Yvette Yien, Ph.D.

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Dr.  Yvette Yien is an Assistant Professor in the Department of Biological Sciences at the University of Delaware.  Dr. Yien grew up in sunny Singapore, where she received her B.Sc. in Life Sciences from the National University of Singapore.  During her undergraduate work, she carried out research in the field of x-ray crystallography.  This research experience sparked a life-long interest in the role of protein complexes and protein-protein interactions which persists to this day in her own lab.  Initially, she was convinced that she wanted to study protein biochemistry until a friend reviewed an entire semester of cell biology lectures that she had skipped right before the test.  During this cramming session, she was won over by the beauty of the apoptosis pathway and promptly joined the lab of Dr. Victor Yu at the Institute of Molecular and Cellular Biology to work on the biochemistry of mitochondrial apoptosis pathway proteins.  The year she spent in Dr. Yu’s lab sparked a life-long fascination with cell biology, and shaped her approach of identifying problems in vivo, and solving them in vitro.  Dr. Yien moved to the US in 2004 and entered the Ph.D. program in Biomedical Sciences at the Mount Sinai School of Medicine in New York City with the goal of learning how cells develop. She worked with Dr. James Bieker, who discovered the Erythroid Kruppel Life Factor, EKLF/KLF1, a master regulator of erythroid transcription and globin switching.  KLF1 turned out to be the founding member of the vertebrate KLF family of zinc-finger transcription factors, which regulate a wide range of critical processes such as development, cell death and proliferation.  Dr. Yien investigated how the function of EKLF/KLF1 could be modulated in a context-specific manner during erythroid differentiation.  During her studies, she observed that EKLF splicing was altered in the bone marrows of pregnant mice and in murine fetal livers.  This made her wonder if pregnancy caused adaptive changes in erythropoiesis to meet the requirements of the pregnant female and developing fetus.  This fascination with sex-specific regulation of hematopoiesis has persisted and is one of the projects in the Yien lab.

During graduate school, Dr. Yien attended a research seminar by Dr. Trista North on the identification of the PGE2/Wnt pathway as a regulator of hematopoietic stem cells.  This seminar opened up the possibility of doing in vivo genetic and imaging experiments in zebrafish that were not possible in mice.  Further, she realized that zebrafish is an excellent model organism in which to examine how cellular development occurs within an organismal context.  Excited by these possibilities, Dr. Yien left for Boston in 2012 to work on the role of mitochondrial iron metabolism in erythroid cell biology in Barry Paw’s zebrafish lab at Brigham and Women’s Hospital.  Her research showed that erythroid cells expressed specialized, mitochondrial membrane proteins which increase the rate transport of heme intermediates and iron during terminal erythroid differentiation.  Further, she identified CLPX as a regulator of heme synthesis in vertebrates.  Her work in these areas earned her a Ruth L. Kirschstein National Research Service Award (F32) and a K01 career development award from NIH/NIDDK.

Dr. Yien started her lab in 2017 at the University of Delaware with the overarching goal of understanding how cells couple nutrient metabolism with cell-type specific requirements.  Although most cells types require the essentially same nutrients for their survival, the specific quantities and fates of these nutrients vary among different cell types as different cells utilize nutrients in varying ways to carry out their specialized functions.  One such nutrient that carries out many ubiquitous, life-essential redox reactions in cells in key processes such as such as respiration, maintenance of the circadian rhythm, and detoxification, is iron.  Iron also plays a central role in cell-specific processes such as dopamine production within the dopaminergic neuron and oxygen transport by red blood cells.  Iron requirements and utilization in different cell types differ widely.  For instance, developing erythroid cells, which synthesize 90% of the body’s heme for hemoglobin production, transport massive quantities of iron and rapidly process them into heme.  This requires expression of erythroid-specific iron transporters and other proteins which increase the activities of heme synthesis enzymes.  Deficiencies in these proteins cause hemoglobinzation defects and developmental defects.  Other tissues, such as the liver, utilize iron for the formation of iron-sulphur clusters, which play a key role in mitochondrial respiration, and for synthesis of liver cytochromes.  The processes that govern iron fate and which couple the rate of iron uptake to its utilization are mostly unknown.  Identification of these regulatory mechanisms is a central goal of the lab.

Currently, the specific goals of the Yien lab are:  1.  To interrogate how iron transport and fate is coupled with to cellular requirements, and to exploit this knowledge to understand mechanisms of hematologic physiology and disease.  The lab hypothesizes that this occurs by the functional and structural interaction of iron transport proteins and heme metabolome with the mitochondrial homeostasis machinery, which may allow crosstalk between iron metabolism with other nutrient metabolism pathways.  2.  To understand how iron is utilized during tissue development, particularly in pathways required for terminal erythroid differentiation and liver development.  3.  To elucidate how pregnancy causes adaptive changes in maternal bone marrow hematopoiesis and iron metabolism, increasing erythroid cell production necessary to keep up with increased maternal blood volume, placental function, and fetal iron requirements.  The lab employs a broad range of model systems and techniques to solve these problems, including yeast and mammalian cell culture, as well as zebrafish and mouse animal models; this is complemented by biochemical techniques such as metabolic labeling, heme synthesis pathway enzymatic assays and metabolomics (the latter two techniques conducted at the University of Utah).   Their long-term goal is to exploit their knowledge of tissue-specific regulation of iron metabolism to more generally understand how nutrient metabolism is regulated in a cell-specific contexts.  The work of the lab is currently funded by a P01 subproject award from the NHLBI, an R35 award from NIGMS, an NIDDK R03, pilot and feasibility grants from the NIDDK administered through Indiana University and the Center for Iron and Heme Disorders at the University of Utah, and a Cooley’s Anemia Foundation fellowship.

In addition to her interests in iron metabolism, mitochondrial biology, and pregnancy, Dr. Yien is also enthusiastic about trainee development and passionate about increasing diversity in the scientific workforce, and accessibility to healthcare for under-served populations.  One of the things her lab does is to focus on research problems that disproportionately affect women and children.  Most of Dr. Yien’s undergraduates have won research awards, and her first postdoc, Dr. Mark Perfetto, was selected for a postdoc exchange program at the Center of Iron and Heme Disorders at the University of Utah.  She is actively recruiting postdoctoral fellows and graduate students who are looking to pursue challenging questions in a supportive and diverse research environment.  More information about the lab can be found here: https://www.bio.udel.edu/people/yyien.

Anne-Ruxandra Carvunis, Ph.D.

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Dr. Anne-Ruxandra Carvunis is an Assistant Professor at the University of Pittsburgh School of Medicine in the Department of Computational and Systems Biology. Dr. Carvunis identifies as an Evolutionary Systems Biologist and is resolutely interdisciplinary in her research philosophy. She opened her laboratory at Pitt in 2017 with the mandate to uncover the fundamental principles of change and innovation during the evolution of living systems. She is particularly interested in understanding what makes each species unique, including how novel species-specific genes emerge “from scratch”. A broad array of eukaryotic species and lineages are investigated in the Carvunis lab, but their current favorite model system is the budding yeast, whose genome was sequenced over twenty years ago but is still full of surprises.

Traditionally, we think of gene evolution akin to how we think of species evolution: a new gene has descended with modification from an ancestral gene. However, it has become clear over the past decade that completely novel protein-coding genes can also evolve de novo from non-genic sequences. How does this extraordinary transformation take place? How often does it happen? How do the new species-specific genes integrate the pre-existing cellular machinery? What are the physiological contributions of these young coding elements? These are only some of the exciting unanswered questions that Dr. Carvunis tackles in her laboratory.

For Dr. Carvunis, the quest to understand the origins of new genes started with an original hypothesis according to which de novo gene “birth” involves the existence and translation of transitory genetic elements called “proto-genes” (Carvunis et al, Nature 2012). Today Dr. Carvunis and her collaborators are actively pursuing research aimed at understanding the biology of these proto-genes and their evolutionary implications. Some questions require thinking deeply about what “function” and “novelty” mean in the genomic world (Keeling et al, eLife 2019), and how these concepts translate to computational methods for identifying novel sequences (Domazet-Loso, Carvunis et al, Molecular Biology and Evolution, 2017; Vakirlis et al, BioRxiv, 2019a). Other questions require directly testing hypotheses with experiments and following clues from genomics data – here again, surprises abound (Vakirlis et al, BioRxiv, 2019b).

Financial support for Dr. Carvunis’ research on gene birth has been generously provided by the NIH Pathway to Independence Award (K99/R00), the Searle Scholars Award, and most recently the NIH Director’s New Innovator Award (DP2). Dr. Carvunis has also received a number of distinctions including a Medal of honorable doctoral work, the national L’Oreal-Unesco Award for Women in Science, and the Trailblazer award from the Ladies Hospital Aid Society. In addition to her research, Dr. Carvunis co-founded the Pittsburgh Center for Evolutionary Biology and Medicine (CEBaM) to help facilitate research and education in evolutionary medicine. She is also the Associate Director of the Pitt graduate program in Integrative Systems Biology (ISB), which now includes a special track in Evolutionary Medicine.

If you would like to learn more about gene birth, please turn to the extensive review of the field Drs Carvunis and Van Oss wrote and posted to Wikipedia (Van Oss and Carvunis, PLoS Genetics 2019). Have fun!

Hossein Khiabanian, Ph.D.

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Hossein Khiabanian is an Assistant Professor of Pathology in Medical Informatics at Rutgers University. His research focuses on computational biology and cancer genomics, based on the idea that studying complexity, dynamics, and stochastic patterns in biological data is critical for understanding how tumors initiate and evolve. Cancer follows clonal, Darwinian evolution, where, as genetic alterations accumulate, fitter clones dominate, ultimately leading to macroscopic disease. During this process, selective pressures can spur tumor evolution and change its mode of progression, often leading to more aggressive and treatment-refractory disease. It is, therefore, imperative to capture the extent of genomic diversity in the subpopulation structure early in a cancer’s evolution.

Dr. Khiabanian received his Sc.B. in Physics from Sharif University of Technology in Tehran, Iran, where he was born and raised. He moved to the United States in September 2001, and entered Brown University to pursue his childhood dream of studying astronomy. There, under the supervision of Dr. Ian Dell’Antonio, he surveyed and analyzed a uniquely large cosmological datasets, and developed a method to reconstruct multi-resolution maps of galaxy clusters and dark matter structures using week gravitational lensing. During this time, he also attended lectures in genetics and immunology, which motivated him to search for research opportunities in computational biology. Soon after defending his Ph.D., he joined Dr. Raul Rabadán’s group at Columbia University in September 2008, and focused on designing statistical approaches to dissect the cellular and molecular heterogeneity that enables clonal populations to evolve and transform. He developed computational and experimental approaches that led to the discovery of genes implicated in development and disease progression in pediatric and adult leukemias and lymphomas. Specifically, his work revealed that some small mutations present prior to treatment at low abundances infer the same clinical phenotype and poor survival as clonal lesions carried by majority of cancer cells. The results by Dr. Khiabanian and his colleagues strongly suggested that limiting the knowledge of tumor genetics to the dominant clone was not sufficient for accurate prediction of a cancer’s outcome.

In August 2015, Dr. Khiabanian started a tenure-track position at Rutgers Cancer Institute of New Jersey. Since then, his lab has successfully designed statistical, information-theoretic approaches to analyze high-throughput, high-depth sequencing data to especially address the challenges in careful interpretation of clinical sequencing results. These methods aim to resolve genomic heterogeneity in both tumor and non-tumor cell populations, which may confound distinguishing subclonal tumor alterations from those possibly originating from the non-tumor component in the microenvironment. Recently, Dr. Khiabanian led an analysis of a large dataset from patients with solid tumors (Severson et al. Blood 2018), which showed that some detected mutations arose from hematopoietic cells infiltrating the tumor microenvironment. In addition to the presence of mutations associated with coexistent hematological malignancies such as myeloproliferative neoplasms (Riedlinger et al. JAMA Oncology 2019), some mutations were detected due to an age-related condition known as clonal hematopoiesis of indeterminate potential (CHIP). This work raised the hypothesis that CHIP exhibits a distinct genomic landscape when enriched in tumor microenvironment and may evolve under solid tumor treatment. Dr. Khiabanian’s lab has been testing these hypotheses and developing computational methods to study tumor evolutionary patterns supported by an R01 award from the National Cancer Institute, three pre- or post-doctoral fellowships from the New Jersey Commission on Cancer Research, an institutional grant from American Cancer Society, and more recently a Translational Grant from the V Foundation. Since joining Rutgers, the Khiabanian lab has contributed to more than 20 publications including the lead or corresponding role in 12 research articles, reviews, and pre-prints.

Dr. Khiabanian is also passionate about bridging communication barriers between computational and clinical fields and building a pathway for quantitative researchers to become translational scientists. He has organized multiple multidisciplinary meetings at Rutgers, NYU, and Columbia, and has mentored graduate students and postdocs with backgrounds in physics, engineering, informatics, and medicine. He has also made an effort to promote interdisciplinary collaborations as well as pre-print and open-access publishing through his participation in the eLife Community Ambassador program, and by providing opportunities for junior scholars to participate in the peer-review process as an academic editor for the journal PeerJ.

Because of his graduate training in physics and cosmology, Dr. Khiabanian gravitates towards putting current research in genomics in the broader historical context of advancements in science. The study of astronomy was marked by important paradigm shifts based on precise observations that were interpreted by the quantitative language of mathematics and geometry. With the advent of high-throughput sequencing methods, genomics has moved into an era that is characterized by vast amounts of unbiased data. The field has embarked on a path to uncover important insights into tumor pathogenesis and its evolutionary dynamics with the goal of helping design potentially more effective therapeutic approaches for the treatment of cancer. Dr. Khiabanian is excited for the opportunity to be a part of these efforts, and is looking for graduate students and postdocs to join this work. You can find more information about the Khiabanian lab at khiabanian-lab.org or on Twitter at @HKhiabanian.

 

Megan Killian, Ph.D.

Megan Killian - NSF Early Career Award

Dr. Megan Killian is an Assistant Professor in the Department of Biomedical Engineering at the University of Delaware. Dr. Killian’s laboratory studies the mechanisms of adaptation and growth of musculoskeletal tissues and joints (e.g., tendon-bone attachment; hip joint) with the goal of leveraging these mechanisms to improve orthopaedic healing and regeneration. To address these challenges, Megan has developed several small animal models to study the onset and progression of mechanically-induced joint disorders. The Killian Lab approaches this problem from an engineering, physiology, and clinical perspective and uses a wide range of tools and techniques such as mechanical testing, optogenetics, transgenic mouse models, and engineered materials to study healing and regeneration.

Megan is a native Michigander and grew up downriver from Detroit in a small, rural town where her father was a steelworker and mother was a tax accountant. Megan was the first in her family to attend a 4-year college and received a B.S. in Biomedical Engineering from Michigan Technological University. At Michigan Tech, Megan was a three-sport athlete (XC, Nordic skiing, and Track and Field) and learned to ski when she joined the team. Her participation in NCAA endurance sports strengthened her interest in movement science and biomechanics. She then pursued her interests in biomechanics at Montana State University, where she completed a M.S. in Exercise Science and Human Movement Biomechanics with Michael Hahn (now Associate Professor and Director of the Bowerman Sports Science Clinic at the University of Oregon). Her interests in biomechanics were strengthened even more, and she returned to Michigan Tech for a Ph.D. in BME with Tammy Haut Donahue (currently the founding chair of BME at the University of Massachusetts Amherst).

Upon completing her Ph.D. in 2010, Megan moved to Saint Louis, Missouri, where she was a postdoctoral fellow in the laboratory of Stavros (Steve) Thomopoulos in Orthopaedic Surgery at Washington University School of Medicine. Her research focused on rotator cuff development and degeneration, and she worked closely with orthopaedic surgeons to develop new animal models of joint instability and degeneration.  Her work in this area earned her the Ruth L. Kirschstein National Research Service Award (F32) and the Children’s Discovery Fellowship.

Megan started her laboratory as an Assistant Professor of Biomedical Engineering at the University of Delaware in 2016 where she continues work in these areas. She was the Co-Chair of the Gordon Research Seminar on Musculoskeletal Biology and Bioengineering in 2016 and a member of the Advocacy Committee for the Orthopaedic Research Society. In 2017, she received a K12 from the Interdisciplinary Rehabilitation Engineering Research Career Development Program. She attended the Training in Grantsmanship for Rehabilitation Research in 2018 and was awarded an R03 from NICHD in 2018 to study the contributions of skeletal muscle loading during rotator cuff maturation and healing. She has also received funding from University of Delaware Research Foundation, Delaware Center for Translational Research, Delaware Biosciences Center for Advanced Technology Applied Research Collaborations, and Delaware Rehabilitation Institution COBRE. In 2018, she was awarded the Journal of Orthopaedic Research Early-Career Award for her work in hip instability.

Megan is passionate about increasing the engagement of women in STEM fields, especially orthopaedics and engineering, which was a major draw for her to UD (which is the headquarters for The Perry Initiative, an outreach program for high school and medical school women aimed at encouraging women to pursue careers in engineering and orthopaedic surgery). Megan’s mentoring style follows principles of the growth mindset and her laboratory is populated with engaged graduate and undergraduate students from diverse educational backgrounds. This diversity brings an array of perspectives and expertise to her research group. She has hosted four high school students and five REU students for summer research and has mentored undergraduate students at UD from a diverse set of majors, including Nursing, Animal Biosciences, Neuroscience, Biomedical Engineering, Biology, Political Science, and Mechanical Engineering.

She is also a peer mentor through UD and led a team of all-women STEM faculty through the UD Faculty Achievement Program. As an active member of New PI Slack, Megan initiated the New PI Slack Faculty Success Program and has organized seven small writing and mentoring groups, which are modeled after the National Center for Faculty Development and Diversity Faculty Success Program “Bootcamp” approach.

For more information about Dr. Killian and her work, find her on Twitter at @megankillian and her website here: https://killianlab.com/

 

 

Katherine Aird, Ph.D.

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Dr. Katherine Aird is an Assistant Professor at Penn State College of Medicine in the Department of Cellular & Molecular Physiology. Her lab is broadly interested in understanding how cellular metabolism regulates cancer initiation and progression with the ultimate goal of exploiting these pathways for new therapies. Dr. Aird’s work has been funded by the NCI, DoD Ovarian Cancer Research Program, W. W. Smith Charitable Trust, and Sandy Rollman Ovarian Cancer Foundation.

Dr. Aird was born in Saudi Arabia, where she lived until she was 6. After moving to Virginia and then Ohio, she began middle school in New Dehli, India. During this time, she developed a passion for science and was especially interested in infectious disease since diseases like leprosy were something she saw on a daily basis. After finishing high school in Singapore,  she attended Johns Hopkins University for her undergraduate degree so that she could have first-hand research experience. During that time, she studied susceptibility to tuberculosis with Dr. Yuka Manabe, which solidified her resolve to obtain a PhD.

For her PhD studies, Dr. Aird moved to Duke University. While she remained interested in infectious disease, she also explored other areas of biomedical science during her rotations. During one particular rotation on cancer biology in Dr. Gayathri Devi’s lab, she was intrigued by the mechanistic cell biology puzzles that remain to be solved in cancer cells. She stayed on in this lab and identified multiple new mechanisms of therapeutic resistance of inflammatory breast cancer (IBC) cells. In 2008, she received a DoD Predoctoral Fellowship from the Breast Cancer Research Program to study mechanisms of resistance to HER2 targeting agents in IBC.  Importantly, her work revealed a new mechanism of action of the HER2 kinase inhibitor lapatinib through increased reactive oxygen species, which suggested that patients taking this drug should not combine it with antioxidants.

Dr. Aird then joined Dr. Rugang Zhang’s lab at Fox Chase Cancer Center, and later moved with him to The Wistar Institute, for her postdoctoral studies. During her interview, Dr. Zhang spoke about From that day on, Dr. Aird has been fascinated by senescence as a biological process and has worked towards discovering how senescence plays a role in both cancer initiation and response to therapy. During her postdoctoral work, she discovered that suppression of nucleotide metabolism is both necessary and sufficient for oncogene-induced senescence. Her work was the first to describe upregulation of a metabolic pathway that could completely overcome senescence and induce proliferation. This work formed the foundation for her K99/R00 Pathway to Independence Award.

In late 2016, Dr. Aird started her independent lab at Penn State College of Medicine. Her love for senescence and excitement about the growing cancer metabolic field has given her a unique niche. The aims to understand the metabolic differences between normal, oncogene-induced senescent, and tumor cells with the overall goals of: 1) elucidating the earliest events in tumorigenesis: and 2) exploiting these pathways for new cancer therapies. For instance, her lab discovered a metabolic pathway through wildtype IDH1 that is upregulated in ovarian cancer compared to normal cells-of-origin. Inhibition of IDH1 in ovarian cancer cells induced senescence through a metabolic-epigenetic axis. This work was recently published in Molecular Cancer Research where it will be highlighted in the August issue. In another project that was recently accepted at Cell Reports and currently available on bioRxiv, Dr. Aird’s lab discovered that the cell cycle inhibitor p16 has a non-canonical role in nucleotide metabolism. They found that suppression of p16 increases nucleotide metabolism to bypass oncogene-induced senescence through regulation of mTORC1. This is one of the first studies to describe a role for p16 outside of the cell cycle. These projects have led to multiple new insights into the ways cells use metabolites and activate metabolic pathways early in transformation. The lab is following up on these studies to determine whether inhibition of these pathways in pre-clinical models results in decreased tumor burden. The next big challenge the Aird lab plans to tackle is whether these metabolic changes alter the tumor microenvironment and how that affects cancer initiation and response to therapy.

Dr. Aird is also passionate about mentoring the next generation of scientists and has been nominated by her postdoctoral fellow for Outstanding Mentor through the PSU Postdoctoral Association. She is the Associate Director for Professional Development for the Penn State College of Medicine Postdoctoral Society and aims to help postdocs develop critical professional skills for the transition to the next phase of their career. Her dedication to her trainees is also evident in their fellowship success rate- both her first graduate student and first postdoc are independently funded through an NCI F31 and Penn State Cancer Institute Fellowship, respectively. You can find more information about open positions and the lab’s projects at airdlab.com. Follow Dr. Aird on Twitter @airdlab.

Joel D. Boerckel, Ph.D.

Joel Boerckel PhD

Dr. Joel D. Boerckel is an Assistant Professor at the University of Pennsylvania, with joint appointments in the Departments of Orthopaedic Surgery and Bioengineering. His lab seeks to understand how mechanical cues influence embryonic development and to apply these principles to regenerative medicine.

The Boerckel lab’s philosophy is that, if one wants to build a tissue, they should look to how the embryo builds that tissue. Thus the lab seeks to recapitulate embryonic development for tissue regeneration. The Boerckel lab’s work focuses on the mechanosensitive transcriptional regulators Yes-associated protein (YAP) and Transcriptional co-activator with PDZ motif (TAZ) in mechanotransduction, morphogenesis, growth, adaptation, and repair. In addition, his lab seeks to develop new tissue engineering strategies for challenging injuries. The Boerckel Lab uses a combination of engineered matrices and bioreactors to study mechanisms of cell mechanotransduction, genetic mouse models to study development and disease, and mouse and rat models to study repair and regeneration.

Dr. Boerckel was born in Jerusalem, Israel, and spent his childhood in La Paz, Bolivia, before moving to Illinois, USA, at age 12. He received his B.S. in Mechanical Engineering from Grove City College in 2006, and his M.S. and Ph.D. degrees, also in Mechanical Engineering, from the Georgia Institute of Technology in 2009 and 2011, respectively. On entering graduate school, he was intent to work on biomechanics and swore never to work on cell biology or signaling. However, in his doctoral work, with Robert Guldberg at Georgia Tech, he discovered that mechanical forces when applied during tissue regeneration can dramatically influence neovascularization, i.e., the formation of new blood vessels. This led him to an interest in understanding how blood vessels form, and he pursued postdoctoral training in endothelial cell biology with Paul DiCorleto at the Cleveland Clinic. There, as a Ruth L. Kirschstein NRSA Fellow, he uncovered a non-canonical role for the MAP kinase phosphatase, MKP-1, in angiogenesis. By serendipity, he also made a new mouse model that happened to have an embryonic-lethal phenotype. Though he has yet to finish and publish this work, this observation led to hours on a microscope looking at embryos. He was immediately hooked, and knew he had to spend the rest of his career studying development.

Coincidentally, as Dr. Boerckel was preparing to transition to a faculty position, a friend from church and also a postdoc at CCF, Munir Tanas (now Assistant Professor of Pathology at the University of Iowa), discovered that genetic defects in the Hippo pathway effectors, TAZ and YAP, cause the vascular sarcoma EHE. One evening over Belgian beers, Tanas mentioned: “This pathway does everything you’re interested in.” In that moment, Boerckel abandoned every idea he’d proposed in his chalk talks to pursue these fascinating proteins.

Dr. Boerckel set up his lab at the University of Notre Dame in 2014 to study YAP/TAZ signaling in bone and blood vessel development, and in 2017 he moved the lab to the McKay Orthopaedic Research Laboratory at the University of Pennsylvania. His lab was the first to identify the roles of YAP and TAZ in bone development (Kegelman+ 2018).  They discovered a mechanism in endothelial cells by which YAP and TAZ are not only activated by the cytoskeleton, but also drive a transcriptional program that feeds back to modulate cytoskeletal tension to enable persistent cell motility (Mason+ 2019). Just this month, they published a paper in Science Translational Medicine which shows how in vivo mechanical forces are required to mimic embryonic development for regeneration of large bone defects (McDermott+ 2019). His laboratory is supported by the American Heart Association, the Penn Center for Musculoskeletal Disorders, and the Center for Engineering Mechanobiology at Penn, and was recently awarded two R01 grants from the National Institutes of Health to continue this work on mechanobiology of bone development and development-inspired tissue engineering.

Dr. Boerckel is passionate about trainee career development and is looking for PhD students, postdocs, and other researchers looking to chase interesting questions in a dynamic and supportive environment. You can find more about the lab at http://www.med.upenn.edu/orl/boerckellab/, hear about his work in person at the 48th International Musculoskeletal Biology Workshop in July where Dr. Boerckel will be presenting thanks to an Alice L. Jee Young Investigator Award, and follow Dr. Boerckel on Twitter at @jboerckel.

Maitreyi Das, Ph.D.

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Dr. Maitreyi Das is an Assistant Professor at the University of Tennessee, Knoxville in the department of Biochemistry and Cellular & Molecular Biology. Dr. Das’s lab is interested in understanding the intracellular signaling patterns that determine cell polarization. To this end, she studies cell polarization events during cell shape establishment and during cytokinesis. Her research is funded by the National Science Foundation (NSF).

Dr. Das grew up in Mumbai, India. She got her Bachelor’s degree in Microbiology from Mumbai University and her Master’s in Biochemistry from M.S. University of Baroda, India. She received her PhD in 2004 from the Indian Institute of Technology, Mumbai in Biosciences. She then moved to Helsinki, Finland to study cell cycle in fission yeast in the lab of Prof. Tomi Makela. She continued her study of fission yeast in the lab of Prof. Fulvia Verde at the University of Miami where she studied cell shape control. As a postdoc, Dr. Das discovered how the conserved NDR kinase maintains cell shape in fission yeast. She also demonstrated how cells establish and maintain their shape via oscillatory dynamics of active Cdc42, a small GTPase central to polarization. In 2013 she started her own lab where she studies fundamental mechanisms that promote cytokinesis and polarized cell growth in fission yeast. When not in the lab she loves to spend time with her husband and young son.

Research in Dr. Das’s lab mainly focuses on the regulation of the small GTPase Cdc42. Cdc42 is a master regulator of cell polarization in most eukaryotes. While the role of Cdc42 in cell shape establishment is well documented, it was previously unclear why cells activated Cdc42 at the division site during cytokinesis. Dr. Das and her lab discovered that Cdc42 was regulated by a unique spatiotemporal activation pattern via its distinct regulators, which in turn regulated distinct steps of the cytokinesis process. This work was published in the journal Molecular Biology of the Cell and given the novelty of the work, it was also selected as an editor’s highlight in the American Society of Cell Biology newsletter.

More recently, Dr. Das’s lab has shown how endocytosis is critical for the later steps in cytokinesis. They found that Cdc42-mediated endocytosis ensures that proteins are uniformly organized along the actomyosin ring to promote centripetal furrow formation. This research was published in the Journal of Cell Science and also highlighted in the same issue.

In addition to these publications, Dr. Das’s lab has also published two preprints in BioRxiv. In the first preprint, her lab has discovered a novel crosstalk between two activators for Cdc42. They find that these activators regulate each other to fine tune Cdc42 activation during cell polarization and cytokinesis. This research provides much needed insight into the significance of multiple activators for Cdc42.  In the second preprint, they have shown how one of the Cdc42 activators, Gef1 is localized to its functional sites. While both the activators for Cdc42 localize to the same sites of function, this research shows that the activators are regulated by different mechanisms

Apart from her research, Dr. Das is also actively involved in outreach to both young investigators and society at large. Her lab is very diverse with students and trainees from different parts of the world, and two of her graduate students hold NSF graduate research fellowships. Dr. Das was also awarded a supplement to fund a professional development seminar series for graduate students. In this series, Dr. Das invited experts from diverse careers to provide the students with an insight into different career options (academic and non-academic) after obtaining a PhD degree. This seminar series was very well received and has been highlighted here and here.

To learn more about Dr. Das’s research, please visit her website here, and you can also follow Dr. Das on Twitter at @DasLab_Pombe.