Inside AJHG: A Chat with Neil Hanchard

Posted By: Sara Cullinan, PhD, Deputy Editor, AJHG

Each month, the editors of The American Journal of Human Genetics interview an author of a recently published paper. This month, we check in with Neil Hanchard, a member of the ASHG Board of Directors and senior author of ‘Whole-Exome Sequencing Reveals Uncaptured Variation and Distinct Ancestry in the Southern African Population of Botswana.’

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Collaborative African Genomics Network (CAfGEN) group at a recent H3Africa meeting. (courtesy Dr. Hanchard)

AJHG: What prompted you to start working on this project? 

Neil: Serendipity. The nidus for the project was the Human Heredity and Health in Africa (H3Africa project), sponsored by the NIH and the Wellcome Trust. Some of our institutional partners in Africa approached us about participating in order to gain insights to the genetics underpinning disease progression in childhood HIV, which, unlike its adult counterpart, hasn’t been extensively studied at the genomic level. They needed someone who knew something about genomic studies and Africa, and I happened to be standing nearby (almost literally). As we started looking for genetic variants influencing the phenotype, it became plainly obvious that without a genomic context, particularly for the individuals from Botswana, we would be going in circles.

AJHG: What about this paper/project most excites you? 

Neil: Two things. First, the degree of uncaptured variation and the unique demographic features in our populations is exciting – if we can exploit them properly, there’s a real prospect of identifying new genes and variants that are relevant to HIV progression in children – that could be a game-changer; second, all the analyses were done by trainees from Botswana and Uganda. They have since taken that genomics experience and expertise back to their home institutions, which bodes well for the future of genomic research in Africa.

AJHG: Thinking about the bigger picture, what implications do you see from this work for the larger human genetics community?

Neil: I hope it will make researchers and clinicians think more broadly about the genetic diversity across the continent. There’s a tendency in the field to think of ‘Africa’ as represented by the predominantly West African groups in publicly available datasets, but that’s only the proverbial tip of the iceberg. I hope this will give people a better understanding of the depth of diversity and genomic complexity that has to be considered in genetic studies of persons of African heritage.

AJHG: What advice do you have for trainees/young scientists?

Neil: I still think of myself as a ‘young scientist’, so I’d have to fall back on the words of my mentor as I was starting my lab – when I asked him what advice he had for me, he said, very unceremoniously, “don’t give up”. At the time, I recall thinking how incredibly underwhelming a response that was, but over time I’ve grown to see it as a genuine pearl of wisdom for a junior faculty (or trainee) enduring what can sometimes seem like a very long time in the academic wilderness.

AJHG: And for fun, tell us something about your life outside of the lab.

Neil: Is there life outside the lab? (jk!) Mostly, I spend my away-from-the-lab time with my family. Accompanying my wife to the various activities my sons are involved in – be it church choir, baseball, or chess – is really enjoyable. Otherwise, I like sports, so I try to make time to play or watch any of swimming, tennis, baseball, football…and on the few occasions when I get to go on vacation, I’m perfectly happy in Jamaica (where I’m from), reading a book beside the beach and listening to the waves crash.

Neil Hanchard, MD, PhD, FACMG, serves as Early-Career Member of the ASHG Board of Directors. He is an Assistant Professor and Clinical Geneticist at Baylor College of Medicine and Texas Children’s Hospital, and has been a member of ASHG since 2010.

Inside AJHG: A Chat with Andy McCallion, Loyal Goff, and Paul Hook

Posted By: Sara Cullinan, PhD, Deputy Director, AJHG

Each month, the editors of The American Journal of Human Genetics interview the authors of a recently published paper. This month, we check in with Andy McCallion (@FunctionalDNA), Loyal Goff (@loyalgoff), and Paul Hook (@paul_hook_HuGen) of Johns Hopkins University to discuss their paper, “Single-cell RNA-seq of mouse dopaminergic neurons informs candidate gene selection for sporadic Parkinson’s disease.”

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(L-R) Paul Hook, Andy McCallion, and Loyal Goff

AJHG: What prompted you to start working on this project?

Andy: The challenge presented by endeavoring to connect common variation identified through genome wide association studies (GWAS) to affected genes and ultimately to the mechanistic understanding of disease gives all of us a headache. Where to start?

Although powerful, GWAS are inherently biologically agnostic. Despite the wealth of loci they implicate in disease, GWAS tell us nothing of the cellular context of disease or how variants mediate their effect/s. This, and the significant distances over which regulatory sequences/variants can act, complicates efforts to systematically identify gene candidates. We wanted to ask whether, beginning with an underlying biological insight into a pathologically vulnerable cell population, we could make progress on this challenge.

AJHG: What about this paper/project most excites you?

Andy: Perhaps the most exciting thing is that this work provides a biologically informed framework that systematically prioritizes candidate genes for an entire field, Parkinson’s Disease (PD). We were able to ask what (if anything) makes the transcriptomes of neurons in the substantia nigra unique among central nervous system dopamine neurons. We reasoned that any differences may contribute to their preferential vulnerability of this population in PD. The data we generated facilitated the exploration of gene networks underpinning the identity of all assayed dopamine subpopulations and in turn revealed that networks most associated with PD are active in the nigral population.

Stepwise integration of this data allowed us to establish a rubric, filtering over 1000 potential genes in 49 PD GWAS intervals to approximately 100. The genuine excitement was driven by the fact that the data holds up! Among these candidates are many established familial/syndromic PD genes. Further, we validate the functional requirement of a gene not previously known to be mutated in PD.

AJHG: Thinking about the bigger picture, what implications do you see from this work for the larger human genetics community?

Andy: Our work demonstrates that starting from an informed biological hypothesis of (one) cellular context in which a subset of variation might be expected to mediate their effect, can yield robust, testable hypotheses of the genes modulated in disease. We’re not naïve enough to think this story is complete; we recognize that much more work needs to be done – similarly evaluating other cell populations, conditions, etc. Many others are similarly seeking ways to reveal what cellular contexts are most pertinent to a range of disorders. We see this as a proof of principle whose observations will (hopefully) synergize with those from other groups.

AJHG: What advice do you have for trainees/young scientists?

Andy: That’s a tough one! My advice would not be technical. I frequently joke with my trainees that life is not complicated – we all have only two responsibilities. First, you need to get the best out of yourself – work hard, be curious, invest in the intellectual and technical platform you create for your science, think rigorously and creatively. Second, you need to get the best out of everyone else – be fair, honest, empathetic; share information generously, recognize what you can learn from the experiences of others.

Hold those things in tension and you will reach for your success, want to ensure the success of others, and simultaneously avoid being a jerk­. The field of genetics/genomics has become so multi-disciplinary that throughout your career, you will need to develop many relationships – networks of colleagues. Hold yourself accountable for how you work and how you build and maintain relationships.

AJHG:  And for fun, tell us something about your life outside of the lab.

Andy: Outside of the lab, Paul is an avid cook and enjoys time in the kitchen. Loyal is a talented photographer and musician but currently spends most of his time chasing after his two young children. I spend much of my free time woodworking – both at home and as the carpenter on the restoration of an active second world war Liberty Ship and living museum, working alongside my teenage son. Collectively our labs (Goff and McCallion) enjoy almost anything that involves food, drink, our families, and a great laugh.

Andy McCallion, PhD; Loyal Goff, PhD; and Paul Hook, BS, study neurogenetics at the Johns Hopkins University McKusick-Nathans Institute of Genetic Medicine. Dr. McCallion, an ASHG member since 2001, served on the Society’s Program Committee from 2012-13 and as its Chair in 2014. Dr. Goff and Mr. Hook have been ASHG members since 2015.

 

 

Inside AJHG: A Chat with Tony Capra and Will Bush

Posted By: Sarah Ratzel, PhD, Science Editor, AJHG

Each month, the editors of The American Journal of Human Genetics interview an author(s) of a recently published paper. This month, we check in with John A. (Tony) Capra and Will Bush, to discuss their paper, “Comprehensive Analysis of Constraint on the Spatial Distribution of Missense Variants in Human Protein Structures.

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Tony Capra, PhD, left, and Will Bush, PhD, right

AJHG: What caused you to start working on this project?

Tony: The roots of this project go all the way back to when I was in graduate school. As a graduate student, I studied how quantifying evolutionary patterns in protein sequences and structures between species could help us understand their functions (e.g., Capra et al. 2009). Then, I transitioned to working on the genetics of recent human evolution and didn’t think much about proteins for several years. When I started my own lab, a colleague came to me with a question about the function of a protein-coding variant in a human protein. As lead author Mike Sivley and I mapped the evolutionary conservation of this variant and its 3D neighborhood across species, we realized that it was silly not to include the wealth of information about genetic variation within human populations in these analyses as well. Around the same time, my colleague Will Bush had a similar idea. Once we got together and implemented a pipeline to map a few variants into protein structures, there was nothing (except lots of debugging!) to stop us from doing it comprehensively. More than 4 million variants later, we had this paper.

Will: I have had a long fascination with structural biology, and have focused much of my work on genomic analyses that are informed in some way by the biological context where variation occurs. This project started for me when multiple studies were published using technologies that explicitly target coding variation, which point to protein-level thinking. Around this time, I met Tony with expertise in protein evolution, and this project felt like the perfect way to start a new collaboration.

AJHG: What about this paper most excites you?

Tony: This paper is a great example of how looking across fields can help solve hard problems. Once we had mapped protein-coding variants into 3D structures, we needed to find a way to quantify whether their spatial patterns exhibited evidence of constraint. After several failed attempts, we realized that this problem had a lot in common with questions that field ecologists commonly ask about the distribution of individuals across physical ranges. A bit of reading revealed the Ripley’s K framework for evaluating and comparing spatial distributions of observations. We had to adapt the methodology for our application, but making this connection to a problem in another field provided the foundation for our solution. I like that an approach from ecology helped us to re-establish a strong link between human genetics and structural biology.

Our results also illustrate why data sharing is so important. By putting two big publicly available databases together, we were able to learn something new about how genetic variants are constrained in 3D space. It would not have been possible without the efforts and foresight of the groups that collected and maintain protein structural data (the Protein Data Bank) and genetic variation data (gnoMAD, COSMIC, TCGA, and ClinVar). Thank you to all of them!

Will: Like Tony, I am excited about the potential of modeling genomic data in a totally different way! The field of geospatial analysis has grown dramatically over the last few years, so using Ripley’s K just scratches the surface of the potential approaches that could be applied in this context. Given all the data that is available for research, the idea of data integration has become quite popular, but there are often many methodological hurdles to combining data of different types or from different domains in a coherent way. I’m excited that our work contributes in this area, and I echo Tony’s thanks to all the wonderful resources that provided the data we used in this work.

AJHG: Thinking about the bigger picture, what implications do you see from this work for the larger human genetics community?

Tony: This paper provides a framework that I believe will improve analysis strategies in both human genetics and structural biology. Both fields have seen substantial increases in the amount of data available over the past 15 years, and our work illustrates the potential to extract insight from the integration of patterns of human genetic variation with 3D structures. We have many new ideas about fully leveraging this combined point of view.

I hope that the human genetics community will recognize that structural biology has many powerful tools that can help us with variant interpretation. However, our results demonstrate that getting the full benefit of the structural perspective requires considering the complex 3D context of variants. This goes beyond the basic structural information, like secondary structure, that is often included in variant pathogenicity predictors.

We also think that we human geneticists have a lot to teach structural biologists, especially about the flexibility and dynamics of their structures. But that’s a topic for another paper!

Will: Beyond our key findings, I hope that this work will inspire other ways to think of the genome in 3D! Chromatin conformation studies are now producing spatial maps of DNA within the nucleus, and we know that these patterns influence gene expression.  Long non-coding RNAs fold into complex forms to achieve their functions – many possibilities exist!

AJHG: What advice do you have for trainees/young scientists?

Tony: Talk to diverse scientists (and non-scientists). This will help you make unexpected connections between fields. Much of the motivation for this project came out of the fact that my office happens to be on the same floor as the Vanderbilt Center for Structural Biology. Different fields have powerful datasets and methods that have direct relevance to important problems (like variant interpretation). The challenge is finding them and then figuring out how they fit together! It is much easier to be creative when you have a broad knowledge of what is state-of-the-art in different fields.

Will: Keep your work organized and persevere. Mike Sivley is a meticulous note-taker, so it was easy at any given moment to go back to prior results and put everything together. Taking good notes is also a great way to know what questions you are asking, and to push through until you have an answer. With any project, there is a time when multiple setbacks make you question the whole endeavor. Looking back over notes from an entire project is the best way to see how much you’ve learned in the process, and that can be a strong motivator to push forward.

AJHG: And for fun, tell us something about your life outside of the lab.

Tony: I secretly want to be a bartender. I suspect this is because I watched too many re-runs of Cheers when I was young. I also hate getting to work before noon.

Will: I intentionally schedule my meetings with Tony before noon, and I really love a good bourbon, especially from Tony’s bar.

Tony Capra, PhD, Assistant Professor at Vanderbilt University, has been an ASHG member since 2012. Will Bush, Assistant Professor at Case Western Reserve University, has been an ASHG member since 2005 and served on the Society’s Communications Committee from 2012-17.

Inside AJHG: A Chat with Christian Schaaf

Posted By: Sarah Ratzel, PhD, Science Editor, AJHG

Each month, the editors of The American Journal of Human Genetics interview an author(s) of a recently published paper. This month, we check in with Christian Schaaf to discuss his paper, “Functional consequences of CHRNA7 copy number alterations in induced pluripotent stem cells and neural progenitor cells.

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Christian Schaaf, MD, PhD, Baylor College of Medicine (courtesy Dr. Schaaf)

AJHG: What caused you to start working on this project?

Christian: My work on copy number variation of chromosome 15q13.3 started with a patient I saw as a genetics resident on the genetics consultation service at Texas Children’s Hospital. As a physician-scientist, all my work has been inspired by patients, and my ultimate goal is to provide a deeper understanding of the mechanisms of disease, which then can be translated into new therapeutic avenues for the respective disorders.

AJHG: What about this paper most excites you?

Christian: There are two aspects that are most exciting to me. First, we have been able to generate a human model of disease, and we can measure functional consequences of a genomic change in the patient-derived cell lines. This may become particularly relevant as we begin thinking about pharmacologic intervention, as it allows us to test new drugs and compounds on these patient-derived neuronal cell lines prior to subjecting actual human patients to those drugs in clinical trials.

Second, one of the most fascinating findings of our study is the fact that increased genomic copy number of the CHRNA7 gene does not necessarily lead to increased functionality of the respective protein. This may have important implications on how we think about this duplication, and how we would consider approaching it therapeutically.

AJHG: Thinking about the bigger picture, what implications do you see from this work for the larger human genetics community?

Christian: We have always been puzzled that for several genomic loci, both deletions and duplications of the same locus predispose to neurodevelopmental disorders that look somewhat similar. One would expect that opposing genomic events cause clinical phenotypes that are also in different direction. For 15q13.3, we now provide first pieces of evidence why opposing genomic events may lead to functional changes that are actually in the same direction. This could be the case for several other genomic disorders, and is kind of a paradigm-shifting concept.

AJHG: What advice do you have for trainees/young scientists?

Christian: For all trainees in the medical field: treat every patient with the care and curiosity as if you could learn something entirely new. All of my research projects started with individual patients. They continue to be the inspiration for everything that I do.

For all trainees and young scientists (MD and PhD): have a hypothesis for every experiment, but be completely open to the outcome. Do not “expect” a certain result. Some of your most important discoveries will originate in the unexpected.

AJHG: And for fun, tell us something about your life outside of the lab.

Christian: I have four children: 6 years, 5 years, 2 years, and 6 months old. Life is crazy at home. Coming to the laboratory feels like vacation to me.

Christian Schaaf, MD, PhD, is an Assistant Professor at Baylor College of Medicine and has been an ASHG member since 2009.

Inside AJHG: A Chat with Diego Calderon, Audrey Fu, and Jonathan Pritchard

Posted by: Sara Cullinan, PhD, Deputy Editor, AJHG

Each month, the editors of The American Journal of Human Genetics interview an author(s) of a recently published paper. This month we check in with Diego Calderon (@diegoisworking), a Stanford University graduate student, along with senior authors Audrey Fu and Jonathan Pritchard (@jkpritch), to discuss their paper, “Inferring Relevant Cell Types for Complex Traits by Using Single-Cell Gene Expression.”

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Diego Calderon, PhD student, Stanford University (courtesy Mr. Calderon)

AJHG: What prompted you to start working on this project?

Diego: Single-cell RNA-seq is a hugely powerful tool for finding novel fine-scale cell types in complex tissues. But if we’re interested in human disease, how can we prioritize potentially trait-involved cells, out of all the newly identified cell types, for further characterization? Our idea was to focus on cell types that tend to specifically express genes near mutations associated with the trait of interest. Surprisingly, when we started thinking about this project, there hadn’t been work published attempting to connect GWAS data and such findings from single-cell assays.

AJHG: What about this paper/project most excites you?

Diego: The development of RolyPoly allowed us to find finer-scale trait-associated cell types from complex tissues; particularly, we focused on neuropsychiatric traits and single-cell data from human brains. There had been hints of immune involvement in Alzheimer’s disease, thus we were intrigued to see this association with microglia, which are the brain’s immune cells. Additionally, there has been wonderful work clustering single-cells into cell states, which we can also scan for links with complex traits. For example, we found that actively replicating cell types from early timepoints of fetal brain development were associated with schizophrenia. These findings are exciting because they can be used to inform the development of cell type or state models that more specifically capture human disease processes.

AJHG: Thinking about the bigger picture, what implications do you see from this work for the larger human genetics community?

Diego: When we began this project, there were only a limited number of human single-cell datasets publicly available. Earlier this year, plans for the human cell atlas were announced, which will result in large publicly accessible datasets of single-cell RNA-seq measurements. Our hope is that researchers can use our tool along with other single-cell methods to further our understanding of biology and complex traits.

AJHG: What advice do you have for trainees/young scientists?

Diego: As a young scientist, you should think deeply about your chosen scientific problem. However, it’s also worth considering how best to communicate your new ideas. The ability to make complex biological or computational concepts accessible is a skill that’s worth refining and will help advance your career regardless of your chosen field. As a result, it takes time and persistence to continue to refine your writing and ideas without becoming discouraged. It took us many months to finalize our manuscript.

AJHG: And for fun, tell us something about your life outside of the lab.

When not in the lab, Diego enjoys throwing clay coffee mugs at the ceramics studio and eating a hot meal after a long day of backpacking. Audrey appreciates listening to opera and singing karaoke. Jonathan is fond of spending time with his family, searching for the best veggie burrito at Stanford, and running through the foothills of Palo Alto.

Diego Calderon, BA, is a graduate student at Stanford and has been an ASHG member since 2014. Audrey Fu, PhD, is an assistant professor at the University of Idaho, and has been an ASHG member since 2014. Jonathan Pritchard, PhD, is a professor of biology and genetics at Stanford, and has been involved with ASHG since 2002.

Inside AJHG: A Chat with Janet Kelso

Posted By: Sarah Ratzel, PhD, Science Editor, AJHG

Each month, the editors of The American Journal of Human Genetics interview an author(s) of a recently published paper. This month, we check in with Janet Kelso, to discuss the paper, “The Contribution of Neanderthals to Phenotypic Variation in Modern Humans.”

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A Neanderthal scene re-created by research group members. (courtesy Dr. Kelso)

AJHG: How did you begin working on this project? 

Janet: We previously studied regions of the genome where there is evidence for Neanderthal DNA in the genomes of present day non-Africans and had inferred, based on the functions of genes nearby to these Neanderthal segments, the influence of Neanderthal DNA by looking at predicted gene functions and at changes in gene expression.

However, directly identifying associations between Neanderthal DNA and phenotypes requires access to large datasets that provide both genetic information as well as well-characterized phenotypes in very large numbers of people. Such datasets were not available until quite recently. In 2016, a study from the Capra group looked specifically at the influence of Neanderthal alleles on disease phenotypes by using medical records for over 25,000 people. They identified a number of really interesting associations between Neanderthal DNA and disease risk. We were interested in extending this idea to include non-disease phenotypes in order to determine what influence Neanderthal DNA might have on ordinary variation in people today.

Because Neanderthal alleles are rather rare in people today, we need to have a really large number of people. The UK Biobank pilot study now provides such an extensive resource, including genetic information as well as information about hundreds of common phenotypes in more than 100,000 individuals. Therefore, we were finally able to investigate the impact of Neanderthal alleles on common phenotypes in modern humans.

AJHG: What about this paper most excites you? 

Janet: A notable aspect of our study is that the growing move to collect both genotype and phenotype information in biobanks, such as the UK Biobank, now provides us with the ability to answer not only biomedical questions but also to understand the evolutionary history of modern human traits.

We were able to determine directly the effect of Neanderthal DNA on the phenotypes of people today. Our findings are consistent with previous inferences that genes involved in skin and hair biology were strongly influenced by Neanderthal DNA. However, in those previous studies it wasn’t possible to determine what aspect of skin or hair biology was affected. We were able to show that it is skin and hair color and the ease with which one tans that are affected.

It was somewhat surprising that we observe multiple different Neanderthal alleles contributing to skin and hair tones. Some Neanderthal alleles are associated lighter tones and others with darker skin tones, and some with lighter and others with dark hair colors. This may indicate that Neanderthals themselves were variable in these traits.

A number of the phenotypes to which Neanderthal DNA contributes in people today seem to be related to sunlight exposure. For example we see contributions to skin and hair pigmentation, mood, sleeping patterns, and smoking status. It is therefore tempting to speculate that Neanderthal contributions may have been important in our adaptation to a modified sunlight regime during the colonization of Eurasia.

AJHG: Thinking about the bigger picture, what implications do you see from this work for the larger human genetics community?

Janet: Our study is notable in that it shows the enormous benefits provided by biobanks in which both genotype and extensive phenotype information are collected. The use of biobanks in in such studies is relatively new, and demonstrates that resources such as the UK Biobank provide us with the ability to answer not only biomedical questions but also to understand the evolutionary history of modern human traits.

More specifically, we have been able to determine directly the effect of Neanderthal DNA on a very broad range of non-disease phenotypes in people today.

AJHG: What advice do you have for trainees/young scientists?

The growing amount of genetic data from both archaic and modern humans provides a tremendous opportunity for creative people to tackle interesting questions in understanding the evolutionary basis of modern human traits and diseases.

Janet Kelso, PhD, is a computational biologist and Group Leader of the Minerva Research Group for Bioinformatics at the Max Planck Institute for Evolutionary Anthropology.

Inside AJHG: A Chat with Wouter de Laat

Posted by: Sarah Ratzel, PhD, Science Editor, AJHG

Each month, the editors of The American Journal of Human Genetics interview an author of a recently published paper. This month, we check in with Wouter de Laat, PhD, to discuss his paper, “Sensitive Monogenic Noninvasive Prenatal Diagnosis by Targeted Haplotyping.”

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Carlo Vermeulen, MSc, first author of the paper (left); and Wouter de Laat, PhD (right) (courtesy Dr. de Laat)

AJHG: How did you begin working on this project? 

Wouter: The realization that our TLA technology is powerful for targeted haplotyping of any genomic locus of interest triggered us to think about clinically relevant applications. Our background in thalassemia research and our close collaborations with the University Medical Centre Utrecht soon made us excited to explore whether TLA haplotyping would enable non-invasive prenatal diagnosis for monogenic diseases.

AJHG: What about this paper most excites you? 

Wouter: Two things. To me, the fact that our knowledge acquired through basic research on the structure and function of our genome led us to develop a novel prenatal diagnostic test emphasizes once more the societal relevance to support fundamental research. I find this important to mention, coming from a country where national policy makers propagate almost exclusively the virtues of translational research. The other very rewarding aspect of this project was our interaction with Dutch, Greek, and Iranian clinicians who work daily with cystic fibrosis and thalassemia families: they made us truly appreciate the clinical impact of this work.

AJHG: Thinking about the bigger picture, what implications do you see from this work for the larger human genetics community?

Wouter: I expect that, now that pre-conception screening programs for severe Mendelian disorders are being implemented in our health care system, non-invasive prenatal diagnosis (NIPD) methods will be very welcome alternatives to the more burdensome invasive tests for giving desired comfort during pregnancy. A genetic test based on a simple blood draw may in the future also provide risk couples opting for embryo selection with an easy means to confirm that the familial disease was not transmitted to the child. And variants of the NIPD method presented here may offer an attractive way to confirm parenthood, for example following in vitro fertilization.

AJHG: What advice do you have for trainees/young scientists?

Wouter: Always, even if you are considering pursuing a tenure track academic position, ask yourself at the end of your PhD and certainly as an early postdoc: am I, and is my CV, in the top among my peers and am I truly passionate about science? If not, realize that there is a world of careers outside of academia that may be equally inspiring and rewarding to you and that this is the moment to start exploring these opportunities.

AJHG: And for fun, tell us something about your life outside of the lab.

Wouter: Scientists are sometimes not very different from other human beings. To recharge the batteries, I love doing sports (soccer, cycling) and love traveling with my wife and three daughters: we just returned from an amazing trip to Sri Lanka.

Wouter de Laat, PhD, is a Professor of Biomedical Genomics at the University Medical Center Utrecht, Professor at Utrecht University, and Founder of Cergentis.