution;” Emilie Marcus, CEO of Cell Press and editor-in-chief of the flagship journal, Cell; and Ari Daniel, an independent science reporter who produces digital videos for PBS NOVA and co-produces the Boston branch of Story Collider.

Among the competitors were five graduate students and three postdocs who hailed from labs scattered throughout Building 68, the Whitehead Institute, the Broad Institute, the Koch Institute for Integrative Cancer Research, and the Picower Institute for Learning and Memory. The storytellers were:

  • Sahin Naqvi, from David Page’s lab, who spoke about the evolution of genetic sex differences in mammals, as well as how these differences impact the likelihood of developing certain diseases based on gender;
  • Sudha Kumari, from Darrell Irvine’s lab, who spoke about her work investigating immune cell interactions — specifically how T cells communicate using physical contact;
  • Deniz Atabay, from Peter Reddien’s lab, who spoke about the ways cells in flatworms self-organize during regeneration to re-form organs, tissues, and even neural circuits;
  • Emma Kowal, from Christopher Burge’s lab, who spoke about her goals to demystify the ways in which certain noncoding regions of genetic sequence, known as introns, contribute to protein production;
  • Xin Tang, from Rudolf Jaenisch’s lab, who spoke about a technique to illuminate the seemingly invisible changes in brain cells that trigger disease, using a glowing enzyme from a firefly;
  • Nicole Aponte, from Troy Littleton’s lab, who spoke about her ability to manipulate brain cell activity in the fruit fly, and study how defects in neuronal connections contribute to developmental disorders;
  • Karthik Shekhar, from Aviv Regev’s lab, who spoke about his efforts to identify and manipulate different types of brain cells, understanding how they assemble into complex networks to facilitate learning, memory, and — in some cases — disease; and
  • Monika Avello, from Alan Grossman’s lab, who spoke about “bacterial sexology,” that is, how and why these organisms choose to block unwanted sexual advances from fellow bacteria.

Vivian Siegel, who oversees the department’s communications efforts, moderated the event. Siegel and the Building 68 communications team joined forces with three members of the Building 68 MIT Postdoctoral Association — Ana Fiszbein, Isabel Nocedal, and Peter Sudmant — to publicize the event and to host two pre-slam workshops, as well as one-on-one training sessions with individual participants.

“Participating in a Science Slam seemed like a great way for our trainees to learn how to communicate to a nonspecialized audience, which is something they will need to be able to do throughout their careers,” Siegel said. “We really wanted to develop a camaraderie among the participants, and bring trainees together from across the department to help each other tell compelling stories about their science.”

Kowal — whose talk was titled “Gone but Not Forgotten: How Do Introns Enhance Gene Expression?”  — ultimately took home both the audience and jury cash prizes. Kowal completed her undergraduate degree in chemical and physical biology at Harvard before coming to MIT for graduate school. Her dream is to write science fiction, so she decided she’d better study science so she’d know what to write about.

“I really enjoyed seeing people get stoked about introns, and the fact that they enhance gene expression,” she said. “It’s a great way to get comfortable explaining your project in a compelling way to a broad audience. Since you’ll probably be telling people about your work for a while, I think it’s a very good use of time to practice doing that.”

Three MIT biologists receive NIH Outstanding Investigator Awards

Graham Walker, Michael Yaffe, and Robert Weinberg earn support from the National Institutes of Health to further their research endeavors.

Raleigh McElvery | Department of Biology
September 19, 2017

This fall, two faculty members from the MIT Department of Biology received R35 Outstanding Investigator Awards sponsored by the National Institute of Environmental Health Sciences (NIEHS), while a third garnered the same distinction from the National Cancer Institute (NCI). These awards provide long-term support to experienced investigators with outstanding records of research productivity as they undertake lengthy projects with unusual potential.

Graham Walker, the American Cancer Society Professor in the Department of Biology at MIT, a member of the Center for Environmental Health Sciences, and affiliate member of the Koch Institute for Integrative Cancer Research, is one of two biology faculty to earn the R35 Outstanding Investigator Award from the NIEHS.

This award is supported by the NIEHS through the Revolutionizing Innovative, Visionary Environmental health Research (RIVER) program. The program recognizes outstanding investigators in the field of environmental health, potentially offering up to $750,000 per year over the next eight years.

The awardees include both mid-career and senior researchers, whose work spans many aspects environmental health science — including technology development, mechanistic, clinical, and epidemiological research. A total of eight investigators received the NIEHS RIVER R35 this year.

“The RIVER program is designed to fund people, not projects,” said David Balshaw, chief of the NIEHS Exposure, Response, and Technology Branch who leads the NIEHS team overseeing this initiative. “It gives outstanding environmental health scientists stable funding, time, and, importantly, flexibility to pursue creative scientific ideas, rather than constantly writing grants to support their research programs.”

Walker will use his award to continue investigating the fundamental mechanisms of mutagenesis and DNA repair, with a special emphasis on the Rev1/3/7-dependent pathway of mutagenic translation synthesis found in eukaryotes, including humans. He and his colleagues recently published evidence suggesting that inhibiting this pathway could potentially improve chemotherapy.

Michael Yaffe, the David H. Koch Professor of Science at MIT, a member of the Koch Institute and the Center for Environmental Health Sciences, and attending surgeon at the Beth Israel Deaconess Medical Center, also received a NIEHS RIVER R35 award.

Yaffe’s work concerns how cells respond to injury, including damage to DNA and RNA molecules arising because of the environment and in response to drugs used to treat cancer. He is also interested in the relationship between inflammation, blood clotting, and cancer. He employs multidisciplinary approaches harnessing techniques from biochemistry, structural and cell biology, computer science, and systems biology/engineering.

Yaffe will use his funds to further a project investigating the roles of protein kinases in coordinating cellular responses to damage to both DNA and RNA molecules.

Robert Weinberg, founding member of the Whitehead Institute, professor of biology at MIT, an affiliate member of the Koch Institute, and director of the MIT Ludwig Center for Molecular Oncology, has received his R35 Outstanding Investigator Award from the NCI.

The award provides up to $600,000 per year over seven years to accomplished cancer researchers, nominated by their institutions, who have served as principal investigators on an NCI grant for the last five years. A total of 18 investigators received the NCI Outstanding Investigator Award this year.

“The NCI Outstanding Investigator Award addresses a problem that many cancer researchers experience: finding a balance between focusing on their science while ensuring that they will have funds to continue their research in the future,” said Dinah Singer, director of NCI’s Division of Cancer Biology. “With seven years of uninterrupted funding, NCI is providing investigators the opportunity to fully develop exceptional and ambitious cancer research programs.”

Weinberg is a pioneer in cancer research, best known for his role in discovering the first human oncogene — a gene that, when activated, can spur tumor growth. His lab is also credited with isolating the first known tumor suppressor gene.

He will use his funds to delve into the mechanisms of metastasis — the process that allows cancer cells to spread. He aims to learn more about how these cells disseminate from primary tumors, as well as how they become established in distant tissues after they metastasize.

Pew recognizes four MIT researchers for innovation in biomedical science

Biophysicist Ibrahim Cissé and cell biologist Gene-Wei Li honored as Pew Scholars; postdocs Ana Fiszbein and María Inda are named Pew Latin American Fellows.

Julia C. Keller | School of Science
June 20, 2017

The Pew Charitable Trusts has named Ibrahim Cissé, assistant professor of physics, and Gene-Wei Li, assistant professor of biology, as 2017 Pew Scholars in the Biomedical Sciences. In addition, two postdocs, Ana Fiszbein and María E. Inda, were named to the 2017 class of Pew Latin American Fellows in the Biomedical Sciences in computational biology and synthetic biology, respectively.

The Pew Scholars program encourages early-career scientists to pursue innovative research to advance the understanding of human biology and disease. This year, 22 Pew Scholars will receive $240,000 over four years and gain inclusion into a select community of scientists that includes three Nobel Prize winners, five MacArthur Fellows, and five recipients of the Albert Lasker Medical Research Award. The applicants, who conduct research in all areas of biomedical sciences, must be nominated by one of 180 invited institutions. To date, the program has invested in more than 900 scholars.

“Pew’s biomedical programs not only provide young scientists with the flexibility to pursue creative ideas; they also spark interdisciplinary thinking and collaborations that can open new paths in the search for answers,” says Craig C. Mello, who won the 2006 Nobel Prize for physiology or medicine, was a 1995 Pew Scholar, and chairs the Pew Scholars National Advisory Committee.

Cissé, the MIT Class of 1922 Career Development Assistant Professor, says “support from Pew at an early stage is great encouragement in pushing my lab further at the frontiers of different fields.”

Cissé’s research group is investigating the fundamental processes involved in gene activation. Using a combination of techniques in cell and molecular biology, biochemistry, genomics, and super-resolution microscopy, he will continue his investigations of the behaviors of the enzyme involved in the transcription of DNA to RNA molecules. The enzyme, RNA polymerase II, has been well-studied in vitro, but Cissé’s work looks at these transient biological interactions within living cells. His findings will deepen the understanding of these processes, disruptions in which are linked to human disease, including most cancers.

Li’s research looks at evolution of cells’ production of proteins to answer a fundamental biological question of how cells specify how much of each type of protein to produce. In Li’s Quantitative Biology Lab, researchers have developed a technique for measuring the precise production rates of every protein in a cell. Combining this approach with other techniques in cell, molecular, and computational biology, Li is comparing a broad range of organisms across evolutionary distances to determine whether all of their proteins are maintained at some preferred level. By artificially perturbing the quantities of selected proteins, Li can explore the mechanisms cells use to reestablish the proper protein balance to better understand when misregulation occurs that leads to disease.

“The success of my research hinges on close integration between expertise in biological and physical sciences, as well as constant stimulation from both disciplines,” says Li, the Helen Sizer Career Development Assistant Professor. “The Pew scholarship will also provide a unique opportunity to interact with the brightest young minds in the biomedical sciences outside my field that will elevate my research to unanticipated levels.”

Each year, current scholars come together to discuss their research and learn from peers in fields outside of their own. “I am looking forward to interacting with other Pew scholars, many of whom are also working on paradigm-shifting ideas,” says Cissé.

Rebecca W. Rimel, president and CEO of The Pew Charitable Trusts calls the scholars an “impressive group” that has demonstrated “the curiosity and courage that drive great scientific advances, and we are excited to help them fulfill their potential.”

The Pew Latin American Fellows program, meanwhile, is intended to support postdocs from Latin America. Winners are awarded two years of funding to conduct research at laboratories and academic institutions in the United States.

The program also provides additional funding to awardees who return to Latin America to launch their own research labs after the completion of their fellowships. About 70 percent of program participants have taken advantage of this incentive and are conducting work on regional and global health challenges in nine Latin American countries, according to The Pew Charitable Trusts.

“Almost 150 young scientists have returned to their home countries and established independent research labs, providing critical groundwork for biomedical research across Latin America,” says Torsten N. Wiesel, the 1981 Nobel laureate in physiology or medicine and chair of the Latin American Fellows National Advisory Committee.

Ten Pew Latin American Fellows were named this year. The fellowship provides a $30,000 salary stipend to support two years of research, as well as an additional $35,000 for laboratory equipment should the fellow return to Latin America to start his or her own lab. Since the program’s inception in 1990, the program has supported almost 150 young Latin American scientists.

Ana Fiszbein is a postdoc working in the Burge Lab, where she researches the role that changes in gene splicing could play in the biology of normal and tumor cells, with the goal of revealing novel targets for cancer therapeutics. “I am very honored to receive this award, it is a privilege and also a responsibility,” she says. Fiszbein is working with Professor Christopher B. Burge, of the departments of Biology and Biological Engineering and the Broad Institute of MIT and Harvard.

“Ana is an exceptionally talented molecular biologist and independent thinker who came to my lab very well trained from her PhD in Alberto Kornblihtt’s lab,” Burge says. “She has developed very interesting hypotheses about the mechanistic connections between transcription and RNA splicing.”

The activity of genes can be regulated on many levels, including how often DNA is read to produce an RNA, where within the gene that reading begins, and which of the gene’s segments are represented in the RNA molecules that ultimately direct the formation of protein. Tumor cells harbor genetic changes that can alter all three of these points of control. However, little is known about the control of these regulatory processes or how they might be interconnected. Fiszbein is working on a sequence study of RNA in different species, with a sequence analysis of human cancer genomes to identify RNAs that may be present more often in cancer cells. She will then assess whether those RNA segments are co-regulated with the sites where the reading of a gene begins.

Inda is a postdoc working in the lab of Timothy Lu, an assistant professor leading the Synthetic Biology Group in the departments of Electrical Engineering and Computer Science and Biological Engineering. In the Lu Lab, she will work on the development of novel noninvasive strategies, for the early diagnosis and alleviation of inflammation in intestinal disorders, such as inflammatory bowel disease (IBD).

“The fellowship provides me a unique opportunity to learn the practical and theoretical underpinnings of cutting-edge research in the synthetic biology field for diagnosis and treatment of serious ailments,” she says.

A variety of bacteria inhabit healthy human intestines, and members of the Lu laboratory have been working to commandeer some of these microbes for use as sentinels that could patrol the gut and secrete therapeutic molecules in areas that appear inflamed. Inda plans to equip bacteria with biosensors that recognize the molecular markers of IBD — and then trigger the release of anti-inflammatory compounds. She will then assess the engineered microbes’ ability to distinguish between diseased and healthy tissue and to treat inflammation in an animal model of IBD.

Wiesel has high praise for the quality of this year’s Latin American Scholars. “The 2017 class is again made up of researchers of outstanding promise who will no doubt continue to enhance the growing biomedical research community in the region,” he says.

Meet Gene-Wei Li
May 4, 2016

Gene-Wei Li is the newest member of the MIT Department of Biology. He opened his lab on the second floor in building 68 about one year ago. But who is Gene? Born in California and raised in Taiwan, Gene fell in love with math and physics and a boyhood dream to figure out quantum teleportation. It was not until he arrived at Harvard that he discovered the field of biophysics. “As a physicist I like thinking about numbers and when I came to Harvard I suddenly realized there was so much biophysics going on in a diversity of labs,” Gene says of his years in graduate school.

In his thesis project, Gene was looking at how transcription factors find their target through single molecule imaging in bacterial cells. He became focused on protein dynamics. Do transcription factors diffuse through cytosol and randomly land on DNA or do they scan through in a directional manner? He discovered they do a bit of both. “As a cell you would optimize the amount of transcription factors searching at any given time and the number of sites. You would not want to crowd the DNA,” Gene explains smiling.

Despite his work in a biological system, Gene admits he still saw himself primarily as a physicist at the beginning of his postdoc. “When I started my postdoc at the Weissman lab at UCSF, I did not even know what ubiquitin was,” he laughs. That was soon to change. At UCSF, Gene utilized a novel method called ribosome profiling which enables the study of protein synthesis rates by looking at ribosome density. “In my postdoc, I was lucky to get a paper published early on and so I had an opportunity to explore what I enjoyed. Quantification is always hard so I decided to see whether there is a good metric to measure, and found a striking result that density corresponds to stoichiometry really well. All the subunits are made in proportion to their stoichiometry. While this makes intuitive sense it was not necessarily obvious before,” Gene describes his postdoctoral experience. What about single subunit proteins? “No protein acts alone,” Gene replies, “we need to look at a whole system — enzymes could be diffusing but receive substrates and the amount of enzyme matters. Make enough but not too much because that would be wasteful.”

Are there physical and quantitative principles behind the precise control of transcription and translation? How do cells fine-tune their RNA and protein production to result in correct stoichiometric complexes? And importantly, if a cell is engineered in the lab to express exogenous proteins are there detrimental effects? Gene’s growing team at MIT (currently, two graduate students, a technician, an undergraduate, and a joint postdoc) are focused on cracking precisely these key questions. “As a mentor, my philosophy is to be supportive but leave freedom for students and postdocs to explore on their own too. In graduate school, I was stuck on a project for two years but was also allowed to follow side stories that both eventually went to fruition.”

Gene’s lab uses bacteria (E.coli and B. subtilis) in their experimental work. “Their operons are surprisingly conserved despite a billion years’ separation. The power is in comparison though – even though the gene order and protein stoichiometry are conserved, these bugs use different tricks of post-transcriptional controls to get the same amount of proteins,” Gene says of his model organisms. Being a young faculty in the MIT Department of Biology is a very humbling experience because it has so much history, he adds. “Boris Magasanik from this department was one of the pioneers of bacterial physiology — we know the system much better now, we can quantitate it better too but he laid the foundation. My lab space is formerly Alexander Rich’s who discovered polysomes — now we are stretching polysomes individually and looking at the actual distribution of ribosomes along the mRNA.”

In his free time, Gene enjoys traveling with his wife though it has become more difficult with the recent birth of their son (congratulations!) and his three-year old brother. He loves meeting people of different backgrounds and thinking about science from different perspectives. “It takes a while to adjust from postdoc to faculty – becoming a manager, accountant, grant writer, colleague, mentor – leaving less time for research,” he says. “The nice thing about the MIT Biology Department is that I can knock on any door and ask for advice on things big and small.”