How many new mutations from Mum and Dad?

30 October 2019
Presented by Chris Smith.

GENETIC RELATEDNESS

How many new mutations did our parents hand on to us?

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This month, join Chris Smith to hear how sleep deprivation sends your endocannabinoids skyrocketing and triggers a tendency to binge, how many new genetic mutations you inherit from your parents, the gene for behaviour that turned out to be nothing of the sort, what good and bad learners have in common with youTube influencers, and from online collective whinge to paper in eLife: the careers of newly appointed PIs.

In this episode

Feet of a sleeping person in bed

00:37 - Endocannabinoids cause post sleep-dep binge

Why tasty treats are more tricky to resist after a sleepless night...

Endocannabinoids cause post sleep-dep binge
Surabhi Bhutani, San Diego State University

It sounds counter-intuitive, but an extra hour or two asleep in bed can help to reduce the risk of becoming obese. Less sleep, on the other hand, seems to be a potent stimulus to over-eat, and especially to binge on high-calorie, fatty and sugary treats. But why is this? As she explains to Chris Smith, Surabhi Bhutani, from San Diego State University, has discovered that sleep deprivation leads to a surge in the body’s own cannabis-like endocannabinoid chemicals. These, she’s found, cause a region of the brain called the insula to slacken it’s inhibitory grip on the brain’s olfactory areas, making delicious treats smell too tempting to resist…

Surabhi Bhutani - There is a huge body of research that suggests that chronic lack of sleep is associated with overall poor health and there is a bunch of data showing that when you do not get enough sleep you increase your food intake, and people become more reactive to unhealthy foods and foods in particular that are high in sugar and fat that we call junk food. What we really wanted to understand was why people crave these high fat foods after a sleepless night.

Chris Smith - Back in the past, when people first began to flush out this association between not getting enough sleep and then rebound overeating, one speculation was that the hunger hormone “ghrelin” - which is produced by the stomach and is suppressed by sleep - that goes up. So there's just a rebound overeating to compensate. So is it as simple as that?

Surabhi Bhutani - It's more complicated than just hunger hormones increasing, because there are a lot of studies showing that people may not really physically feel hungry, but they still go for all those foods that are high in calories. So there has to be a different mechanism where, basically, it connects your sleep loss with consumption of very high calorie foods; so your brain, or your body, saying that I really want a doughnut, or I really want potato chips!

Chris Smith - So you're saying that there's a switch in terms of food choices but it's not necessarily just driven by overall increase in hunger?

Surabhi Bhutani - Exactly.

Chris Smith - And what do you think underpins that then?

Surabhi Bhutani - We definitely think that there are some brain signals that may be playing a role in overeating of not-so-healthy foods, and past research primarily has shown that sleep deprivation increases certain endocannabinoids. So these endocannabinoids are basically these naturally produced neurotransmitters that bind to some of the receptors in the brain and affect feeding behaviour. So they're very similar to cannabis-like compounds that can cause cannabis-related munchies. On the other hand, we also kind of know that sense of smell is also really tightly related to how we choose food items and, in particular, animal studies have shown that these endocannabinoids enhance food intake by increasing the activity of brain areas that process odours. So what we thought was that, maybe we can put all of this together and ask if what people choose to eat when they are sleep deprived is related to how the brain responds to food smells.

Chris Smith - Where in the pathway would you see this effect manifest then? Would it be at the receptor level - how sensitive the receptors are to the molecules that make foods smell and taste the way it does? Would it be in the olfactory bulb where the first processing occurs? Or would it be a cortical level, where the olfactory tracts go into the brain and start depositing signals relative to what they think they're smelling?

Surabhi Bhutani - That's a very interesting question, because it's very difficult to tell exactly where the processes are happening. So, you mentioned olfactory bulb: you really can’t image olfactory bulb in humans. But what we found in our study was that, when people were sleep deprived so they only slept for four hours, the following day when we scanned their brains inside an MRI scanner and made them smell these delicious food odours and also some of the non-food odours, the piriform cortex - the region of the brain where smells are processed - in that particular region the patterns of food versus non-food odours were significantly different in the sleep deprived state. So what this means in simple terms is the smell processing region in the brain goes into this “hyperdrive” - it sharpens the food odours for the brain so it can better differentiate between food and non-food odours.

Chris Smith - And how do you tie that to changes in the end0cannabinoid system, these natural brain chemicals that mimic cannabis?

Surabhi Bhutani - The piriform cortex also sends signals or information out to other brain regions, in particular insula cortex. So insula receives signals that are important for food intake, and when a person is sleep-deprived, signaling between the piriform cortex - the smell processing region - and the insula, that connection was not as strong. So the signaling actually reduced. And we also found that, because of this reduction in communication, people ended up eating more energy-dense food. Now, how is it connected to the endocannabinoids, or the neurotransmitters? When we did the blood analysis, we saw that people had certain components of this endocannabinoid system very high in the blood. And those people also consumed very high energy-density food. So, putting all this together, our results suggest that the sleep deprivation really influences this endocannabinoid system, which in turn alters this connection between piriform cortex and insula cortex and, ultimately, leads to a shift towards foods which are high in calories.

Chris Smith - What would happen if you did this experiment then in an anosmic individual, or people with, say, Kalman syndrome who can’t smell things, or people who've had head injuries and the nose doesn't work properly; are they immune to the appetite-boosting effects of sleep deprivation?

Surabhi Bhutani - That is a very interesting question. So, interestingly, there aren't really any studies done in this area with anosmic individuals, so there is no research out there showing that sleep deprivation can really affect those people who can't really smell. So it'll be interesting to do those kinds of research in future and kind of see whether they are more protected towards these effects of overeating or sleep related overeating or not.

How many new mutations did our parents hand on to us?

07:11 - How many mutations do parents pass on?

What's the rate at which new genetic changes emerge in sperms and eggs?

How many mutations do parents pass on?
Thomas Sasani, The University of Utah

Every one of us got half of our genetic information from each of our parents. But how many new mutations did Mum, or Dad, hand on to us? And if Mum and Dad had waited a few more years before they had us, how much difference would that have made? Now, thanks to a remarkable study looking at whole families conceived over significant periods of time, we know. Thomas Sasani is at the University of Utah…

Thomas - Every generation, we receive half of our DNA from each of our parents. But what we're really interested in figuring out is how many sorts of new mutations are present in the DNA that we inherit. Essentially, how many “spelling errors” are there in the genetic code that we receive from our parents?

Chris - Did we not know that already?

Thomas - So the actual estimated number - this sort of number of spelling errors - was actually pretty well appreciated, and it's been estimated at a number of times before. But what's less well appreciated is how all sorts of different other factors, like the age of your parents when you're born, actually affects that number.

Chris - Because we often say “have your children when you're young, because A you're more fertile and B the risk of having things like chromosomal abnormalities increases with parental age”. So, is that true then?

Thomas - Yes that's absolutely true. In this study actually we were a little bit less interested in sort of the large chromosomal changes - things like the aneuploidy that you mentioned - and more interested in sort of individual spelling errors. So single letter changes in the DNA that you inherit from your parents a “T” instead of a “C”...

Chris - Did you have to therefore go and laboriously read the genetic code of loads and loads of individuals to work out how different they are from each parent?

Thomas - Essentially yeah, that's exactly what we did. In practice, what this amounts to is you sequence the entire genome of both parents, and you sequence the genomes of all of their children, and then you sort of go child by child and compare their genome sequence to the sequence of both of their parents and you just look for the places in the genome where they're different; where even though you would expect that child to share half of their DNA with each parent, at a small number of sites they'll actually have unique mutations that neither of their parents had.

Chris - And have you done the experiment where you could, for instance, take a family and the parents who are obviously correspondingly younger when they have one child, and older when they have subsequent children, and then you could compare how many changes there are all in each of the subsequent children and therefore relate that to parental age?

Thomas - Yes that's exactly right. And really one of the fantastic things about the dataset that we were working with, normally when studies like this are done you use two parents and maybe one or two children. But in this study we had some families that had up to 16 children. And so those children represent - as you were saying - parents when they were, say, 20 years old all the way up to when they were maybe 40 years old. And so we are able to compare the number of new mutations we see in children born to young parents and children born to that same set of parents, but when they were much older.

Chris - What trends emerged?

Thomas - So, overall, on average the number of these new mutations that you see in kids definitely increases as parents get older. So it amounts to about one and a half new mutations every year dads get older, and about point five additional mutations every year mum gets older.

Chris - That's quite a lot isn't it? And interesting that there's that disparity between the sexes. Does that reflect the fact that sperm are made as a continuous process from ongoing divisions in stem cells, whereas eggs get made when actually the individual is themselves developing from an egg and therefore the chances of the DNA in the egg becoming mutated is lower?

Thomas - Yeah. That's a really great question and I think for a long time that's really been the sense in the field is that every year after puberty, sperm cells - or the stem cells that will eventually develop into sperm cells - they're constantly dividing and the idea is that every time you have to copy your genome there's a chance for an error to occur. Now it turns out that there's a hypothesis that the constant sperm cell divisions are not the only reason that there's this kind of bias of de novo mutations in fathers, and that there may be things like accumulating DNA damage and other causes. But, certainly, the increased number of divisions in the sperm cells are probably contributing a little bit to that bias that we see in dads.

Chris - When you say a little bit, do you have a feeling for when most of these mutations are acquired? Because one other possibility, surely, is that not just the sperm and the eggs contributing, but if the embryo itself is not faithfully copying DNA, maybe quite a big amount of that mutation burden could occur after fertilisation has occurred?

Thomas - Yeah that's a great point. We actually were able to get a sense of this in our paper, largely owing to the fact that we had a lot of these large and three generation families. So we were able to apply a strategy whereby we were able to figure out essentially if these new mutations had occurred after the sperm and the egg came together to produce an embryo, or if they happened before. And we actually found that about 10 percent of all of these new mutations that we saw were likely occurring in that embryo.

Chris - And was that itself influenced by the age of the sperm and the egg? So were older parents more likely to have highly mutating embryos, or was the mutation rate in the embryo at about 10 percent regardless of parental age?

Thomas - Yes. So in the embryo at least, we didn't see that the number of new mutations was really affected by the age of the parents. However, overall, the mothers and fathers in our study were generally under the age of 40 or 50. And it's possible that there may be an affected age in much much older parents, but we really weren't able to detect that, at least in our dataset.

Chris - So although you can say that, with increasing parental age, there does appear to be a higher mutation burden being handed on to kids, but, presumably, one constraint to this study is you can't say at the moment whether or not that's going to have a clinical impact?

Thomas - Yeah that's right. So if you think about the number of mutations that we're seeing - 70 new mutations on average in a child - and the number of new mutations might increase by one point five or point five per year depending on the parent you're looking at. But again this is out of - you know - 3 billion or 6 billion total letters in the human genome. And so, in practice, not very many of these mutations are actually landing in genes - regions of the genome - that actually make functional protein. And so at least at this point it's it's tough to say how frequently we'd expect these to be damaging, or cause disease, but certainly there are a number of rare genetic diseases caused by these kinds of mutations. And so having a good handle on how frequently they occur is I think important in its own right.

Yellow gene mutant drosophila

14:10 - Gene for behaviour turns out not to be

Flies with the “yellow” gene aren’t very lucky in love, and it's not down to behaviour...

Gene for behaviour turns out not to be
Jonathan Massey, Harvard University

And now to a genetic mystery that’s taken a hundred years to solve: scientists have finally discovered why flies with the “yellow” gene aren’t very lucky in love. And it’s not, as the first geneticists thought, anything to do with behaviour. From Harvard, and speaking with Chris Smith, Jonathan Massey...

Jonathan - In the early 20th Century, in Thomas Hunt Morgan's fly lab, he was one of the first geneticists to ever work with fruit flies. He started collecting the first mutants in the lab and the reason why he was able to find them is because they had these pigmentation malformations in the bodies of the flies. So when he would dump his fruit flies out of his bottle into the microscope he noticed about one in several thousand when it have the right colour eyes or when it have the right coloured body. One of the first mutants was a yellow coloured fly that he discovered and so he took this yellow fly bred them together with other yellow flies and he found out they bred true which just means that that yellow colour was heritable. And so that became what is known as the yellow mutant fly.

Chris - And did he work out roughly how many genes it's, a single gene isn't it the influences that were involved because those breeding experiments mapped onto the numbers that Mendel had produced in his pea plant. So we know when you've got one single gene influencing a factor you get a certain proportion of different characteristics in the first generation, second generation zone and so on.

Jonathan - That's right. So that's a good question. His undergrad student at the time, Alfred Sturtevant, in 1915 or so created the first genetic map ever. So Alfred Sturtevant, through genetic crosses, discovered that genes are inherited on chromosomes and chromosomes are linear pieces of genetic material. And so, through genetic crosses just like Gregor Mendel did with his pea plants, they were able to discover not only that yellow was a single gene but that yellow was a gene that was linked to the 'X' chromosome, which is inherited from mothers just like in humans and flies.

Chris - Were they intrigued by the fact that these were pretty rare these flies, so the fact that this gene was mutated and these mutants were cropping up but then they didn't get an increase in numbers of them argued that there was something wrong with yellow flies. Were they intrigued by that?

Jonathan - Yes so Alfred Sturtevant had many broad interests. He wanted to understand the basics of genetics; how chromosomes work; how they're inherited, but he also was really interested in speciation and biodiversity. He noticed it was difficult to maintain these flies, and he wanted to understand why. And so he did a very basic experiment: he took the yellow mutant males and he put them in a chamber with normal female flies and he noticed that, while they courted the females like normal flies do, they very rarely were able to actually mate with them successfully. So he wrote a little paper in 1919 describing this result, and it wasn't until the 1950s that it was picked up again.

Chris - And what did people conclude when they revisited the work? What was their conclusion as to why these flies were not maintained in the population?

Jonathan - Yeah it's a fascinating history. Margaret Bastock a behavioural biologist in Nikolaas Tinbergen's lab in the 1950s she concluded after Alfred Sturtevant's work that, indeed, the flies courted normally but they didn't mate, just like Sturtevant described. Her conclusion from a beautiful study using a tape recorder to describe the behaviour of the fly over time was that, although they courted like normal flies, they did not do so in such an excited way.

Chris - Did people think then that this gene was in some way affecting the nervous system of the animals? Because pigmentation is intrinsically tied up with other chemicals that are also employed as neurochemicals - I'm thinking of dopamine, for example, which is made from the same precursor tyrosine that you can turn into a range of different things. Did they think that the colouration was a side effect of different neurochemistry, and that's why the behaviour was wrong and that's why they weren't mating very much?

Jonathan - So in the 1950s they didn't know what yellow did as a protein and - believe it or not - in 2019 we still don't know what the yellow protein does. But it wasn't until the 1980s and the 1990s that part of that biochemical work was worked out, and, as a consequence of that, like you suggest for the most part geneticists concluded that - well - the reason yellow mutant flies have abnormal behaviour is because they have low or abnormal dopamine levels in their brains.

Chris - And is that true? How have you gone about testing that because obviously you've visited this and said right let's take a modern look at this quite old problem?

Jonathan - Exactly. So, in 2016, an undergraduate Diane Chung and I decided to team up to try to solve the problem. And I, like geneticists for the last 30 years, also believed the problem dwelled with dopamine. And the way we went about asking the question is to selectively remove the yellow gene from the brain of the fly and ask what happens to their behaviour. And what we've found is the flies behaved completely normally. Not only did they court normally, but they mated normally, so they didn't behave like the yellow mutants do. From that study, we were able to conclude that, really, its function outside the nervous system is what's important for behaviour.

Chris - So what is it then?

Jonathan - We know that yellow is required to make black pigments or black melanin in the fly. That's why, when you remove the function of yellow, the fly turns yellow. What we discovered is that, specifically, yellow function in making black pigments in these structures on their legs that are called "sex combs" is required for a fly's ability to mate. So, when you remove yellow protein from these very tiny structures on the front legs of the males, the males lose the ability to grab the females and that's what disrupts their ability to mount and finish the mating sequence.

Chris - How did the earlier workers miss that?

Jonathan - It wasn't until about 15 years ago that geneticists developed tools in flies to be able to answer these targeted questions. They didn't have the ability to remove the function of the allergen in different tissues of the fly. The other thing that was critical for this project is we used a high speed video camera that slowed down the mating sequence to 1000 frames per second, so you could see all of the really fascinating details of how the fly is moving. And it was at that point we decided this is likely what's wrong. We noticed that, though they were courting fine, that last sequence, in which they tried to grab the female, seemed disrupted and that's what pointed us towards the sex comb hypothesis.

Birds learn best when presented with a song tuned to their abilities

20:60 - Are there good learners and bad learners?

A study on birds confirms that the way in which information is presented is key to effective education...

Are there good learners and bad learners?
David Mets, University of California San Francisco

Some people are better learners than others. Or so we thought. Actually, it turns out that there might just be a disparity between the way they learn best and the way the information is being presented. Speaking with Chris Smith, UCSF’s David Mets explains what he's been finding with his songbirds…

David - Some people learn better, and others learn worse. And there's some evidence that some of that is genetically-driven. But we know that some of that can be environmentally driven. So one question is, can we provide a better environment for some genetic makeups to increase learning outcomes.

Chris - In other words, if I'm a genetic poor learner, can you nonetheless compensate by changing the environment to one to which I am better adapted to learn in?

David - That's right and, additionally, you might not be genetically a poor learner you just prefer to learn with a specific type of presentation, and so you might seem poor because the stimulus isn't presented in a way that is tuned to your preferences. But, if you tune it more accurately, you're actually quite a good learner.

Chris - And how have you been looking into this?

David - The system where we study this is in songbirds, and they learn their vocalisations in a process very similar to how humans learn speech. They listen to their dad early in life and then they go on to practice, practice, practice and, ultimately, produce a very complex vocalisation. And this is a powerful system, because we can vary the environmental parameters and we also can vary the genetics, so we can ask very specific questions about Is this the right environment for this individual based on their genetic makeup, or is it the wrong environment.

Chris - How did you actually do that then? How did you vary the genetics and vary the environmental parameters in order to test that and tease apart the two?

David - So in this particular population of finches where we work we know that some individuals are biased genetically to sing faster and some are biased to sing slower. We can go in and take individuals we know to be genetically biased to sing faster and we can take some individuals and present them with a tutor song that is similarly fast, or a tutor song that is at sort of an average rate, or at a very slow rate. And then we can see how well they learn in those three different environments. And we can do that for fast learners, medium learners, and also slow learners.

Chris - So this is a bit like I go to a lecture at medical school and some lecturers teach with overheads, some teach with PowerPoint, and some are in the dark ages with talk and chalk, and it suits some of the class better than others. And so you're varying the different teaching styles. But how about the genetics, because you mentioned you can also mix that up?

David - Yeah. So in this case we basically took a population that is a genetically heterogeneous population, so there's lots of different individuals with a different genetic makeup, and we can measure how that genetic bias works. So, basically, we take individuals from all different genetic backgrounds and we provide them with one tutor song and we see what they end up being biased to sing. Basically we have a fixed environment and we see if they behave as their father behaved, and so we can then estimate whether that bird is biased to sing fast or slow based on their genetics.

Chris - And then the obvious question you're going to be asking is "right, okay, a bird that doesn't learn well in one setting, if we vary the conditions, it might be a slow learner in one setting but then we switch modality and it learns much better?"

David - Yes that's right. One possibility is that you see better and worse learning and the best stimulus will be the average song. So we provide everybody with an average song and some individuals appear to be poor learners, some individuals appear to be good learners. The birds who in that context appear to be poor learners we take those guys and we say oh what's their genetic bias, or these guys were all genetically biased to sing slowly, and so we'll provide them with a slow stimulus and we'll see what happens. And for all of the birds, for slow birds members and fast birds, providing a stimulus matched to their genetics increased their learning and, in many cases, it increased it to the point of being essentially equivalent across the different genetic backgrounds.

Chris - So it really is horses for courses when it comes to learning isn't it! Why do you think this relationship exists?

David - I think that this relationship exists mostly because there is genetic diversity. Individuals are different and their brains are built in different ways and they're more adept at thinking about things in this dimension or that dimension. To some degree, that's determined genetically, but the mind has such capacity for adaptation and plasticity and taking in information that, really, these genetic influences are tamped by that ability. But, tuning it a little bit to be slightly more appropriate results in better learning, and so I think it really is just a product of having - you know - organisms that are to some degree influenced by their genetic structure and then also an incredibly adaptive neural system that that helps them learn.

Chris - The parallels with humans - now you talk about it, and as I come to think about it - are really potentially very striking aren't they? When you think "how does advertising work? What's the best way to teach children in a classroom? Are influencers on YouTube influential because of whom they're talking to and the way they're doing it?"

David - Yes, it's an excellent question. We focus in the paper on the case of trying to adapt learning stimuli to individuals to increase outcomes, and we have been actually quite slow at applying that kind of idea in in educational settings, but Google and YouTube and Facebook and so on are extremely good at figuring out our individual proclivities, and providing you with an ad that matches you perfectly; matches your biases and shifts you even further in a specific direction...

A show of raised hands

26:59 - Life as a scientific group leader

How do UK universities treat their early-career group leaders?

Life as a scientific group leader
Sophie Acton, UCL

In the words of co-author Sophie Acton, who took Chris Smith through what happened, it began as an online whinge on Twitter. But, as responses poured in, it rapidly transformed into a valuable, publishable dataset that’s now a paper in eLife, and documents the - frankly mixed - experiences of early-career lab group leaders...

Sophie - Well, in the end, it was more than we expected: it was about 385 people responded, primarily people who work in the life sciences. We have all started independent research labs at various universities in the last five years and we collected this data mostly through advertising via Twitter. We are all our generation of researchers we're very active in social media. We're trying to get our voices and our research heard and the word just spread. It just took off so everybody responded to a survey that we'd put together and added their comments when we saw the data. We really should publish this.

Chris - And what was it you were seeking to probe mostly?

Sophie - Mostly I think just unfairness that these are a bunch of really bright people, they've been very successful in their training to that point. They have great ideas. They've been given grant funding and we just want everybody to have equal opportunities to make the most of that. And some people were reporting that they were really being stuck, they were having trouble with getting lab space, they were having trouble recruiting people. They were being swamped with teaching load - all these various issues - and other people were swimming through and having a great time. But we are we were all starting at the same level, and we wanted everybody to have the opportunity to show what they could do.

Chris - And when you began to unpack and decode the data you had collected what messages emerged. I mean what did you find from this?

Sophie - The one very surprising issue that we found was a gender disparity that I genuinely did not expect. And that came through in starting salaries. It came through in the research group size of people recruiting. It came through in teaching load, it came through in administration, working in committees and they're very small differences, but I can imagine that these may compound over the years and if you're starting off unequal that's something we should really take notice of and fix.

Chris - Does seem rather strange doesn't it? Because, you know, when we hire people, for instance in the medical job I do, I was doing some interviews this week. It's not the individual that attracts a salary, it is the role that they're going to do. You hire a person and they earn whatever that role is specified to earn; and I thought that academic salaries were the same...

Sophie - I thought so too! And certainly the way I was recruited it wasn't really given as an option. There was no negotiation of salary; I was told that, if you join this department in this role, you bring that funding. This is your starting salary. But, I presume there must be a little bit of wiggle-room in certain situations where people are asking for just a couple more increment points on a scale here and there. That's being awarded and that those little negotiations tend to be done by the male applicants.

Chris - I'll read you one of the quotes that you put from one of your respondents in the survey because it really it made me laugh - for the right reason - but also made me think and this person says "I feel like I'm trying to do three separate jobs research, management, admin, teaching" - there's a slash between management and admin which is why she says three - "as well as be a mother; to be my own postdoc because I can't afford one; to be a lab technician, because I can't afford one; to be the lab manager, because I can't afford one; to be a good mentor for my PhD students" etc.. The point that's being made here is that this is a very stressful position because all the time prior to this in a scientific career a person is largely having their life sorted out for them on their university we get spoon fed, as a PhD student we're often handed a project and guided through it; as a postdoc we're part of a moving train; and, suddenly, you have to stand on your own two feet and - it sounds to me - from this that so many of your respondents are feeling that they could be better directed, or better supported, in the in the early ramp up to get their careers airborne?

Sophie - Absolutely that! The people who responded who were happy in their positions, stressful as it may be, were the ones that had mentorship; that had supportive heads of department; who were eased into these various roles gradually when they have no experience of management, teaching, all of those things they can come gradually with the right preparation or people have been on training courses and leadership courses. But there are others in that cohort who were just thrown into all of these things at once. So get grant money hire students set up your lab be on these committees teach this many hours a week and that's so different from the training that they'd received to that point we all had. We focus on one research project as a postdoc, we focused purely on the site and getting out something new. And then as soon as you're managing a group even if it's a group of two or three people there's all these other roles that we're just not adequately trained for.

Chris - So it could really use a bit of input on that front?

Sophie - I think there's some really simple interventions that would just level the playing field for everybody.

Chris - It looks like also from your survey that the universities across the country - and these are Russell Group universities heavily represented in your data, so these are some of the foremost institutions in the world let alone in the UK - they're trying to have their cake and eat it here aren't they? Because some of the people who've responded to your survey are really high flyers. They've brought in enormous amounts of grant money, but they've been given a soft contract and they're being handed some cases enormous teaching burdens, more than people who are full time teachers at universities!

Sophie - I know I don't know how that can be possible but it is happening. We do have individuals in our cohort that report that they have got a full teaching load and they may have brought in multi-million pound research grants and they just feel like their hands are tied and they cannot do it all. And people going to these very prestigious institutions should be treated like they are those high flyers and mentored into being the next generation of amazing scientists not burdened with everything in and set up for failure.

Chris - Helpfully, at the end of your paper, you've got this survival guide - what amounts to a survival guide - for PIs. This is advice from you collectively as a group who've made it, but also from the survey data isn't it. What would be your top few tips for people who may be listening to this and they're about to start a group or they're about to embark on this particular career track?

Sophie - Yes and they have been our main audience; I have to say the number of people who've said this transparency has been amazing. The most important point I think that we raise here are to have as much transparency as you can when you're negotiating. There may not be very much to negotiate, but get in writing the things that you need. Get your head of department to really adhere to those things in writing before you start. You may also take from the datasets what the starting salary should be, or the average starting salaries are. So, if you feel like you're on the lower levels of those, you can now take these datasets, show them that - it's published - and say why are you suggesting that I'm on this grade when actually I know a lot of people on the same funding that I'm bringing in are recruited as a senior lecturer level and vice versa. So you can have those conversations when you're applying a little bit more with a bit more backing I suppose.

Chris - So play a little bit "harder to get" from the get-go would appear to be the moral of that story! Sophie Acton there she is an immunologist at UCL. 

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