TERRY GROSS, HOST:
This is FRESH AIR. I'm Terry Gross. More and more people are looking to genetics to understand where they come from and what their future might be. Genetic sequencing can tell us about our ancestry and warn us about the risks we inherited of certain diseases and conditions. Meanwhile, scientists are exploring ways of altering genes to prevent or cure illnesses. My guest, Carl Zimmer, has written a new book about state of the art genetic research and the history of genetic research that led us to where we are today. The book is called "She Has Her Mother's Laugh: The Powers, Perversions, And Potential Of Heredity." Zimmer is a science columnist for The New York Times. He teaches science writing at Yale University. He's written previous books about viruses, parasites and evolution.
Carl Zimmer, welcome back to FRESH AIR. How accurate do you think the DNA ancestry traces are now?
CARL ZIMMER: I like to think of them as telescopes in the 1700s. You know, they're pretty good. You know, you could look up in the sky with a telescope in the 1700s, and you could see things that you couldn't see with your naked eye. But it was pretty blurry, and there might be things you saw that weren't real and there'd be a lot of things you didn't see. So if you go from one testing company to another in terms of ancestry, you're going to get different percentages. People have done this, and that's what they find. The statistics are still very rough. They are going to get better because what's going to happen is more and more DNA is going to go into these databases, and it may even be possible in the future to zero in at least some of your ancestry to, you know, let's say a town or a village in someplace where people don't move around a lot. So, you know, you shouldn't look at that as sort of absolute truth. We like to look at our DNA as some sort of divine revelation about who we are, but really what you're getting from these tests is, you know, the best guess that scientists can use with the information that they have.
GROSS: What did you learn medically from your DNA?
ZIMMER: I was working with a genetics counselor when I was getting my genome sequenced. You know, I wanted to know if there was anything I needed to worry about. And I have two kids, and I wanted to talk with them about anything that was of serious concern first before even thinking about writing about this. My genetics counselor called me one day and said, OK, your genome's sequenced and we've had a chance to look at it. And I said, OK. And she said, we can just have this conversation over the phone, (laughter) which I thought was weird if she was going to tell me about some terrible, disturbing problem I had that I didn't know about. And she said, you're fine. You have a boring genome. And it's funny how I felt somehow a little crestfallen. Like, I wanted something exciting and exotic, you know, like, I have some obscure, bizarre syndrome that nobody else has and I'll be cool. (Laughter) But she pointed out, no, a boring genome is a really good genome. And so all that means is that I don't have any of these mutations that on their own can knock you down with a particular disease. You know, I have, you know, lots of genes with mutations that raise my risk a little bit for this disease or that. But we all do.
What was actually really interesting to me is that when I showed my genome to some scientists, they said, you know, you actually have an interesting mutation here in this one gene. This isn't a gene that raises your risk of disease. It is actually extremely protective. So I have a mutation that protects me from certain autoimmune diseases. And when I started to learn about what this mutation does and how it sort of tamps down my immune system so it doesn't go out of control, I discovered that scientists have been studying this mutation in other people and have developed a drug based on the biology which has just gone on the market recently and is used for autoimmune diseases. So there's no end of these sorts of things to discover. You know, I can now look to my parents and say, you know, there's a mutation I inherited from each of you on a gene called FTO, and, you know, that makes people on average a few pounds heavier. So, you know, I wish you had given me the other one. (Laughter).
GROSS: No, but they gave you the great one, the one that protects against autoimmune disease.
ZIMMER: That's true. Well, one of them did. I have one copy. (Laughter).
GROSS: But that's good enough, isn't it? No?
ZIMMER: Yeah, it is. I don't know which one personally to thank, though. (Laughter).
GROSS: You know, a question in terms of heredity has always been, like, nature versus nurture. Like, what potentials and problems are you born with - I guess that are inherited through your genes - and what's going to shape you from the world around you, the experiences you've had, the environment you're brought up in, the way your parents raise you. And you say that line is growing increasingly more blurry, and that's in part because of our knowledge of epigenetics, which is a whole new field about how parts of your genetics can actually be changed by the world around you. Would you explain the basic premise of epigenetics?
ZIMMER: Sure. So we have genes, and our cells use genes to make proteins and other molecules. And those genes can be switched on, or they can be switched off. And the way that happens is that our cells have molecules that are hovering around our DNA, and they clamp onto certain genes and silence them. We can actually coil up our DNA to hide genes, and that shuts them down, as well. And these are long-term changes so that, you know, when an embryo is developing and starting to develop muscle and brain tissue and different organs, the cells in each of those tissues are permanently turning off certain genes and turning on others. And that whole area of turning genes on and off is sometimes called epigenetics. And what's fascinating is that, actually, it looks as if some kinds of experiences that we have in the environment around us may alter that epigenetic pattern in ourselves. So it's conceivable that in your own life your experiences can change how your genes work.
This is a very controversial area for a lot of reasons. One is that it's actually surprisingly hard to really pin down what those changes are and what's causing them, but that hasn't stopped epigenetics from becoming incredibly trendy. And where this gets even more exciting but also controversial is the idea that maybe if your experience changes that epigenetics (unintelligible), maybe you could pass it down to children, and maybe they could pass it down to their children. So perhaps, some people argue, epigenetics could be a completely separate channel of heredity.
GROSS: So there was a study related to epigenetics that was done with mice, and what they did was they totally stressed out mice to see if that stress was inherited by the mice offspring. Would you describe that study and tell us how definitive it is? Like, what did we really learn from it?
ZIMMER: These studies are really fascinating because what they're doing is, they are putting mice under stress, male mice in particular. And then these mice are mating. And then researchers are looking at their offspring and later descendants. And you have to think about this that all the male is contributing to its offspring is just sperm. It's not as if females are getting stressed, and that affects the environment in the uterus where an animal is developing. So it's just what...
GROSS: So the stressed-out mice were just male mice.
ZIMMER: That's right. So it's just male mice, and all they are contributing is what's in that sperm cell. And some of these experiments suggested that their descendants seemed to be altered through the experiences of their father or grandfather. And then scientists have actually gone into these individual sperm cells, and they have pulled out some of the molecules that control genes, and they've actually then just taken those molecules and then gone over to some other mouse sperm and inject them into that, and then use that to fertilize mice. And just transferring those molecules into other mice seems to then produce these offspring that also have this kind of altered personality.
This is incredibly tantalizing research. And, you know, it makes you think about how the experiences of our ancestors might alter us. But a lot of scientists are really strongly skeptical about it. They are arguing that these are very small studies, that they're just very random effects that are being picked up and people are claiming that they're real. So, you know, the jury is definitely still out on mice, let alone people. But, you know, that doesn't mean that epigenetics isn't real.
GROSS: Let me reintroduce you. If you're just joining us, my guest is New York Times science columnist Carl Zimmer, who's the author of a new book about the history of genetic research and current state-of-the-art research. The book is called "She Has Her Mother's Laugh: The Powers, Perversions And Potential Of Heredity." We'll be right back after a break. This is FRESH AIR.
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GROSS: This is FRESH AIR. And if you're just joining us, my guest is Carl Zimmer. He's the author of a new book about the history of genetic research and current state-of-the-art research. It's called "She Has Her Mother's Laugh: The Powers, Perversions And Potential Of Heredity." And he's a science columnist for The New York Times.
Let's talk about CRISPR, which is the word that's used for the process of what's called genetic splicing, like genetic editing - basically changing a gene. And, you know, when you hear genetic splicing, at least for me - I work in radio - I picture, like, audio editing, audio splicing, where in the old days we would remove a piece of tape and splice the remaining pieces of tape together or now digitally edit out a few words or a few sounds. But CRISPR, from what I understand, isn't anything like that (laughter).
ZIMMER: Actually, I think that's not a bad metaphor (laughter).
ZIMMER: Yeah. Because what happens with CRISPR is that scientists will design a molecule. Think of it as a probe. And it will search around in the DNA in a cell until it finds a very specific short sequence, and it'll grab on to it. And it brings along with it basically molecular scissors, which will then cut the DNA at that spot, kind of like cutting tape. And you can cut out a segment of DNA. And if you just do that, then the DNA will heal itself. Basically, the two loose ends will stitch themselves back together, and now that piece is just missing. Or you can add in a little piece of different DNA, and you can actually get the cell to put in that new piece of DNA where you just cut out the old one.
GROSS: Right. So that's pretty remarkable. But it's not like scientists are, like, taking razorblades or anything (laughter) in the lab and changing DNA. You're basically programming - what? - programming other molecules to go in and do the job for you?
ZIMMER: Yeah. You're creating molecules that are going to be able to attach to just one particular place in all of your DNA. And so they are zeroing in with greater and greater precision to just particular spots in the DNA. You know, wherever you want to go, you just craft a molecule that will recognize that place and lock on to it. And then it brings with it these molecular scissors that will make the cuts.
GROSS: I'm confident that if I asked you to explain it more, in more scientific detail, that I would not understand it. So instead of doing that, I'm (laughter) going to ask you for an example of how that's being used now, how this kind of gene editing is being used.
ZIMMER: So here's an example which I think really drives home the potential for CRISPR. It's that scientists can create lines of mice that have some of the diseases that we have. So for example, there is a kind of mouse that gets a muscle disease called muscular dystrophy. And this is caused by a particular mutation on the X chromosome. And it's a really devastating disease in humans, and these mice will develop it too. So you have these mice that, unless otherwise treated, are going to basically waste away. Their muscles are essentially going to turn into, like, a jelly-like substance. And then they're not going to be able to breathe anymore, and they're going to die.
Now, what scientists can do is they can inject these CRISPR molecules into the mice. And these CRISPR molecules make their way into muscle cells, and they then cut out that mutation and repair the DNA. So the mutation that caused the disease is no longer there in those cells. And these mice then become stronger, and they live longer. They are being treated, if not cured of this disease.
GROSS: That's - yeah.
ZIMMER: That's the kind of thing that CRISPR can do.
GROSS: That's pretty remarkable. Is it being used with human beings yet?
ZIMMER: We're just on the verge of human trials. They will be starting hopefully very soon for diseases like sickle cell anemia. There is actually a lot of research on muscular dystrophy as well. There are a few key diseases where scientists think these would be the good - the best places to start, to basically inject CRISPR molecules into people's bodies. These CRISPR molecules will then go to certain kinds of cells and repair one particular spot in their DNA. And that treats the disease.
GROSS: So this could be the future of genetic diseases, genetically inherited diseases?
ZIMMER: It very well could be. Yeah. I mean, we shouldn't look at this as a panacea because it may turn out that these CRISPR molecules, maybe they don't do a very good job of reaching their targets in the human body, or maybe there are going to be side effects. Like, for example, maybe they get distracted by another piece of DNA, and they accidentally cut that as well. I mean, there are a lot of reasons to sort of just kind of hold on because it's so exciting that you want it to work.
But we've been here before. I mean, there have been earlier kinds of treatments known as gene therapy, where you would basically try to add an extra gene into someone's cells. And that seems like it was just a slam dunk, but then it turned out to not work very well for years and years. And that's only starting to recover now after, like, 20 years of research. So CRISPR could be even more exciting and truly revolutionary. We just have to wait and see what these first generation of human clinical trials show us.
GROSS: Is CRISPR being used for genetically modified foods, or is that completely different process?
ZIMMER: It - they are being used for genetically modified foods. They're just beginning to. And it's - the basic logic, is, again, the same in the sense that, you know, plants have DNA, and CRISPR works on DNA. So what scientists are doing in that case is they're not just trying to, say, cure a disease in a plant. They're actually trying to produce new breeds of plants. And so, you know, if you know that there is a gene that controls how a plant deals with high temperature, and you're saying, well, we need to prepare new kinds of plants for climate change, you can test out new kinds of genetics by using CRISPR to rewrite that gene a little bit and see how well it does at those higher temperatures.
GROSS: There are some people who will not eat genetically modified food if they can avoid it. And I'm wondering, after having done all this research for your new book, what your thoughts are about the pros and cons of genetically modified food?
ZIMMER: Well, you know, the fact is that, you know, when plant breeders were producing new kinds of plant varieties, like in the 1900s, you know, they would use methods like basically pointing X-ray machines at seeds and just blasting them and then just seeing if any interesting mutations came out of that and then breeding up some crops from that. That's like a very random, almost blind process. And so there's no reason to think that actually going in strategically and tinkering with one particular gene that you already have a lot of evidence is very important for that trait that you want to change could be any worse. You know, in fact, you might have good reason to think that it would actually be safer.
There's no evidence that genetically modified foods are harmful to our health. And so there's even less reason to think that this new generation of CRISPR foods will necessarily be more dangerous to us. We may object to genetically modified foods for other reasons - for social and economic reasons. And I find those arguments to be totally valid in the sense that - you know, do we want to leave the control of agriculture in the hands of small-scale farmers? Or does everybody have to go to, you know, one big chemical company and buy their seeds each year from these people and be not even allowed to plant those seeds the next year. That's a different argument though. That's a social argument. And it's not - it doesn't have to do with safety.
GROSS: There's also a fear that the genetically modified plants will spread their DNA to places where that genetic modification is not wanted. And then they'll just kind of, like, take over.
ZIMMER: There has been concern about that. But, you know, there's no evidence of that actually happening in any sort of significant way. You know, so genetically modified crops have been around now for a number of years. And in the United States, you know, a lot of, like, you know, the soybeans and cotton and so on are - these plants are genetically modified. And you don't see that sort of a runaway process happening.
GROSS: My guest is Carl Zimmer. His new book is called "She Has Her Mother's Laugh: The Powers, Perversions And Potential Of Heredity." After a break, we'll talk about altering genes in mosquitoes to prevent malaria and how DNA was used to track down the Golden State Killer. And Maureen Corrigan will review two mystery novels she thinks are great for summer reading. I'm Terry Gross, and this is FRESH AIR.
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GROSS: This is FRESH AIR. I'm Terry Gross back with New York Times science columnist Carl Zimmer. His new book "She Has Her Mother's Laugh: The Powers, Perversions, And Potential Of Heredity" is about state-of-the-art genetic research and early genetic research that led us to where we are today. When we left off, we were talking about research into how genes can be modified to prevent diseases.
So another area that applies to modifying genes for genetic reasons to prevent disease has to do with genetically modifying insects that carry disease, such as trying to genetically modify mosquitoes so that those mosquitoes can no longer carry malaria. What's being done in this research?
ZIMMER: So for the research for my book, I went to California and went to the lab of a scientist named Anthony James. And he runs what he calls an insectarium, which is basically a giant room full of mosquitoes. He raises thousands and thousands of mosquitoes. And he's genetically engineered them so that they are resistant to malaria. Malaria is spread by a parasite. And so these mosquitoes basically kill off the parasite if it tries to get in their bodies. And the idea behind these mosquitoes is that, maybe in the future, we would release them into the wild. And these mosquitoes have been genetically engineered in another way so that they will basically push this resistance gene into all of their offspring. And those offspring will push it into all of their offspring as well. So they basically override the normal rules of heredity.
And the theory is that if you were just to release a few hundred of these mosquitoes into a region where you have a lot of malaria - within a few years, the malaria might be gone. This could be a way of eradicating malaria period. And so now there's a huge amount of interest in this from a lot of foundations and governments around the world, focusing on using this new way of tinkering with heredity to maybe attacking malaria.
GROSS: Is there a possible downside of doing that?
ZIMMER: The downside is that once you set these kinds of organisms loose out in the wild and you kind of change the rules of heredity, it might be hard to undo what you've done. You know, we've sort of seen an analogy of this with invasive species - you know, that people brought cane toads from South America to Australia because they thought they would be great at eating the insects that were destroying sugar cane plantations. And it turned out the cane toads like to eat lots of native species, and they've exploded over the continent. And there's just no way of taking them back. So maybe these crisper, altered mosquitoes might do something that we can't predict, and they're just going to keep reproducing and just be part of the environment. And we really don't know much about how to take them back. So there is a lot of research going on into how to make this gene-drive technology super safe and being able to undo any damage that you might do to wild species.
GROSS: So the insectarium that you went to with all the thousands and thousands of mosquitoes - would you describe it to us?
ZIMMER: So yeah. It's kind of amazing. I mean, first of all, you have to gown-up before you go in there. And then...
GROSS: That sounds like a good thing.
ZIMMER: Yeah. Absolutely. Absolutely. But it does sort of remind you, you're doing something serious here. And then you go through an air lock, and then you're in this room where there are the mosquitoes living in all their different life cycles. So there is a dark room where the female mosquitoes are laying their eggs 'cause they like to do it in the dark. And then the scientists pull the eggs out from these rooms, and they inject DNA into them. And then they put them in water 'cause that's where mosquito larvae like to develop.
And so you go into this other room where there are these tubs of water, and these, like, snakelike things are slithering around in there. And then they develop into adults, and then, you know, the females need to drink blood. And so they have these - they found that the containers for movie popcorn work really well. What they do is they basically clamp a warm container of calf's blood on top of them, and then the mosquitoes are underneath - on the underside of the plastic lid basically poking through and drinking the blood and fattening themselves up. And then the cycle repeats itself. It's kind of spooky. And, you know, when you leave, you go back into the air lock. And then you just look at this white door making sure that no mosquitoes came out with you (laughter) because they - for now, those mosquitoes need to stay in there. We do not want them getting anywhere. It's a very intense experience.
GROSS: So when you were in the room all gowned up, were the mosquitoes wild or are they contained like in an aquarium where everything's behind glass?
ZIMMER: The mosquitoes were always in containers. So they were, you know, in - they were in jars, or they were in these little plastic tubs if they were still in their larval stage. So no, you were not getting bitten by mosquitoes. There were not swarms of mosquitoes in your face. They were all very much where they needed to be in different rooms for different parts of their lifecycle. But, you know, it's always possible that one mosquito might get out. And, you know, they have all sorts of things in place to basically kill any mosquitoes that might escape. These are actually mosquitoes that are native to India, and this is Irvine, Calif. So, you know, even if one were to get out, it would probably just die right away because it's so dry there. It's so unlike their native habitat. So all sorts of things have been put in place to minimize the chance of anything going wrong.
GROSS: And you didn't have any bites when you left?
ZIMMER: No. No...
ZIMMER: ...I did not. You know, but the flipside is - I mean, there's a - certainly it's a little spooky to be looking at, you know, movie popcorn containers full of blood-engorged mosquitoes. But on the other hand, you look at them and, actually, you can tell that they've been genetically altered 'cause they have red eyes, which is kind of spooky. But, you know, they - you look at that. And you say, well, that means that these could be the cure for malaria. It really - that really could happen. And hundreds of thousands of people die every year of malaria. We've thrown everything we can at it, and this parasite is still knocking us down worldwide. So maybe this could be it, and so that's actually quite exciting.
GROSS: Let me reintroduce you here. If you're just joining us, my guest is science journalist Carl Zimmer. His new book is called "She Has Her Mother's Laugh: The Powers, Perversions, And Potential Of Heredity." And it's about the history of genetic research and the state-of-the-art, current genetic research. We'll take a short break and then be right back. This is FRESH AIR.
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GROSS: This is FRESH AIR. And if you're just joining us, my guest is Carl Zimmer. He's a science columnist for The New York Times and author of a new book about genetics, the history of genetic research and current state-of-the-art genetic research. It's called "She Has Her Mother's Laugh: The Powers, Perversions And Potential Of Heredity."
So one of the big stories lately involving genetics was how genetic research - how DNA was used to track down the Golden State Killer in California. And this had been a cold case for years. So how was DNA used to solve that case?
ZIMMER: They were taking an advantage of a pattern in heredity, which is that, you know, as parents pass down DNA to their kids, the DNA on the chromosomes gets shuffled a little bit. And so what that means is that, you know, you and a sibling will share a lot of very long identical stretches of DNA. But you and your cousin will share fewer of these sequences, and they'll be shorter. That's because there's been more shuffling happening over two generations instead of one. And the same is true for three generations back and so on.
So geneticists have actually been able to come up with a method for comparing DNA, identifying these long stretches and saying, ah, these two people must be related. So this method of identifying relatives has become incredibly popular thanks to the rise of websites like ancestry.com, 23andMe. And, you know, they'll offer you this relative-finder service, and basically all they're doing is looking for people in their database with very long stretches of DNA that match yours.
And so for the Golden State Killer case, what somebody decided to do was to take the DNA that they had from these crime scenes and upload it to one of these open-access sites, not a commercial site, and then just see if they could find any close matches. And they found that, you know, there were some people who looked like they were distant cousins of this person. And then they went and did the genealogical research to figure out, well, how would they be related? And then said, OK, who are the possible relatives that this person could be, and where do they live? And that actually helped narrow down their search until they made an arrest.
GROSS: Now, if you just send your DNA to get, like, an ancestry search through one of the companies, like 23andMe, would that mean that your DNA was available for a crime search like that?
ZIMMER: So the commercial companies said, when they were asked about this during the Golden State Killer news, that they won't do this - I mean, that they will not invade people's privacy in this way. Now, what the police did in this case is that they went to an open-access, sort of crowdsourced site called GEDmatch. And there, basically, you know, it's sort of a group effort. And everybody uploads their DNA and works on the software together, and it's sort of a joint effort. And so you know, everybody is free to just try to match up their own DNA to anybody in the database. I don't know how many people thought about the police coming in and secretly comparing their own DNA to a possible suspect.
You know, this is a broad civil liberties issue. There is - has been some long-running concern about police trying to find evidence of crimes by looking for the relatives of criminals with DNA because, you know, things get less and less precise. And there have actually been people who have been arrested because it looked as if, you know, their DNA matched that of somebody in one of these genealogical databases. Like, they looked like they were related. And they said, oh, that's good enough for us, and they would make an arrest. And then it turned out this person was innocent. So this is not the last time we're going to see this coming up in news about crime.
GROSS: Well, getting back to the commercial companies like 23andMe and Ancestry, what kind of privacy agreements do you sign with them?
ZIMMER: So you can choose sort of different levels of privacy with a lot of these services. And so for example, some people will say, I want you to look at my DNA. I want you to tell me about my ancestry. I want you to tell me about - you know, for 23andMe, they'll give you a few bits of information about your medical conditions. And that's it. But they will try to get you to opt in to sharing your data for their own basic research.
So at 23andMe, for example, there's a whole team of researchers who are studying all sorts of things, all sorts of diseases, sleep patterns and so on. And then they will also go into partnerships with drug development companies, who will take their data looking at, say, 50,000 people with lupus and 50,000 people who don't have lupus and try to look for the genetic differences. Those could point the way towards possible drugs.
GROSS: So to sum up, there's some amazing breakthroughs being made in genetic research, but there's so many questions that remain. I know I'm stating the obvious here. But it sounds like there's a lot that's still really inconclusive.
ZIMMER: Yes. You know, if you just look at the genome and look at all the things that we inherit genetically from our ancestors, you know, there's just a lot of it that scientists really can't tell you much about at all. It's still a pretty poorly explored frontier. And, you know, heredity is so important to us. It really is how we explain who we are and how we got that way, by looking to our ancestors and saying, what did we inherit from them? And so we really want it to tell us all sorts of things. And now that we can start to look at our own DNA, we want those answers right now. And the simple fact is that a lot of those answers either aren't there yet, or we'll never find them in our DNA.
GROSS: So - and you decided to have your genome sequenced. And that was really part of the research for this book because you knew you'd be writing this book. Had you braced yourself for the possibility of bad news, that you would find out that you had a gene that showed you would be more inclined to have, say, early-onset Alzheimer's or an inherited illness?
ZIMMER: I was definitely concerned. My father's parents both died pretty young. And in both those cases, they were diseases - you know, heart disease in one case and cancer in another. And so I thought, oh, boy, like I could very well have inherited whatever genes that put them at risk. And, you know, my father is Ashkenazi Jewish background. And so, you know, I immediately started thinking about this gene that people may have heard of called BRCA1, which is a gene that, if it's mutated, can really raise your risk of breast cancer. I have two daughters. And so that got me very anxious as well.
So, yeah, I would say that it was a very nerve-wracking experience going into it. You know, I think we all like think back to, you know, our relatives who got sick and then wonder, well, you know, is that in me. I mean, I have someone else in my family who had an intellectual disability. And I thought, well, is that inherited? I mean, I just - you just keep thinking about these issues. And, you know, I wasn't actually going to write about my genome if something turned up. And, you know, I was going to personally have to deal with a serious medical condition or, you know, have to talk with my daughters about it. I mean, I wouldn't want to sort of, you know, kind of air their genetic laundry, as it were.
But, you know, I have lots of genes that slightly increase my risk of some things and decrease my risk of other things - just, you know, nudging the needle a little bit. And that's pretty typical. You know, it's only a pretty small fraction of people who will get their genome sequenced and discover there's something really serious that they have to attend to. And that could be a lot of people. I think there could be a lot of value to people having their genome sequenced in general. But I think any one person if they really have their fingers crossed that they're going to find some weird exotic mutation may be disappointed. And that's a good thing.
GROSS: Carl Zimmer, a pleasure to talk with you again. Thank you so much.
ZIMMER: Thank you. It's been great.
GROSS: Carl Zimmer is the author of the new book "She Has Her Mother's Laugh: The Powers, Perversions, And Potential Of Heredity."
Are you looking for good mysteries to read this summer? Our book critic Maureen Corrigan will have a couple of suggestions after a break. This is FRESH AIR.
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TERRY GROSS, HOST:
This is FRESH AIR. For our book critic Maureen Corrigan, suspense and summer go together like gin and tonic. Here's her review of two very different kinds of mystery novels - one that's been out for a while, the other brand-new, both featuring memorable female heroines.
MAUREEN CORRIGAN, BYLINE: Summer offers some breathing room for me to catch up on good books I've missed - as well as to ferret out promising new arrivals. And in the more relaxed days of summer, my hands reflexively reach out for a mystery. My first pick after Memorial Day was "The Dime" by Kathleen Kent, which was one of the nominees for this year's Edgar Award for best mystery. I've been curious about this novel because Kent's heroine, Brooklyn-born police detective Betty Rhyzyk, is gay. And there's been a dearth of queer detectives in mainstream mystery fiction over the last decade or so. If Kent decides to write more novels starring Betty Rhyzyk, it will be a boost both for the genre and for the cause of diversifying the detectives who walk down the mean streets of hard-boiled fiction.
"The Dime" opens in Dallas, Texas, where Betty has reluctantly relocated because her partner, a radiologist named Jackie, needed to be closer to her ailing and homophobic mother. The family friction, along with the routine razzing that Betty faces from male colleagues on the force, is simply part of the daily nastiness of her world - along with an escalating drug cartel war. Kent doesn't overplay the social commentary. Instead, she shows how Betty has to navigate situations differently - how, for instance, she feels pressure to always be ready with a cheeky comeback to the taunts to safeguard her standing and restore the karmic balance in the station house.
What really makes "The Dime" special is not just the fact that it features a lesbian detective. Rather, it's the fact that it shoves its lesbian detective into one of the most breathless, inventive and - be forewarned - violent suspense plots I've read in a long time. Halfway through, "The Dime" accelerates into warp speed, and Betty has to draw on all her Brooklyn, Polish, tough-girl moxie to fight her way out of an imprisonment that would have made Harry Houdini hang his head in defeat. I don't want to ruin things by talking any more about the plot, but I'll just say that the opening epigraph of "The Dime" should reassure anxious readers. It's identified as a Chinese proverb that says a patient woman can roast an ox with a lantern.
If "The Dime" caught my attention because of its progressive heroine, Ruth Ware's just-published mystery, "The Death Of Mrs. Westaway," genuinely knocked me out by its flawless, faithful adherence to tradition. This is a suspense tale so old-fashioned I'm hard-pressed to recall even one element that doesn't derive straight from the it-was-a-dark-and-stormy-night playbook. Among other Gothic delights, there's a crumbling mansion, a disputed inheritance, an orphaned heroine and a grim housekeeper whose signature supper dish is gristle stew.
"The Death Of Mrs. Westaway" is a perfectly executed mystery very much in the mode of Daphne du Maurier's "Rebecca." Somehow Ware takes all these tarnished suspense tropes, gives them a brisk working-over with a polishing cloth and recovers the ageless beauty of the tried and true. The novel opens on - well, on a dark and stormy night as a lone young woman scurries her way homeward along a deserted seaside promenade.
Harriet Hal Westaway is 21 years old. She never knew her father's identity. Ever since the hit-and-run death of her mother three years ago, Hal has been eking out a living reading tarot cards in a seedy resort town on the English Channel. When she arrives home to her chilly flat, Hal surveys the bills that have come in that day's mail. Two letters stand out in the pile. One is a threat from a loan shark she naively borrowed money from months ago. The other is a missive from a solicitor's firm in Cornwall informing her of the death of her maternal grandmother and summoning Hal to a reading of the will. The tantalizing phrase substantial size of the estate catches Hal's eye.
The only catch is Hal knows that her mother's mother died decades ago. The lawyer must have confused her with another Harriet Westaway. Hal is a person of integrity, but she's also desperate. That loan shark has a reputation for cutting deadbeats like her to ribbons. Mulling over her options, Hal resolves to travel to Cornwall and use the cold-reading skills she's developed to suss out personal details about her tarot card clients to pass herself off as the missing Westaway granddaughter. When she arrives at the family mansion, she's shown to an attic bedroom whose small window features iron bars and the words help me scratched into the glass.
"The Death Of Mrs. Westaway" is superb. In addition to its brooding atmosphere and labyrinthine mistaken-identity plot, this novel also gives us a heroine of real depth in Hal. As Ware vividly depicts, Hal is hemmed in by her poverty as much as she is by the iron bars of her bedroom. I predict that lovers of first-class suspense will want to shut out the sunny delights of summer, burrow into one or both of these very different books and read until the stunning endgames here are played out.
GROSS: Maureen Corrigan teaches literature at Georgetown University. She reviewed "The Dime" by Kathleen Kent and "The Death Of Mrs. Westaway" by Ruth Ware. Tomorrow on FRESH AIR, my guest will be Paul Schrader, the writer and director of the new film "First Reformed," and its star, Ethan Hawke, who plays a minister in a spiritual crisis.
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ETHAN HAWKE: (As Ernst Toller) Hope and despair. A life without despair is a life without hope. Holding these two ideas in our head is life itself.
GROSS: "First Reformed" has echoes of Schrader's early film "Taxi Driver." I hope you'll join us.
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GROSS: Fresh Air's executive producer is Danny Miller. Our technical director and engineer is Audrey Bentham. Our associate producer for digital media is Molly Seavy-Nesper. Roberta Shorrock directs the show. And I'm grateful to Dave Davies for hosting last week while I took the week off. I'm Terry Gross.
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