There are huge changes taking place in the world of biosciences, and whether it’s new discoveries in stem cell research, new reproductive technologies, or genetics being used to make predictions about health and behavior, there are legal ramifications for everything. Journal of Law and the Biosciences is a new journal published by Oxford University Press in association Duke University, Harvard University Law School, and Stanford University, focused on the legal implications of the scientific revolutions in the biosciences. We sat down with one of the Editors in Chief, I. Glenn Cohen, to discuss the rapidly changing field, emerging legal issues, and the new peer-reviewed and open access journal.
Why have you decided to launch Journal of Law and the Biosciences?
This is an incredibly exciting time to be working in these areas and in particular the legal aspects related to these areas. We are seeing major developments in genomics, in neuroscience, in patent law, and in health care. We want to be in the forefront of this, and we think that a peer-review journal led by the leading research institutions working in this area in the United States is the way to go.
How has this subject changed in the last 10 years?
The genomics revolution, the reality of cheap whole genome sequencing, further developments in the ability to examine neuroscience, the realization that biosciences are a crucial aspect of criminal investigations, and the importance of research ethics have all become more prominent, as have roles that law and the biosciences play in the criminal justice system, health care delivery, and our understanding of ourselves.
What are the major intersections of law and the biosciences?
Neuroscience, genetics, research ethics, human enhancement, development of drugs and devices in biologics, and medical ethics, and many others.
What is it that makes this such a fast growing area of law?
First, we are fuelled by development in the biosciences, which is moving at an increasingly fast pace since we can build new technologies over old technologies. Second, there is increasing interest by jurists and by lawyers in these areas. Third is an increase in interest in health care and sciences more generally. From President Obama’s announcement of a major enterprise in studying the human brain to the passing of the Affordable Care Act, we are seeing a golden age in this field.
What do you expect to see in the coming years from both the field and the journal?
The ethical issues that have always been in the background are going to be made much more pressing, such as with cheap whole genome sequencing, fetal blood tests called non-invasive genetic testing, and increasingly science-based attempts to restrict abortion rights. All of these are raising questions that have always been present but are making them more pressing and also making it more likely that courts and legislatures will have to be the ones to wrestle with them correctly. We are hoping that the journal plays a role in answering those questions.
Last year, with the Advanced Notice of Proposed Rulemaking (ANPRM) and revisions to the common rule in human subjects’ research, there has also been a lot more emphasis and rethinking about the rules by which science operates at the level of human subject research regulation.
What do you hope to see in the coming years from both the field and the journal?
Increasing number of law students and non-lawyers realizing the important role that law has to play in these disputes and enabling discourse at a deeper level than we have seen to this date.
What does Journal of Law and the Biosciences expect to focus on within the field (trends / new approaches)?
Stem cell technology, reproductive technologies, law and genetics, law and neuroscience, human subjects’ research, human enhancement, patent law, food and drug regulation, and predictive analytics and big data . . . but those are just off the top of my head. We are hoping to get submissions in many more areas as well.
Nita Farahany, I. Glenn Cohen, and Henry T. (Hank) Greely are the Editors of the Journal of Law and the Biosciences. I. Glenn Cohen, JD, is Professor of Law and Co-Director of the Petrie-Flom Center for Health Law Policy, Biotechnology & Bioethics at Harvard Law School. Cohen’s current projects relate to reproduction and reproductive technology, research ethics, rationing in law and medicine, health policy, and medical tourism. Nita Farahany, PhD, JD, is Professor of Law & Philosophy at Duke Law School and Professor of Genome Sciences and Policy at the IGSP. Since 2010, she has served on Obama’s Presidential Commission for the Study of Bioethical Issues. Henry T. (Hank) Greely, JD, is the Deane F. and Kate Edelman Johnson Professor of Law at Stanford University, where he directs the Center for Law and the Biosciences. He chairs the California Advisory Committee on Human Stem Cell Research, is a founder and director of the International Neuroethics Society, and belongs to the Advisory Council for the National Institute for General Medical Sciences and the Institute of Medicine’s Neuroscience Forum.
The Journal of Law and the Biosciences (JLB) is the first fully Open Access peer-reviewed legal journal focused on the advances at the intersection of law and the biosciences. A co-venture between Duke University, Harvard University Law School, and Stanford University, and published by Oxford University Press, this open access, online, and interdisciplinary academic journal publishes cutting-edge scholarship in this important new field. The Journal contains original and response articles, essays, and commentaries on a wide range of topics, including bioethics, neuroethics, genetics, reproductive technologies, stem cells, enhancement, patent law, and food and drug regulation.
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This is the latest post in our regular OUPblog column SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: what is gene mutation?
By Jonathan Crowe
In my last three posts I’ve introduced you to the world of biological information, taking you from the storage of biological information in libraries called genomes, which house information in individual books called chromosomes (themselves divided into chapters called genes), to the way the cell makes use of that stored information to manufacture the molecular machines called proteins.
But what happens when the storage of information goes wrong? If we’re reading a recipe and that recipe contains a mistake, chances are that the end-result of our culinary endeavour won’t end up as it should. And so it is at the level of cells. If the information the cell is using is somehow wrong, the end result will also be wrong – sometimes with catastrophic results.
I’ve mentioned in previous posts how biological information is captured by the sequence of the building block ‘letters’ from which DNA is constructed. The sequence of letters is ultimately deciphered by a molecular machine called the ribosome, which reads the sequence of letters in sets of three, and uses each trio to determine which amino acid – the building block of proteins – should be used next in its mission to construct a particular protein. It should come as no surprise that, if the recipe for the protein is changed – if the sequence of DNA ‘letters’ is altered – the protein that is manufactured will probably contain errors as a result. And if a protein contains errors, it won’t be able to function correctly, just as flat-packed furniture will end up being decidedly wobbly if you construct it from the wrong parts.
Imagine a snippet of DNA has the sequence GGTGCTAAG. The ribosome would ‘read’ this sequence, and would use it as the recipe for building a chain of three amino acids: Glycine-Alanine-Lysine. Now imagine that we alter just one letter in our original sequence so that it becomes GGTCCTAAG. All we’ve done is swap a G for a C at the fourth position in the DNA sequence. However, this change is sufficient to affect the composition of the protein that is produced when the sequence is deciphered: the ribosome will now build a chain with the composition Glycine-Proline-Lysine.
Surely such a small change won’t actually cause significant problems in a cell, though. Right? Wrong. Amazingly (and perhaps unnervingly) the tiniest error can have really quite significant consequences.
Let’s take just one example. Sickle cell anaemia is a condition that affects the red blood cells of humans. Red blood cells fulfil the essential role of transporting oxygen from our lungs to all the living cells of our body: they continually circulate through our arteries and veins, shuttling oxygen from one place to another. A healthy red blood cell looks a bit like a ring doughnut (though it doesn’t actually have a hole right through the middle); by contrast, the red blood cells of individuals with sickle cell anaemia become warped into crescent-like shapes (like a sickle, the grass-cutting tool, after which the disease is named). These sickle cells no longer pass freely through our arteries and veins. Instead, they tend to get entangled with each other. As a result, the flow of oxygen round the body is impeded, and
By Jonathan Crowe
What links a queen honeybee to a particular group of four atoms (one carbon and three hydrogen atoms, to be precise)? The answer lies in the burgeoning field of epigenetics, which has revolutionized our understanding of how biological information is transmitted from one generation to the next.
The genetic information stored in our genome – the set of chromosomes that we inherit from our parents – directs the way in which we develop and behave. (We call the attributes and behaviours exhibited by an organism its ‘phenotype’.) Traditionally, the genetic information was thought to be encoded solely in the sequence of the four different chemical building blocks from which our DNA is constructed (that is, our genome sequence). If a DNA sequence changes, so the resulting phenotype changes too. (This is why identical twins, with genomes whose DNA sequences are identical, look the same, but other individuals, whose genomes comprise different DNA sequences, do not.) However, the field of epigenetics opens up a strong challenge to this traditional view of our DNA sequence being the sole dictator of phenotype.
So what actually is epigenetics? In broad terms, epigenetics refers to the way that the information carried in our genome – and the phenotype that results when this information is ‘deciphered’– can be modified not by changes in DNA sequence, but by chemical modifications either to the DNA itself, or to the special group of proteins called histones that associate with DNA in the cell. (It’s a bit like taking a book, with a story told in the author’s words, and adding notes on the page that alter how the story is interpreted by the next person to read it.)
But what has epigenetics to do with the group of four atoms, the one carbon and three hydrogen atoms mentioned at the start of this blog post? These four atoms can combine to form a methyl group – a central carbon atom, with three hydrogen atoms attached; the addition of methyl groups to both DNA and histone proteins in a process called methylation is a primary way in which epigenetic modification occurs. For example, the addition of a methyl group to one of the four chemical building blocks of DNA (called cytosine, C) either when it appears in the sequence CG (where G is the building block called guanine) or the sequence CNG (where N represents any of the four chemical building blocks of DNA) appears to result in that stretch of DNA being ‘switched off’. Consequently, the information stored in that stretch of DNA is not actively used by the cell; that stretch of DNA falls silent.
But what of our queen honeybee? Where does she fit into our story? A queen honeybee has an identical DNA sequence to her workers. Yet she bears some striking differences to them in terms of physical appearance and behavior (amongst other attributes). These differences are more than just skin-deep, however: the pattern of methylation between queen and worker larvae differs. Their genomes may be the same at the level of DNA sequence, but their different patterns of methylation direct different fates: the queen honeybee and her workers develop into quite distinct organisms.
Things take an interesting turn when we consider the cause of these different methylation patterns: the diets that the queen and workers experience during their development. The queen is fed on large quantities of royal jelly into adulthood, while worker larvae face a more meager feast, being switched to a diet of pollen and nectar early on. It is these diets that influence the way in which the queen and worker bees’ genes are switched on and off.
It is not just the queen honeybee whose genome is affected by the environment (in her case, diet). Mice exposed to certain chemicals during pregnancy have be
