Author: mantulin

3 Questions: Professors Adam Martin and Joel Volman on updating MIT’s undergraduate curriculum

Professors Adam Martin and Joel Volman explain the genesis, scope, and objectives of the recently launched Task Force on the MIT Undergraduate Academic Program.

Office of the Vice Chancellor
March 19, 2024

In late February, Vice Chancellor for Undergraduate and Graduate Education Ian A. Waitz and Faculty Chair Mary Fuller announced the formation and launch of the Task Force on the MIT Undergraduate Academic Program (TFUAP). The effort fulfills a critical recommendation of the Task Force 2021 and Beyond RIC1 (Undergraduate Program) and draws upon several, prior foundational working groups — some focused on the current General Institute Requirements (GIRs) and others on updating recent studies for the purposes of this review.

In this interview, task force co-chairs Adam Martin, professor of biology, and Joel Voldman, the William R. Brody Professor of Electrical Engineering and Computer Science describe the TFUAP’s goals, approach, and next steps.

Q: The charge of the task force is quite ambitious, including “reviewing the current undergraduate academic program and considering improvements with a focus on both the curriculum and pedagogy.” Can you explain your approach?

Martin: For context, it’s important to know that the undergraduate program is multifaceted and consists of many components, including majors, electives, experiential learning, and of course the GIRs — arguably one of the best-known acronyms at MIT! Moreover, the GIRs include science core classes; humanities, arts, and social sciences classes; certain electives in science and engineering; and a lab requirement, each of which serves a slightly different purpose and dovetails with majors and minors in unique ways.

Some aspects of the academic program are determined by the faculty, either MIT-wide or within a particular department. Others can be customized by students, in consultation with faculty and staff advisors, from the broad array of curricular and co-curricular offerings at MIT. The task force will look holistically at all of these aspects, considering both what MIT requires of all students, and the options we make available as students chart their own paths.

As part of this holistic approach, the TFUAP will zero in on both content and pedagogy. Obviously, the content we cover is important; our goal must remain to provide undergraduates with the world-class education they expect. But how we teach is of fundamental importance, as well. The pedagogy we adopt should be inclusive, supported by research, and designed to help students not only understand what they are learning, but why they are learning it — how it relates to their majors, potential careers, and their lives.

Voldman: I think your question’s description of our charge as “ambitious” is noteworthy. We feel that the task force is ambitious, too, but perhaps in a different sense from the question. That is, we believe our job is to not only think about nuts-and-bolts issues of the academic program requirements but also to consider the big picture. What are the most expansive possibilities? How can we push the envelope? That’s the MIT way, after all.

Q: The task force is building upon quite a bit of past work and benefits from some major accomplishments recommended by Task Force 2021 (TF2021). For example, how does the creation of the Undergraduate Advising Center, and in general, the desire to provide more personal and professional support to all students, fit in with the potential updates to the undergraduate curriculum?

Martin: You’re absolutely right — our work benefits greatly from years of conversations focused on the undergraduate academic program, particularly in the last decade or so. These include the 2014 Task Force on the Future of Education; the 2018 Designing the First-Year Experience Class; Task Force 2021 and Beyond (TF2021); the Foundational Working Groups (part of the RIC 1 implementation) that have studied the existing MIT undergraduate program; and the Committee on the Undergraduate Program. The valuable work of these past committees and their findings will certainly inform our thought process.

In the past, groups that evaluated the undergraduate curriculum were also charged with tackling related topics, such as undergraduate advising or revamping classrooms. Taking on any one of these three issues is ambitious by any measure! What’s changed in the past decade is that advances have been made in these other critical areas, so the TFUAP can focus solely on curriculum and pedagogy. For example, thanks to recent accomplishments by TF2021 and others, we have implemented a new advising system for all undergraduates in the form of the Undergraduate Advising Center.

We envision the TFUAP being a highly collaborative process, bringing in voices across the entire Institute and beyond. We welcome input from members of the community via email at tfuap@mit.edu. We will also be reaching out to student groups, alumni, individual faculty, faculty groups, and administrative staff across the Institute to hear their perspectives.

Q: Part of what TFUAP will have to confront, no doubt, are some of the most pressing issues of our time, like the rise of computing and AI, climate change (what President Kornbluth calls an existential threat to our way of life), and the changing nature of learning (online, hybrid, etc.). How are you thinking about all of these factors?

Voldman: That is a good question! It’s early days, and our work is just beginning, but we know that these and other issues loom over all of us. For example, we are keenly aware of the influx of students into computing-related majors and classes, and we need to think deeply about the implications. Furthermore, we want a curriculum that prepares students for current and upcoming global challenges as well as changes in the technology and tools available to address those challenges. However, we can expect that our students will need to be agile and curious, lifelong learners, collaborative and compassionate teammates, and creative and thoughtful problem-solvers.

As we work with the community to design the next version of an MIT undergraduate education, it will be important to build a structure that can incorporate the biggest challenges and opportunities of the day, while staying flexible and responsive to an ever-evolving world.

Faculty Ömer Yilmaz and Seychelle Vos among MIT faculty selected for Cancer Grand Challenges

Joining three teams backed by a total of $75 million, MIT researchers will tackle some of cancer’s toughest challenges.

Bendta Schroeder | Koch Institute
March 18, 2024

Cancer Grand Challenges recently announced five winning teams for 2024, which included five researchers from MIT: Michael Birnbaum, Regina Barzilay, Brandon DeKosky, Seychelle Vos, and Ömer Yilmaz. Each team is made up of interdisciplinary cancer researchers from across the globe and will be awarded $25 million over five years.

Birnbaum, an associate professor in the Department of Biological Engineering, leads Team MATCHMAKERS and is joined by co-investigators Barzilay, the School of Engineering Distinguished Professor for AI and Health in the Department of Electrical Engineering and Computer Science and the AI faculty lead at the MIT Abdul Latif Jameel Clinic for Machine Learning in Health; and DeKosky, Phillip and Susan Ragon Career Development Professor of Chemical Engineering. All three are also affiliates of the Koch Institute for Integrative Cancer Research At MIT.

Team MATCHMAKERS will take advantage of recent advances in artificial intelligence to develop tools for personalized immunotherapies for cancer patients. Cancer immunotherapies, which recruit the patient’s own immune system against the disease, have transformed treatment for some cancers, but not for all types and not for all patients.

T cells are one target for immunotherapies because of their central role in the immune response. These immune cells use receptors on their surface to recognize protein fragments called antigens on cancer cells. Once T cells attach to cancer antigens, they mark them for destruction by the immune system. However, T cell receptors are exceptionally diverse within one person’s immune system and from person to person, making it difficult to predict how any one cancer patient will respond to an immunotherapy.

Team MATCHMAKERS will collect data on T cell receptors and the different antigens they target and build computer models to predict antigen recognition by different T cell receptors. The team’s overarching goal is to develop tools for predicting T cell recognition with simple clinical lab tests and designing antigen-specific immunotherapies. “If successful, what we learn on our team could help transform prediction of T cell receptor recognition from something that is only possible in a few sophisticated laboratories in the world, for a few people at a time, into a routine process,” says Birnbaum.

“The MATCHMAKERS project draws on MIT’s long tradition of developing cutting-edge artificial intelligence tools for the benefit of society,” comments Ryan Schoenfeld, CEO of The Mark Foundation for Cancer Research. “Their approach to optimizing immunotherapy for cancer and many other diseases is exemplary of the type of interdisciplinary research The Mark Foundation prioritizes supporting.” In addition to The Mark Foundation, the MATCHMAKERS team is funded by Cancer Research UK and the U.S. National Cancer Institute.

Vos, the Robert A. Swanson (1969) Career Development Professor of Life Sciences and HHMI Freeman Hrabowksi Scholar in the Department of Biology, will be a co-investigator on Team KOODAC. The KOODAC team will develop new treatments for solid tumors in children, using protein degradation strategies to target previously “undruggable” drivers of cancers. KOODAC is funded by Cancer Research UK, France’s Institut National Du Cancer, and KiKa (Children Cancer Free Foundation) through Cancer Grand Challenges.

As a co-investigator on team PROSPECT, Yilmaz, who is also a Koch Institute affiliate, will help address early-onset colorectal cancers, an emerging global problem among individuals younger than 50 years. The team seeks to elucidate pathways, risk factors, and molecules involved in the disease’s development. Team PROSPECT is supported by Cancer Research UK, the U.S. National Cancer Institute, the Bowelbabe Fund for Cancer Research UK, and France’s Institut National Du Cancer through Cancer Grand Challenges.

Scientists develop a rapid gene-editing screen to find effects of cancer mutations

With the new technique, MIT researchers hope to identify mutations that could be targeted with new cancer therapies.

Anne Trafton | MIT News
March 12, 2024

Tumors can carry mutations in hundreds of different genes, and each of those genes may be mutated in different ways — some mutations simply replace one DNA nucleotide with another, while others insert or delete larger sections of DNA.

Until now, there has been no way to quickly and easily screen each of those mutations in their natural setting to see what role they may play in the development, progression, and treatment response of a tumor. Using a variant of CRISPR genome-editing known as prime editing, MIT researchers have now come up with a way to screen those mutations much more easily.

The researchers demonstrated their technique by screening cells with more than 1,000 different mutations of the tumor suppressor gene p53, all of which have been seen in cancer patients. This method, which is easier and faster than any existing approach, and edits the genome rather than introducing an artificial version of the mutant gene, revealed that some p53 mutations are more harmful than previously thought.

This technique could also be applied to many other cancer genes, the researchers say, and could eventually be used for precision medicine, to determine how an individual patient’s tumor will respond to a particular treatment.

“In one experiment, you can generate thousands of genotypes that are seen in cancer patients, and immediately test whether one or more of those genotypes are sensitive or resistant to any type of therapy that you’re interested in using,” says Francisco Sanchez-Rivera, an MIT assistant professor of biology, a member of the Koch Institute for Integrative Cancer Research, and the senior author of the study.

MIT graduate student Samuel Gould is the lead author of the paper, which appears today in Nature Biotechnology.

Editing cells

The new technique builds on research that Sanchez-Rivera began 10 years ago as an MIT graduate student. At that time, working with Tyler Jacks, the David H. Koch Professor of Biology, and then-postdoc Thales Papagiannakopoulos, Sanchez-Rivera developed a way to use CRISPR genome-editing to introduce into mice genetic mutations linked to lung cancer.

In that study, the researchers showed that they could delete genes that are often lost in lung tumor cells, and the resulting tumors were similar to naturally arising tumors with those mutations. However, this technique did not allow for the creation of point mutations (substitutions of one nucleotide for another) or insertions.

“While some cancer patients have deletions in certain genes, the vast majority of mutations that cancer patients have in their tumors also include point mutations or small insertions,” Sanchez-Rivera says.

Since then, David Liu, a professor in the Harvard University Department of Chemistry and Chemical Biology and a core institute member of the Broad Institute, has developed new CRISPR-based genome editing technologies that can generate additional types of mutations more easily. With base editing, developed in 2016, researchers can engineer point mutations, but not all possible point mutations. In 2019, Liu, who is also an author of the Nature Biotechnology study, developed a technique called prime editing, which enables any kind of point mutation to be introduced, as well as insertions and deletions.

“Prime editing in theory solves one of the major challenges with earlier forms of CRISPR-based editing, which is that it allows you to engineer virtually any type of mutation,” Sanchez-Rivera says.

When they began working on this project, Sanchez-Rivera and Gould calculated that if performed successfully, prime editing could be used to generate more than 99 percent of all small mutations seen in cancer patients.

However, to achieve that, they needed to find a way to optimize the editing efficiency of the CRISPR-based system. The prime editing guide RNAs (pegRNAs) used to direct CRISPR enzymes to cut the genome in certain spots have varying levels of efficiency, which leads to “noise” in the data from pegRNAs that simply aren’t generating the correct target mutation. The MIT team devised a way to reduce that noise by using synthetic target sites to help them calculate how efficiently each guide RNA that they tested was working.

“We can design multiple prime-editing guide RNAs with different design properties, and then we get an empirical measurement of how efficient each of those pegRNAs is. It tells us what percentage of the time each pegRNA is actually introducing the correct edit,” Gould says.

Analyzing mutations

The researchers demonstrated their technique using p53, a gene that is mutated in more than half of all cancer patients. From a dataset that includes sequencing information from more than 40,000 patients, the researchers identified more than 1,000 different mutations that can occur in p53.

“We wanted to focus on p53 because it’s the most commonly mutated gene in human cancers, but only the most frequent variants in p53 have really been deeply studied. There are many variants in p53 that remain understudied,” Gould says.

Using their new method, the researchers introduced p53 mutations in human lung adenocarcinoma cells, then measured the survival rates of these cells, allowing them to determine each mutation’s effect on cell fitness.

Among their findings, they showed that some p53 mutations promoted cell growth more than had been previously thought. These mutations, which prevent the p53 protein from forming a tetramer — an assembly of four p53 proteins — had been studied before, using a technique that involves inserting artificial copies of a mutated p53 gene into a cell.

Those studies found that these mutations did not confer any survival advantage to cancer cells. However, when the MIT team introduced those same mutations using the new prime editing technique, they found that the mutation prevented the tetramer from forming, allowing the cells to survive. Based on the studies done using overexpression of artificial p53 DNA, those mutations would have been classified as benign, while the new work shows that under more natural circumstances, they are not.

“This is a case where you could only observe these variant-induced phenotypes if you’re engineering the variants in their natural context and not with these more artificial systems,” Gould says. “This is just one example, but it speaks to a broader principle that we’re going to be able to access novel biology using these new genome-editing technologies.”

Because it is difficult to reactivate tumor suppressor genes, there are few drugs that target p53, but the researchers now plan to investigate mutations found in other cancer-linked genes, in hopes of discovering potential cancer therapies that could target those mutations. They also hope that the technique could one day enable personalized approaches to treating tumors.

“With the advent of sequencing technologies in the clinic, we’ll be able to use this genetic information to tailor therapies for patients suffering from tumors that have a defined genetic makeup,” Sanchez-Rivera says. “This approach based on prime editing has the potential to change everything.”

The research was funded, in part, by the National Institute of General Medical Sciences, an MIT School of Science Fellowship in Cancer Research, a Howard Hughes Medical Institute Hanna Gray Fellowship, the V Foundation for Cancer Research, a National Cancer Institute Cancer Center Support Grant, the Ludwig Center at MIT, a Koch Institute Frontier Award, the MIT Research Support Committee, and the Koch Institute Support (core) Grant from the National Cancer Institute.

Postdoc Andrew Savinov among 2024 Infinite Expansion Award recipients

Nine postdocs and research scientists honored for contributions to the Institute.

School of Science
March 3, 2024

The MIT School of Science has announced nine postdocs and research scientists as recipients of the 2024 Infinite Expansion Award, which highlights extraordinary members of the MIT community.

The following are the 2024 School of Science Infinite Expansion winners:

  • Sarthak Chandra, a research scientist in the Department of Brain and Cognitive Sciences, was nominated by Professor Ila Fiete, who wrote, “He has expanded the research abilities of my group by being a versatile and brilliant scientist, by drawing connections with a different area that he was an expert in from his PhD training, and by being a highly involved and caring mentor.”
  • Michal Fux, a research scientist in the Department of Brain and Cognitive Sciences, was nominated by Professor Pawan Sinha, who wrote, “She is one of those figurative beams of light that not only brilliantly illuminate scientific questions, but also enliven a research team.”
  • Andrew Savinov, a postdoc in the Department of Biology, was nominated by Associate Professor Gene-Wei Li, who wrote, “Andrew is an extraordinarily creative and accomplished biophysicist, as well as an outstanding contributor to the broader MIT community.”
  • Ho Fung Cheng, a postdoc in the Department of Chemistry, was nominated by Professor Jeremiah Johnson, who wrote, “His impact on research and our departmental community during his time at MIT has been outstanding, and I believe that he will be a worldclass teacher and research group leader in his independent career next year.”
  • Gabi Wenzel, a postdoc in the Department of Chemistry, was nominated by Assistant Professor Brett McGuire, who wrote, “In the one year since Gabi joined our team, she has become an indispensable leader, demonstrating exceptional skill, innovation, and dedication in our challenging research environment.”
  • Yu-An Zhang, a postdoc in the Department of Chemistry, was nominated by Professor Alison Wendlandt, who wrote, “He is a creative, deep-thinking scientist and a superb organic chemist. But above all, he is an off-scale mentor and a cherished coworker.”
  • Wouter Van de Pontseele, a senior postdoc in the Laboratory for Nuclear Science, was nominated by Professor Joseph Formaggio, who wrote, “He is a talented scientist with an intense creativity, scholarship, and student mentorship record. In the time he has been with my group, he has led multiple facets of my experimental program and has been a wonderful citizen of the MIT community.”
  • Alexander Shvonski, a lecturer in the Department of Physics, was nominated by Assistant Professor Andrew Vanderburg, who wrote, “… I have been blown away by Alex’s knowledge of education research and best practices, his skills as a teacher and course content designer, and I have been extremely grateful for his assistance.”
  • David Stoppel, a research scientist in The Picower Institute for Learning and Memory, was nominated by Professor Mark Bear and his research group, who wrote, “As impressive as his research achievements might be, David’s most genuine qualification for this award is his incredible commitment to mentorship and the dissemination of knowledge.”

Winners are honored with a monetary award and will be celebrated with family, friends, and nominators at a later date, along with recipients of the Infinite Mile Award.

How early-stage cancer cells hide from the immune system

A new study finds precancerous colon cells turn on a gene called SOX17, which helps them evade detection and develop into more advanced tumors.

Anne Trafton | MIT News
February 28, 2024

One of the immune system’s primary roles is to detect and kill cells that have acquired cancerous mutations. However, some early-stage cancer cells manage to evade this surveillance and develop into more advanced tumors.

A new study from MIT and Dana-Farber Cancer Institute has identified one strategy that helps these precancerous cells avoid immune detection. The researchers found that early in colon cancer development, cells that turn on a gene called SOX17 can become essentially invisible to the immune system.

If scientists could find a way to block SOX17 function or the pathway that it activates, this may offer a new way to treat early-stage cancers before they grow into larger tumors, the researchers say.

“Activation of the SOX17 program in the earliest innings of colorectal cancer formation is a critical step that shields precancerous cells from the immune system. If we can inhibit the SOX17 program, we might be better able to prevent colon cancer, particularly in patients that are prone to developing colon polyps,” says Omer Yilmaz, an MIT associate professor of biology, a member of MIT’s Koch Institute for Integrative Cancer Research, and one of the senior authors of the study.

Judith Agudo, a principal investigator at Dana-Farber Cancer Institute and an assistant professor at Harvard Medical School, is also a senior author of the study, which appears today in Nature. The paper’s lead author is MIT Research Scientist Norihiro Goto. Other collaborators include Tyler Jacks, a professor of biology and a member of MIT’s Koch Institute; Peter Westcott, a former Jacks lab postdoc who is now an assistant professor at Cold Spring Harbor Laboratory; and Saori Goto, an MIT postdoc in the Yilmaz lab.

Immune evasion

Colon cancer usually arises in long-lived cells called intestinal stem cells, whose job is to continually regenerate the lining of the intestines. Over their long lifetime, these cells can accumulate cancerous mutations that lead to the formation of polyps, a type of premalignant growth that can eventually become metastatic colon cancer.

To learn more about how these precancerous growths evade the immune system, the researchers used a technique they had previously developed for growing mini colon tumors in a lab dish and then implanting them into mice. In this case, the researchers engineered the tumors to express mutated versions of cancer-linked genes Kras, p53, and APC, which are often found in human colon cancers.

Once these tumors were implanted in mice, the researchers observed a dramatic increase in the tumors’ expression of SOX17. This gene encodes a transcription factor that is normally active only during embryonic development, when it helps to control development of the intestines and the formation of blood vessels.

The researchers’ experiments revealed that when SOX17 is turned on in cancer cells, it helps the cells to create an immunosuppressive environment. Among its effects, SOX17 prevents cells from synthesizing the receptor that normally detects interferon gamma, a molecule that is one of the immune system’s primary weapons against cancer cells.

Without those interferon gamma receptors, cancerous and precancerous cells can simply ignore messages from the immune system, which would normally direct them to undergo programmed cell death.

“One of SOX17’s main roles is to turn off the interferon gamma signaling pathway in colorectal cancer cells and in precancerous adenoma cells. By turning off interferon gamma receptor signaling in the tumor cells, the tumor cells become hidden from T cells and can grow in the presence of an immune system,” Yilmaz says.

Without interferon gamma signaling, cancer cells also minimize their production of molecules called MHC proteins, which are responsible for displaying cancerous antigens to the immune system. The cells’ insensitivity to interferon gamma also prevents them from producing immune molecules called chemokines, which normally recruit T cells that would help destroy the cancerous cells.

Targeting SOX17

When the researchers generated colon tumor organoids with SOX17 knocked out, and implanted those into mice, the immune system was able to attack those tumors much more effectively. This suggests that preventing cancer cells from turning off SOX17 could offer a way to treat colon cancer in its earliest stages.

“Just by turning off SOX17 in fairly complex tumors, we were able to essentially obliterate the ability of these tumor cells to persist,” Goto says.

As part of their study, the researchers also analyzed gene expression data from patients with colon cancer and found that SOX17 tended to be highly expressed in early-stage colon cancers but dropped off as the tumors became more invasive and metastatic.

“We think this makes a lot of sense because as colorectal cancers become more invasive and metastatic, there are other mechanisms that create an immunosuppressive environment,” Yilmaz says. “As the colon cancer becomes more aggressive and activates these other mechanisms, then there’s less importance for SOX17.”

Transcription factors such as SOX17 are considered difficult to target using drugs, in part because of their disorganized structure, so the researchers now plan to identify other proteins that SOX17 interacts with, in hopes that it might be easier to block some of those interactions.

The researchers also plan to investigate what triggers SOX17 to turn on in precancerous cells.

The research was funded by the MIT Stem Cell Initiative via Fondation MIT, the National Institutes of Health/National Cancer Institute, and a Koch Institute-Dana Farber Harvard Cancer Center Bridge Project grant.

What can super-healing species teach us about regeneration?

Albert Almada PhD ’13 studies the mechanics of how stem cells rebuild tissues. “Digging deep into the science is what MIT taught me,” he says.

Lillian Eden | Department of Biology
February 21, 2024

When Albert E. Almada PhD ’13 embarks on a new project, he always considers two criteria instilled in him during his time as a graduate student in the Department of Biology at MIT.

“If you want to make a big discovery, you have to approach it from a unique perspective — a unique angle,” Almada says. “You also have to be willing to dive into the unknown and go to the leading edge of your field.”

This is not without its challenges — but with an innovative spirit, Almada says, one can find ways to apply technologies and approaches to a new area of research where a roadmap doesn’t yet exist.

Now an assistant professor of orthopedic surgery and stem cell biology and regenerative medicine at the Keck School of Medicine of the University of Southern California (USC), Almada studies the mechanics of how stem cells rebuild tissues after trauma and how stem cell principles are dysregulated and drive conditions like degenerative disease and aging, exploring these topics through an evolutionary lens.

He’s also trying to solve a mystery that has intrigued scientists for centuries: Why can some vertebrate species like fish, salamanders, and lizards regenerate entire body parts, but mammals cannot? Almada’s laboratory at USC tackles these critical questions in the musculoskeletal system.

Almada’s fascination with muscle development and regeneration can be traced back to growing up in southern California. Almada’s brother had a degenerative muscle disease called Duchenne muscular dystrophy — and, while Almada grew stronger and stronger, his brother grew weaker and weaker. Last summer, Almada’s brother, unfortunately, lost his battle with his disorder at the age of 41.

“Watching his disease progress in those early years is what inspired me to become a scientist,” Almada recalls. “Sometimes science can be personal.”

Almada went to the University of California at Irvine for his undergraduate degree, majoring in biological sciences. During his summers, he participated in the Undergraduate Research Program (URP) at the Cold Spring Harbor Laboratory and the MIT Summer Research Program-Bio (now the Bernard S. and Sophie G. Gould MIT Summer Research Program in Biology, BSG-MSRP-Bio), where he saw the passion, rigor, and drive that solidified his desire to pursue a PhD.

Despite his interest in clinical applications, skeletal muscle, and regenerative biology, Almada was drawn to the Department of Biology at MIT, which is focused on basic fundamental research.

“I was willing to bet that it all came down to understanding basic cellular processes and things going wrong with the cell and how it interacts with its environment,” he says. “The MIT biology program really helped me define an identity for myself and gave me a template for how to tackle clinical problems from a molecular perspective.”

Almada’s PhD thesis work was based on a curious finding that Phillip Sharp, Institute Professor emeritus, professor emeritus of biology, and intramural faculty at the Koch Institute for Integrative Cancer Research, had made in 2007 — that transcription, the process of copying DNA into a messenger molecule called RNA, can occur in both directions at gene promoters. In one direction, it was long understood that fully formed mRNA is transcribed and can be used as a blueprint to make a protein. The transcription Sharp observed, in the opposite direction, results in a very short RNA that is not used as a gene product blueprint.

Almada’s project dug into what those short RNA molecules are — their structure and sequence, and why they’re not produced the same way that coding messenger RNA is. In two papers published in PNAS and Nature, Almada and colleagues discovered that a balance between splicing and transcription termination signals controls the length of an RNA. This finding has wider implications because toxic RNAs are produced and can build up in several degenerative diseases; being able to splice out or shorten RNAs to remove the harmful segments could be a potential therapeutic treatment.

“That experience convinced me that if I want to make big discoveries, I have to focus on basic science,” he says. “It also gave me the confidence that if I can succeed at MIT, I can succeed just about anywhere and in any field of biology.”

At the time Almada was in graduate school, there was a lot of excitement about transcription factor reprogramming. Transcription factors are the proteins responsible for turning on essential genes that tell a cell what to be and how to behave; a subset of them can even theoretically turn one cell type into another.

Almada began to wonder whether a specialized set of transcription factors instructs stem cells to rebuild tissues after trauma. After MIT, Almada moved on to a postdoctoral position in the lab of Amy Wagers, a leader in muscle stem cell biology at Harvard University, to immerse himself in this problem.

In many tissues in our bodies, a population of stem cells typically exists in an inactive, non-dividing state called quiescence. Once activated, these stem cells interact with their environment, sense damage signals, and turn on programs of proliferation and differentiation, as well as self-renewal, which is critical to maintaining a pool of stem cells in the tissue.

One of the biggest mysteries in the field of regenerative biology is how stem cells transition from dormancy into that activated, highly regenerative state. The body’s ability to turn on stem cells, including those in the skeletal muscle system, declines as we age and is often dysregulated in degenerative diseases — diseases like the one Almada’s brother suffered from.

In a study Almada published in Cell Reports several years ago, he identified a family of transcription factors that work together to turn on a critical regenerative gene program within hours of muscle trauma. This program drives muscle stem cells out of quiescence and speeds up healing.

“Now my lab is studying this regenerative program and its potential dysregulation in aging and degenerative muscle diseases using mouse and human models,” Almada says. “We’re also drawing parallels with super-healing species like salamanders and lizards.”

Recently, Almada has been working on characterizing the molecular and functional properties of stem cells in lizards, attempting to understand how the genes and pathways differ from mammalian stem cells. Lizards can regenerate massive amounts of skeletal muscle from scratch — imagine if human muscle tissue could be regrown as seamlessly as a lizard’s tail can. He is also exploring whether the tail is unique, or if stem cells in other tissues in lizards can regenerate faster and better than the tail, by comparing analogous injuries in a mouse model.

“This is a good example of approaching a problem from a new perspective: We believe we’re going to discover new biology in lizards that we can use to enhance skeletal muscle growth in vulnerable human populations, including those that suffer from deadly muscle disorders,” Almada says.

In just three years of starting his faculty position at USC, his work and approach have already received recognition in academia, with junior faculty awards from the Baxter Foundation and the Glenn Foundation/American Federation of Aging Research. He also received his first RO1 award from the National Institutes of Health with nearly $3 million in funding. Almada and his first graduate student, Alma Zuniga Munoz, were also awarded the HHMI Gilliam Fellowship last summer. Zuniga Munoz is the first to be recognized with this award at USC; fellowship recipients, student and advisor pairs, are selected with the goal of preparing students from underrepresented groups for leadership roles in science.

Almada himself is a second-generation Mexican American and has been involved in mentoring and training throughout his academic career. He was a graduate resident tutor for Spanish House at MIT and currently serves as the chair of the Diversity, Equity, and Inclusion Committee in the Department of Stem Cell Biology and Regenerative Medicine at USC; more than half of his lab members identify as members of the Hispanic community.

“The focus has to be on developing good scientists,” Almada says. “I learned from my past research mentors the importance of putting the needs of your students first and providing a supportive environment for everyone to excel, no matter where they start.”

As a mentor and researcher, Almada knows that no question and no challenge is off limits — foundations he built in Cambridge, where his graduate studies focused on teaching him to think, not just do.

“Digging deep into the science is what MIT taught me,” he says. “I’m now taking all of my knowledge in molecular biology and applying it to translationally oriented questions that I hope will benefit human health and longevity.”

Nancy Hopkins awarded the National Academy of Sciences Public Welfare Medal

The MIT professor emerita and influential molecular biologist is being honored for her advocacy for women in science.

Bendta Schroeder | Koch Institute
January 30, 2024

The National Academy of Sciences has awarded MIT biologist Nancy Hopkins, the Amgen Professor of Biology Emerita, with the 2024 Public Welfare Medal in recognition of “her courageous leadership over three decades to create and ensure equal opportunity for women in science.”

The award recognizes Hopkins’s role in catalyzing and leading MIT’s “A Study on the Status of Women Faculty in Science,” made public in 1999. The landmark report, the result of the efforts of numerous members of the MIT faculty and administration, revealed inequities in the treatment and resources available to women versus men on the faculty at the Institute, helped drive significant changes to MIT policies and practices, and sparked a national conversation about the unequal treatment of women in science, engineering, and beyond.

Since the medal was established in 1914 to honor extraordinary use of science for the public good, it has been awarded to several MIT-affiliated scientists, including Karl Compton, James R. Killian Jr., and Jerome B. Wiesner, as well as Vannevar Bush, Isidor I. Rabi, and Victor Weiskopf.

“The Public Welfare Medal has been awarded to MIT faculty who have helped define our Institute and scientists who have shaped modern science on the national stage,” says Susan Hockfield, MIT president emerita. “It is more than fitting for Nancy to join their ranks, and — importantly — celebrates her critical role in increasing the participation of women in science and engineering as a significant national achievement.”

When Hopkins joined the faculty of the MIT Center for Cancer Research (CCR) in 1973, she did not set out to become an advocate for equality for women in science. For the first 15 years, she distinguished herself in pioneering studies linking genes of RNA tumor viruses to their roles in causing some forms of cancer. But in 1989, Hopkins changed course: She began developing molecular technologies for the study of zebrafish that would help establish it as an important model for vertebrate development and cancer biology.

To make the pivot, Hopkins needed more space to accommodate fish tanks and new equipment. Although Hopkins strongly suspected that she had been assigned less lab space than her male peers in the building, her hypothesis carried little weight and her request was denied. Ever the scientist, Hopkins believed the path to more lab space was to collect data. One night in 1993, with a measuring tape in hand, she visited each lab to quantify the distribution of space in her building. Her hypothesis appeared correct.

Hopkins shared her initial findings — and her growing sense that there was bias against women scientists — with one female colleague, and then others, many of whom reported similar experiences. The senior women faculty in MIT’s School of Science began meeting to discuss their concerns, ultimately documenting them in a letter to Dean of Science Robert Birgeneau. The letter was signed by professors Susan Carey, Sylvia Ceyer, Sallie “Penny” Chisholm, Suzanne Corkin, Mildred Dresselhaus, Ann Graybiel, Ruth Lehmann, Marcia McNutt, Terry Orr-Weaver, Mary-Lou Pardue, Molly Potter, Paula Malanotte-Rizzoli, Leigh Royden, Lisa Steiner, and Joanne Stubbe. Also important were Hopkins’s discussions with Lorna Gibson, a professor in the Department of Materials Science and Engineering, since Gibson had made similar observations with her female colleagues in the School of Engineering. Despite the biases against these women, they were highly accomplished scientists. Four of them were eventually awarded the U.S. National Medal of Science, and 11 were, or became, members of the National Academy of Sciences.

In response to the women in the School of Science, Birgeneau established the Committee on the Status of Women Faculty in 1995, which included both female faculty and three male faculty who had been department chairs: Jerome Friedman, Dan Kleitman, and Robert Silbey. In addition to interviewing essentially all the female faculty members in the school, they collected data on salaries, space, and other resources. The committee found that of 209 tenured professors in the School of Science only 15 were women, and they often had smaller wages and labs, and were raising more of their salaries from grants than equivalent male faculty.

At the urging of Lotte Bailyn, a professor at the MIT Sloan School of Management and chair of the faculty, Hopkins and the committee summarized their findings to be presented to MIT’s faculty. Struck by the pervasive and well-documented pattern of bias against women across the School of Science, both Birgeneau and MIT President Charles Vest added prefaces to the report before it was published in the faculty newsletter. Vest commented, “I have always believed that contemporary gender discrimination within universities is part reality and part perception. True, but I now understand that reality is by far the greater part of the balance.”

Vest took an “engineers’ approach” to addressing the report’s findings, remarking “anything I can measure, I can fix.” He tasked Provost Robert Brown with establishing committees to produce reports on the status of women faculty for all five of MIT’s schools. The reports were published in 2002 and drew attention to the small number of women faculty in some schools, as well as discrepancies similar to those first documented in the School of Science.

In response, MIT implemented changes in hiring practices, updated pay equity reviews, and worked to improve the working environment for women faculty. On-campus day care facilities were built and leave policies were expanded for the benefit of all faculty members with families. To address underrepresentation of individuals of color, as well as the unique biases against women of color, Brown established the Council on Faculty Diversity with Hopkins and Philip Clay, then MIT’s chancellor and a professor in the Department of Urban Studies and Planning. Meanwhile, Vest spearheaded a collaboration with presidents of other leading universities to increase representation of women faculty.

MIT increased the numbers of women faculty by altering hiring procedures  — particularly in the School of Engineering under Dean Thomas Magnanti and in the School of Science under Birgeneau, and later Associate Dean Hazel Sive. MIT did not need to alter its standards for hiring to increase the number of women on its faculty: Women hired with revised policies at the Institute have been equally successful and have gone on to important leadership roles at MIT and other institutions.

In the wake of the 1999 report the press thrust MIT — and Hopkins — into the national spotlight. The careful documentation in the report and first Birgeneau’s and then Vest’s endorsement of and proactive response to its findings were persuasive to many reporters and their readers. The reports and media coverage resonated with women across academia, resulting in a flood of mail to Hopkins’s inbox, as well as many requests for speaking engagements. Hopkins would eventually undertake hundreds of talks across the United States and many other countries about advocating for the equitable treatment of women in science.

Her advocacy work continued after her retirement. In 2019, Hopkins, along with Hockfield and Sangeeta Bhatia, the John J. and Dorothy Wilson Professor of Health Sciences and Technology and of the Department of Electrical Engineering and Computer Science, founded the Boston Biotech Working Group — which later evolved into the Faculty Founder Initiative — to increase women’s representation as founders and board members of biotech companies in Massachusetts.

Hopkins, however, believes she became “this very visible person by chance.”

“An almost uncountable number of people made this happen,” she continues. “Moreover, I know how much work went on before I even set foot on campus, such as by Emily Wick, Shirley Ann Jackson, Sheila Widnall, and Mildred Dresselhaus. I stood on the shoulders of a great institution and the long, hard work of many people that belong to it.”

The National Academy of Sciences will present the 2024 Public Welfare Medal to Hopkins in April at its 161st annual meeting. Hopkins is the recipient of many other awards and honors, both for her scientific achievements and her advocacy for women in science. She is a member of the National Academy of Sciences, the National Academy of Medicine, the American Academy of Arts and Sciences, and the AACR Academy. Other awards include the Centennial Medal from Harvard University, the MIT Gordon Y. Billard Award for “special service” to MIT, the MIT Laya Wiesner Community Award, the Maria Mitchell Women in Science Award, and the STAT Biomedical Innovation Award. In addition, she has received eight honorary doctorates, most recently from Rockefeller University, the Hong Kong University of Science and Technology, and the Weizmann Institute.

Capsid of HIV-1 behaves like cell’s cargo receptor to enter the nucleus

Biologists demonstrate that HIV-1 capsid acts like a Trojan horse to pass viral cargo across the nuclear pore.

Lillian Eden | Department of Biology
January 24, 2024

Retroviruses cannot replicate on their own — they must insert their genetic code into the DNA of a host and exploit the host cell’s resources to make more copies of themselves, furthering infection. Some retroviruses only infect cells as they divide, when the nuclear envelope that protects the host’s genetic material breaks down, making it easily accessible. HIV-1 is a type of retrovirus, called a lentivirus, that can infect non-dividing cells.

HIV-1 delivers its genome into the nucleus by packaging it into a large, cone-shaped structure called a capsid — but the exact mechanism has remained elusive for decades. Travel through the nuclear envelope occurs through, and is regulated by, nuclear pores, doughnut-shaped protein assemblies. Human cells have about 2,000 nuclear pores perforating the nuclear envelope. Some earlier evidence suggested that the capsid remains intact during its delivery into the nucleus — but this created a dimensional conundrum. The cone-shaped HIV-1 capsid is about 120 nanometers long and 60 nm wide — too large, researchers thought, to fit through the opening of the nuclear pore, measured at only 43 nm wide.

Members of the Schwartz Lab at MIT, in the Department of Biology, became interested in this question when a postdoc in the lab used cryo-electron tomography, slicing up sections of frozen cells to examine structures, to show that nuclear pores in the nuclear envelope are larger than 43nm. They deflate and shrink, it turns out, when removed from their native conditions. In native conditions, the nuclear pore complex is about 60nm wide — wide enough to accommodate the HIV-1 capsid.

Knowing that it could fit, a question remained: How can the capsid navigate the dense mesh of spaghetti-like proteins that act like a sieve in the nuclear pore channel? That spaghetti-like mesh allows small cargo to diffuse through, but prevents large cargo from entering unless it is escorted by proteins called nuclear transport receptors.

In an open-access paper published today in Nature, researchers present evidence that the HIV-1 capsid mimics the cell’s transport receptors to traverse the nuclear pore.

To support that conclusion, the researchers showed three things in vitro: that an HIV-1 capsid can deliver cargo through a nuclear pore analog; that the capsid can interact with the sieve of proteins in the nuclear pore channel; and that the capsid targets the nuclear pore in the absence of native transport proteins.

Nuclear transport receptors escort large cargo through the nuclear pore by “batting away” the spaghetti-like mesh of proteins inside the channel — like someone holding your hand and guiding you across a crowded dance floor. The HIV-1 capsid interacts with the spaghetti-like proteins, but its purpose is more like a Trojan horse — the capsid encapsulates the viral cargo, protecting it from detection in the cytoplasm and as it enters the nuclear pore complex.

“What’s really amazing about cells is that they are incredibly complex. What’s really difficult about studying cells is that they are incredibly complex,” jokes co-first author Erika Weiskopf, a graduate student in the Schwartz lab. “Biochemists are constantly trying to find ways to study their system in a simplified context, but still give it a flavor of cell biology.”

To do that, the Schwartz lab collaborated with Dirk Görlich, the director of cellular logistics at the Max Planck Institute for Multidisciplinary Sciences. Görlich is a co-senior author on the paper with MIT’s Boris Magasanik Professor of Biology Thomas Schwartz. Görlich’s lab has produced concentrated droplets of the spaghetti-like proteins found inside the nuclear pore, and those droplets allow and exclude cargo the same way a nuclear pore will. In experiments, fluorescently-labeled cargo did not enter the droplets, but fluorescently-labeled cargo packaged in an HIV-1 capsid was delivered. This indicated that the capsid could deliver cargo through a nuclear pore.

Using a biophysical binding assay, the researchers also showed that the HIV-1 capsid interacts with the proteins inside the channel. Different spaghetti-like proteins are found in different channel sections, such as at the cytoplasmic side’s entrance or only inside the channel; there are 10 such proteins in human cells. The capsid is a promiscuous binder — it can interact with all the spaghetti-like proteins found in the channel.

The capsid can target the nuclear pore complex even without the cell’s transport receptors, indicating that it is not commandeering native transport receptors to find and enter the nuclear pore. The team used a classic assay in the nucleocytoplasmic transport field to collect this evidence: When cells are treated with digitonin, their membranes become porous. Everything in the cytoplasm will leak out of the cells, but the nuclear envelope will remain intact. Despite the absence of native proteins, the capsid was attracted to the nuclear pore complex, a behavior indicative of a nuclear transport receptor.

Although the capsid behaves like a nuclear transport receptor to penetrate the nuclear pore, it is fundamentally different. A transport receptor doesn’t need to conceal material for delivery the way the capsid does to avoid detection.

These findings open new lines of inquiry for what the nuclear pore complex is capable of accommodating.

“The HIV-1 capsid is one of the largest things that we now know can go through the nuclear pore complex intact,” Weiskopf says. “It raises all kinds of questions — what other things could be going through the pore that we thought was impossible?”

Schwartz said another question is whether all of the 2,000 nuclear pores in human cells are identical or whether there is something that makes certain pores more amenable to allowing the capsid through.

The capsid is also known to be unusually elastic, a property that may be key for passage through the pore. Another interesting question for the field is whether the cone-shaped capsid gains entry into the pore by squeezing through.

Although the team has shown that the capsid can enter the pore, what happens at the other end of the channel is still unknown — whether the capsid fully or partially enters the nucleus or breaks down inside the channel. Weiskopf is working on perturbing parts of the capsid or the spaghetti-like proteins to learn more about which interactions are most important for successful capsid entry.

Although these results have expanded our understanding of the nuclear pore, much remains unknown, both for HIV-1 infection and for the transport process through the nuclear pore complex.

“The nuclear pore is such an important element of cell biology, we thought it would be interesting to understand it better — and that’s how we figured out that the pore is much bigger than we anticipated,” Schwartz says. “We will certainly try to see whether we can understand the mechanism of HIV-1 infection, how the capsid is released on the other side of the channel, and what factors are important there — and to what extent you can manipulate it or influence it for therapeutic applications.”

Pulin Li among recipients of 2023 School of Science teaching prizes

Roger Levy, Pulin Li, and David McGee were nominated by peers and students for their exceptional instruction.

School of Science
January 10, 2024

The MIT School of Science has announced the winners of its 2023 Teaching Prizes for Graduate and Undergraduate Education. The prizes are awarded to School of Science faculty members who demonstrate excellence in teaching. Winners are chosen from nominations by their students or colleagues.

Roger Levy, a professor in the Department of Brain and Cognitive Sciences, was awarded a prize for developing and teaching class 9.19 (Computational Psycholinguistics). Levy’s nominators highlighted his success in adapting courses to synchronous and asynchronous instruction during the first year of the Covid-19 pandemic and in leading an engaging and challenging course for students across disciplines.

Pulin Li, the Eugene Bell Career Development Professor of Tissue Engineering in the Department of Biology and a member of the Whitehead Institute for Biomedical Research, was awarded the prize for teaching classes 7.06 (Cell Biology) and 7.46/7.86: (Building with Cells). Nominators praised Li’s talent for teaching complex topics effectively and her exceptional accomplishments as a teaching partner.

David McGee, associate professor and associate department head for diversity, equity, and inclusion in the Department of Earth, Atmospheric and Planetary Sciences, was awarded the prize for achieving an outstanding level of community learning in class 12.000 (Solving Complex Problems), also known as “Terrascope.” Nominators noted McGee’s extraordinary investment in both the class material and his students’ learning experiences.

The School of Science welcomes nominations for the teaching prize at the end of each semester. Nominations can be submitted at the school’s website.

Food for thought

Biology graduate student Juana De La O is building connections through her thesis work in mouse development and her passion for cooking and baking.

Lillian Eden | Department of Biology
January 10, 2024

MIT graduate student Juana De La O describes herself as a food-motivated organism, so it’s no surprise that she reaches for food and baking analogies when she’s discussing her thesis work in the lab of undergraduate officer and professor of biology Adam Martin.

Consider the formative stages of a croissant, she offers, occasionally providing homemade croissants to accompany the presentation: When one is forming the puff pastry, the dough is folded over the butter again and again. Tissues in a developing mouse embryo must similarly fold and bend, creating layers and structures that become the spine, head, and organs — but these tissues have no hands to induce those formative movements.

De La O is studying neural tube closure, the formation of the structure that becomes the spinal cord and the brain. Disorders like anencephaly and craniorachischisis occur when the head region fails to close in a developing fetus. It’s a heartbreaking defect, De La O says, because it’s 100 percent lethal — but the fetus fully develops otherwise.

“Your entire central nervous system hinges on this one event happening successfully,” she says. “On the fundamental level, we have a very limited understanding of the mechanisms required for neural closure to happen at all, much less an understanding of what goes wrong that leads to those defects.”

Hypothetically speaking

De La O hails from Chicago, where she received an undergraduate degree from the University of Chicago and worked in the lab of Ilaria Rebay. De La O’s sister was the first person in her family to go to and graduate from college — De La O, in turn, is the first person in her family to pursue a PhD.

From her first time visiting campus, De La O could see MIT would provide a thrilling environment in which to study.

“MIT was one of the few places where the students weren’t constantly complaining about how hard their life was,” she says. “At lunch with prospective students, they’d be talking to each other and then just organically slip into conversations about science.”

The department emails acceptance letters and sends a physical copy via snail mail. De La O’s letter included a handwritten note from department head Amy Keating, then a graduate officer, who had interviewed De La O during her campus visit.

“That’s what really sold it for me,” she recalls. “I went to my PI [principal investigator]’s office and said, ‘I have new data’” and I showed her the letter, and there was lots of unintelligible crying.”

To prepare her for graduate school, her parents, both immigrants from Mexico, spent the summer teaching De La O to make all her favorite dishes because “comfort food feels like home.”

When she reached MIT, however, the Covid-19 pandemic ground the world to a halt and severely limited what students could experience during rotations. Far from home and living alone, De La O taught herself to bake, creating the confections she craved but couldn’t leave her apartment to purchase. De La O didn’t get to work as extensively as she would have liked during her rotation in the Martin lab.

Martin had recently returned from a sabbatical that was spent learning a new research model; historically a fly lab, Martin was planning to delve into mouse research.

“My final presentation was, ‘Here’s a hypothetical project I would hypothetically do if I were hypothetically going to work with mice in a fly lab,’” De La O says.

Martin recalls being impressed. De La O is skilled at talking about science in an earnest and engaging way, and she dug deep into the literature and identified points Martin hadn’t considered.

“This is a level of independence that I look for in a student because it is important to the science to have someone who is contributing their ideas and independent reading and research to a project,” Martin says.

After agreeing to join the lab — news she shared with Martin via a meme — she got to work.

Charting mouse development

The neural tube forms from a flat sheet whose sides rise and meet to create a hollow cylinder. De La O has observed patterns of actin and myosin changing in space and time as the embryo develops. Actin and myosin are fibrous proteins that provide structure in eukaryotic cells. They are responsible for some cell movement, like muscle contraction or cell division. Fibers of actin and myosin can also connect across cells, forming vast networks that coordinate the movements of whole tissues. By looking at the structure of these networks, researchers can make predictions about how force is affecting those tissues.

De La O has found indications of a difference in the tension across the tissue during the critical stages of neural tube closure, which contributes to the tissue’s ability to fold and form a tube. They are not the first research group to propose this, she notes, but they’re suggesting that the patterns of tension are not uniform during a single stage of development.

“My project, on a really fundamental level, is an atlas for a really early stage of mouse development for actin and myosin,” De La O says. “This dataset doesn’t exist in the field yet.”

However, De La O has been performing analyses exclusively in fixed samples, so she may be quantifying phenomena that are not actually how tissues behave. To determine whether that’s the case, De La O plans to analyze live samples.

The idea is that if one could carefully cut tissue and observe how quickly it recoils, like slicing through a taught rubber band, those measurements could be used to approximate force across the tissue. However, the techniques required are still being developed, and the greater Boston area currently lacks the equipment and expertise needed to attempt those experiments.

A big part of her work in the lab has been figuring out how to collect and analyze relevant data. This research has already taken her far and wide, both literally and virtually.

“We’ve found that people have been very generous with their time and expertise,” De La O says. “One of the benefits we, as fly people, brought into this field is we don’t know anything — so we’re going to question everything.”

De La O traveled to the University of Virginia to learn live imaging techniques from associate professor of cell biology Ann Sutherland, and she’s also been in contact with Gabriel Galea at University College London, where Martin and De La O are considering a visit for further training.

“There are a lot of reasons why these experiments could go wrong, and one of them is that I’m not trained yet,” she says. “Once you know how to do things on an optimal setup, you can figure out how to make it work on a less-optimal setup.”

Collaboration and community

De La O has now expanded her cooking repertoire far beyond her family’s recipes and shares her new creations when she visits home. At MIT, she hosts dinner parties, including one where everything from the savory appetizers to the sweet desserts contained honey, thanks to an Independent Activities Period course about the producers of the sticky substance, and she made and tried apple pie for the first time with her fellow graduate students after an afternoon of apple picking.

De La O says she’s still learning how to say no to taking on additional work outside of her regular obligations as a PhD student; she’s found there’s a lot of pressure for underrepresented students to be at the forefront of diversity efforts, and although she finds that work extremely fulfilling, she can, and has, stretched herself too thin in the past.

“Every time I see an application that asks ‘How will you work to increase diversity,’ my strongest instinct is just to write ‘I’m brown and around — you’re welcome,’” she jokes. “The greatest amount of diversity work I will do is to get where I’m going. Me achieving my goals increases diversity inherently, but I also want to do well because I know if I do, I will make everything better for people coming after me.”

De La O is confident her path will be in academia, and troubleshooting, building up protocols, and setting up standards for her work in the Martin Lab has been “an excellent part of my training program.”

De La O and Martin embarked on a new project in a new model for the lab for De La O’s thesis, so much of her graduate studies will be spent laying the groundwork for future research.

“I hope her travels open Juana’s eyes to science being a larger community and to teach her about how to lead a collaboration,” Martin says. “Overall, I think this project is excellent for a student with aspirations to be a PI. I benefited from extremely open-ended projects as a student and see, in retrospect, how they prepared me for my work today.”