Research Area: Human Disease

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
Harvey F. Lodish

Education

  • PhD, 1966, Rockefeller University
  • BS, 1962, Chemistry and Mathematics, Kenyon College

Research Summary

Harvey Lodish has been a leader in molecular cell biology as well as a biotechnology entrepreneur for over five decades. Much of his early research focused on the regulation of messenger RNA translation and the biogenesis of plasma membrane glycoproteins. Beginning in the 1980s, his research focused on cloning and characterizing many proteins, microRNAs, and long noncoding RNAs important for red cell development and function. His laboratory was the first to clone and sequence mRNAs encoding many hormone receptors, mammalian glucose transport proteins, and proteins important for adipose cell formation and function. He went on to identify and characterize several genes and proteins involved in insulin resistance and stress responses in adipose cells. Over the years, he has mentored hundreds of undergraduates, PhD and MD/PhD students, and postdoctoral fellows, and continues to teach award-winning undergraduate and graduate classes on biotechnology.

Harvey Lodish closed his lab in 2020 and is no longer accepting students.

Awards

  • Wallace H. Coulter Award for Lifetime Achievement in Hematology, American Society of Hematology, 2021
  • Donald Metcalf Award, International Society for Experimental Hematology, 2020
  • American Society for Cell Biology WICB Sandra K. Masur Senior Leadership Award, 2017
  • Pioneer Award, Diamond Blackfan Anemia Foundation, 2016
  • Mentor Award in Basic Science, American Society of Hematology, 2010
  • President, American Society for Cell Biology, 2004
  • Associate Member, European Molecular Biology Organization (EMBO), 1996
  • National Academy of Sciences, Member, 1987
  • American Academy of Arts and Sciences, Fellow, 1986
  • John Simon Guggenheim Memorial Foundation, Guggenheim Fellowship, 1977
Rudolf Jaenisch

Education

  • MD, 1967, University of Munich

Research Summary

We aim to understand the epigenetic regulation of gene expression in mammalian development and disease. Embryonic stem cells are important because they have the potential to generate any cell type in the body and, therefore, have great potential for regenerative medicine. We study the way somatic cells reprogram to an embryonic pluripotent state, and use patient specific pluripotent cells to study complex human diseases.

Awards

  • German Society for Biochemistry and Molecular Biology, Otto Warburg Medal, 2014
  • New York Academy, Medicine Medal, 2013
  • Franklin Institute, Benjamin Franklin Medal, 2013
  • National Science Foundation, National Medal of Science, 2011
  • National Science Foundation, National Medal of Science, 2010
  • National Academy of Sciences, Member, 2003
Susumu Tonegawa

Education

  • PhD, 1968, University of California, San Diego
  • BS, 1963, Chemistry, Kyoto University

Research Summary

We are interested in the molecular, cellular and neural circuit mechanisms underlying learning and memory in rodents. We generate genetically engineered mice, and analyze them through multiple methods including molecular and cellular biology, electrophysiology, microscopic imaging, optogenetic engineering, and behavioral studies. Ultimately, we aim to detect the effects of our manipulations at multiple levels in the brain — deducing which behaviors or cognitions are causally linked to specific processes and events taking place at the molecular, cellular, and neuronal circuit levels.

Awards

  • The Nobel Foundation, Nobel Prize in Physiology or Medicine, 1987
  • Albert and Mary Lasker Award in Basic Research, 1987
  • National Academy of Sciences, Member, 1986
New player in cellular signaling

Researchers have identified a key nutrient sensor in the mTOR pathway that links nutrient availability to cell growth.

Nicole Giese Rura | Whitehead Institute
November 9, 2017

To survive and grow, a cell must properly assess the resources available and couple that with its growth and metabolism — a misstep in that calculus can potentially cause cell death or dysfunction. At the crux of these decisions is the mTOR pathway, a cellular pathway connecting nutrition, metabolism, and disease.

The mTOR pathway incorporates input from multiple factors, such as oxygen levels, nutrient availability, growth factors, and insulin levels to promote or restrict cellular growth and metabolism. But when the pathway runs amok, it can be associated with numerous diseases, including cancer, diabetes, and Alzheimer’s disease. Understanding the various sensors that feed into the mTOR pathway could lead to novel therapies for these diseases and even aging, as dialing down the mTOR pathway is linked to longer lifespans in mice and other organisms.

Although the essential amino acid methionine is one of the key nutrients whose levels cells must carefully sense, researchers did not know how it fed into the mTOR pathway — or if it did at all. Now, Whitehead Institute Member David Sabatini and members of his laboratory have identified a protein, SAMTOR, as a sensor in the mTOR pathway for the methionine derivative SAM (S-adenosyl methionine). Their findings are described in the current issue of the journal Science.

Methionine is essential for protein synthesis, and a metabolite produced from it, SAM, is involved in several critical cellular functions to sustain growth, including DNA methylation, ribosome biogenesis, and phospholipid metabolism. Interestingly, methionine restriction at the organismal level has been linked to increased insulin tolerance and lifespan, similar to the antiaging effects associated with inhibition of mTOR pathway activity. But the connection between mTOR, methionine, and aging remains elusive.

“There are a lot of similarities between the phenotypes of methionine restriction and mTOR inhibition,” says Sabatini, who is also a Howard Hughes Medical Institute investigator and a professor of biology at MIT. “The existence of this protein SAMTOR provides some tantalizing data suggesting that those phenotypes may be mechanistically connected.”

Sabatini identified mTOR as a graduate student and has since elucidated numerous aspects of its namesake pathway. He and his lab recently pinpointed the molecular sensors in the mTOR pathway for two key amino acids: leucine and arginine. In the current line of research, co-first authors of the Science paper Xin Gu and Jose Orozco, both graduate students Sabatini’s lab, identified a previously uncharacterized protein that seemed to interact with components of the mTOR pathway. After further investigation, they determined that the protein binds to SAM and indirectly gauges the pool of available methionine, making this protein — SAMTOR — a specific and unique nutrient sensor that informs the mTOR pathway.

“People have been trying to figure out how methionine was sensed in cells for a really long time,” Orozco says. “I think that this is the first time in mammalian cells a mechanism has been found to describe the way methionine can regulate a major signaling pathway like mTOR.”

The current research indicates that SAMTOR plays a crucial role in methionine sensing. Methionine metabolism is vital for many cellular functions, and the Sabatini lab will further investigate the potential links between SAMTOR and the extended lifespan and increased insulin sensitivity effects that are associated with low methionine levels.

“It is very interesting to consider mechanistically how methionine restriction might be associated in multiple organisms with beneficial effects, and identification of this protein provides us a potential molecular handle to further investigate this question,” Gu says. “The nutrient-sensing pathway upstream of mTOR is a very elegant system in terms of responding to the availability of certain nutrients with specific mechanisms to regulate cell growth. The currently known sensors raise some interesting questions about why cells evolved sensing mechanisms to these specific nutrients and how cells treat these nutrients differently.”

This work was supported by the National Institutes of Health, the Department of Defense, the National Science Foundation, and the Paul Gray UROP Fund.

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.
A new workflow for natural product characterization comes ashore with red algae
October 30, 2017

CAMBRIDGE, Mass. – A few years ago while paddling off the coast near La Jolla, California, avid surfer Roland Kersten noticed a piece of red algae (Laurenica pacifica) bobbing alongside his surfboard. Kersten, whose background is in natural product chemistry, was intrigued.

Natural products—chemicals from living organisms such as plants and algae—represent a rich source of potential therapeutics. A majority of anti-cancer drugs are natural product-based or inspired. One such well-known natural product—the potent anti-cancer drug Taxol—was identified in the bark of a yew tree.

Marine algae, like the red algae Kersten found, are often rich in compounds called sesquiterpenes, some of which have been shown to have potential medicinal attributes. Since the 1970s, scientists identified many sesquiterpenes produced by Laurencia species with anti-cancer properties. The identification techniques usually required about tens of milligrams of purified compounds, which were obtained from more than a kilogram of algae. Because Laurencia and the reef ecosystems in which it thrives are protected, and such large-scale harvesting for scientific or medicinal purposes is no longer tenable, Kersten had to devise a different approach to analyze its sesquiterpenes.

Kersten received a collection permit to clamber over the rocky shore at deep low tide to collect a hand-sized sample of the red algae. Now a postdoctoral fellow in the lab of Whitehead Member and Massachusetts Institute of Technology assistant professor of biology Jing-Ke Weng, Kersten’s first task was to search the RNA sequences of all genes expressed in his red algae sample to find those whose product seemed likely to be enzymes that make sesquiterpenes.  In order to determine the product generated by these enzymes, he engineered them in yeast and isolated its sesquiterpene products.

In order to define the first step in the biogenesis of sesquiterpenes in red algae, Kersten wanted to see the precise 3-D structure of the isolated sesquiterpene. But the small handful of algae he had obtained produced only a fraction of the amount required for x-ray crystallography, the established method for determining a compound’s absolute structure. So Kersten tried a method recently developed by collaborator Makoto Fujita at the University of Tokyo that requires only a few nanograms of material: soaking extracted compounds into a special crystalline sponge, which supports the sample’s molecular shape while it is bombarded with x-rays to accurately determine the 3-D conformation of a molecule. A new combination of the crystalline sponge method and nuclear magnetic resonance spectroscopy by the Fujita group revealed the structure of prespatane.

With the compound’s structure in hand, Kersten is closer to understanding how Laurenciabiosynthesizes its sesquiterpenes and how to engineer yeast to produce the same molecules for medicinal research at scale—without touching the red algae flourishing on protected reefs. And the novel workflow—spanning genomics, metabolomics, synthetic biology, and x-ray crystallography with crystalline sponges—established by Weng, Kersten, and their collaborators may expedite the identification of other promising compounds produced by organisms from both land and sea.

Other contributors to this work include Shoukou Lee of Tokyo University, Daishi Fujita of Tokyo University and Whitehead Institute, Tomáš Pluskal of Whitehead Institute.  The team also collaborated with researchers from Scripps Institution of Oceanography and Salk Institute of Biological Sciences.

This work was supported by Howard Hughes Medical Institute, the Simons Foundation, the Helen Hay Whitney Foundation, the Pew Scholars Program in the Biomedical Sciences, the Searle Scholars Program, and the Japan Science and Technology Agency.

 Written by Nicole Giese Rura
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Jing-Ke Weng’s primary affiliation is with Whitehead Institute for Biomedical Research, where his laboratory is located and all his research is conducted. He is also an assistant professor of biology at Massachusetts Institute of Technology.
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Full Citation:
“A Red Algal Bourbonane Sesquiterpene Synthase Defined by Microgram-scale NMR-coupled Crystalline Sponge XRD Analysis”
Journal of the American Chemical Society, online October 30, 2017.
Roland D. Kersten (1,6), Shoukou Lee (2,6) , Daishi Fujita (1,2) , Tomáš Pluskal (1) , Susan Kram (3), Jennifer E. Smith (3) , Takahiro Iwai (2) , Joseph P. Noel (4) , Makoto Fujita (2), Jing-Ke Weng (1,5).
1. Whitehead Institute for Biomedical Research, 455 Main Street, Cambridge, MA, United States
2. Graduate School of Engineering, The University of Tokyo, JST-ACCEL, Tokyo, Japan
3. Scripps Institution of Oceanography, University of California San Diego, La Jolla, CA, United States
4. Howard Hughes Medical Institute, Jack H. Skirball Center for Chemical Biology and Proteomics, The Salk Institute for Biological Studies, La Jolla, CA, United States
5. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, United States
6. These authors contributed equally
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
Genetic body/brain connection identified in genomic region linked to autism
October 6, 2017

CAMBRIDGE, Mass. – For the first time, Whitehead Institute scientists have documented a direct link between deletions in two genes—fam57ba and doc2a—in zebrafish and certain brain and body traits, such as seizures, hyperactivity, enlarged head size, and obesity.

“Finding the molecular connections between a brain and a body phenotype is indeed really paradigm shifting,” says Whitehead Institute Member Hazel Sive, who is also a professor of biology at MIT. “It lets us think about the common control of these two aspects of phenotype, which is very interesting and could be useful for developing therapies for these phenotypes.”

Both genes reside in the 16p11.2 region of human chromosome 16. About 1 in 2000, or around 4 million people worldwide, have deletions in this region, and these deletions are associated with multiple brain and body symptoms, including autism spectrum disorders, developmental delay, intellectual disability, seizures, and obesity.

Scientists have had difficulty teasing apart the relationship between specific traits and deletions in this region, because it includes at least 25 genes, and because there is not a one-to-one mapping of gene to phenotype. Instead, multiple genes seem to create a web of interactions that produce a variety of characteristics.

To solve such a complex puzzle, Jasmine McCammon, a postdoctoral researcher in Sive’s lab, enlisted the zebrafish as a “living test tube”.  The Sive group uses zebrafish to study the genetic/phenotype connections associated with human disorders. Like the human genome, the zebrafish genome has two copies of each gene, and scientists can remove the function of multiple genes to produce phenotypes that are reminiscent of human symptoms.

The results from McCammon’s initial screen with zebrafish indicate that two genes in the 16p11.2 region could be key for brain development: fam57ba and doc2a. (fam57b encodes a ‘ceramide synthase’ that makes a kind of lipid, and doc2a encodes a regulator of secretion.) McCammon investigated further by deleting one copy of fam57ba and doc2a individually; the effect was minimal. However, simultaneously removing a copy of both genes revealed significant synergy between them. Compared with controls, fish with only one copy of each gene exhibit hyperactivity, increased propensity for seizures, increased body and head size, and fat content. When both copies of only fam57ba are removed, the fish are much larger and with a higher fat content. All of the study’s results are published in the journal Human Molecular Genetics.

Although her findings use zebrafish and are far from the clinic, McCammon was struck by how much people affected by deletions in this genome identified with her results.

“When I spoke with the parents of some kids with neurodevelopmental disorders, I was surprised how much the brain/body connection that we described resonated with them,” she says. “They said that yes, their child has autism, but he also has really weak muscle tone. Or she has a gastrointestinal problem and that’s been more problematic than her behavior issues. For me, it’s been really revealing to talk to people who’ve actually experienced this as opposed to reading about statistics in journals.”

The mechanisms underlying this brain/body connection are still not well understood. One of the identified genes, fam57ba, provides some intriguing hints as to how metabolism and brain function could be intertwined, because it produces an enzyme that plays a role in lipid production and is believed to be a metabolic regulator.  The lipid type, ceramide, also has a functional role in various signaling pathways and affects synaptic function, although its primary role is not in the synapse, but providing structure in cell membranes.

For Sive, the two identified genes could be just the beginning. “Our data suggest that there may be metabolic genes involved in human neurodevelopmental disorders,” she says.  “This is a nascent field, that we’re very interested in going forward.”

This work was supported by Jim and Pat Poitras, Len and Ellen Polaner, and the Markell-Balkin-Weinberg Postdoctoral Fellowship.

Written by Nicole Giese Rura
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Hazel Sive’s primary affiliation is with Whitehead Institute for Biomedical Research, where her laboratory is located and all her research is conducted. She is also a professor of biology at Massachusetts Institute of Technology.
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Full Citation:
“The 16p11.2 homologs fam57ba and doc2a generate certain brain and body phenotypes”
Human Molecular Genetics, Volume 26, Issue 19, 1 October 2017.
Jasmine M. McCammon(1), Alicia Blaker-Lee(1), Xiao Chen(2), and Hazel Sive (1,2).
1. Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA
2. Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
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.”