A personal overview of the Science is Vital “R&D to 0.8%” campaign


by Paula Salgado

Science is Vital is a grass roots campaign of UK scientists and supporters of science who believe that a strong science base is vital to the UK’s economy and reputation. It launched its latest initiative to persuade the Government to increase investment in research and  development (R&D) in the 2015-16 budget, details of which will be announced on June 26. ICaMB’s blog own Paula Salgado, member of the Science is Vital Executive Committee, recalls the earlier campaigns and explains all about the current petition and ongoing survey.


It all started in September 2010, when a speech by the then recently appointed BIS secretary, Vince Cable, and rumours from the Government suggested major cuts – up to 25-35% – could hit the science budget. That led Jenny Rohn to a call for action and many scientists and non-scientists responded.

I am happy and proud to say I was of the initial wave of supporters. In only a few hours, there’s a Facebook page, in next couple of days the domain was registered and a  page created: the Science is Vital campaign was born. From the first moment, there was a clear intent to make this campaign about a key point: cutting science funding is not good for the economy. For me, having taken part in many demonstrations and campaigns as a student back in Portugal, this was a crucial point that made believe this was a campaign with a difference.

Delivering Science is Vital petition with ~33K signatures to N.10 (Photo by Joe Dunckley)


A petition gathered over 33,000 signatures in roughly 6 weeks, including many notable scientists and public figures, as well as the support of many learned societies, patient organisations and other NGO groups.



Lobbying Parliament to protect Science Funding (2010)


The campaign also included letters to MPs and a parliamentary lobby session, where we had an opportunity to directly address the issues with our representatives.



Finally, the campaign culminated with a rally in front of the Treasury:

Scientists in white lab coats and many non-scientist supporters at the rally in October 2010

Stewarding at the rally

I was there, helping as a steward (still not sure how that happened!) and seeing a constant stream of white coats and many non-scientist supporters streaming from the tube station was a very memorable sight. I even met a Portuguese colleague that had also been in many of those demonstrations back home and we couldn’t help comparing the situations and behaviours.

The result: cash-freeze

Despite the massive support gathered in such a short period of time, many of those involved, including me, were still unsure of how successful we could be at avoiding cuts… When the announcements were made and it was revealed that the science budget would be frozen for the next 4 years, we felt relieved, happy. I must admit I was also surprised: this was the first campaign I had taken part that was somewhat successful!

However, this was clearly a bitter-sweet victory: we were protected from deep cuts, but a cash-freeze means at least a 10% reduction in real terms due to inflation alone and cuts of up to 50% in capital spending and in many departments R&D budgets meant this was not great news for science in the UK in the long term.

Inspired by this result, SiV has continued to campaign, focusing on issues such as Science Careers and I continued to volunteer and help when I could. Last summer, at the First AGM, I was elected to become a member of the Executive Committee and have therefore become more involved in all aspects of the campaign.

Reverse the decline in science funding – R&D to 0.8% campaign

Despite the welcomed injections of capital by the Government, that somewhat minimised the effects for specific areas, the effects of the cash-freeze and other cuts are already being felt. A recent study by CaSE (Campaign for Science and Engineering) clearly shows that, at the end of the spending review period (2014-15), there will still be a significant shortfall in science funding in real terms, estimated to be around .

This reduction is already having its effects in the research community and it must be reversed if the UK is to remain at the the forefront of scientific research.

Why a new campaign now?

As you might have heard, the Government is currently discussing a budget review for 2015-16, the results of which will be announced on June 26. There are many indicators of further cuts to announced so there is cause for concern. Despite reassurances from Vince Cable that science funding will be protected, we understand that the Treasury favours a continuation of the cash-freeze. This will continue the current decline and will send dangerous signals against long-term public investment in science.

Bringing in the big names

Our first question was: how can we raise awareness of this renewed threat to science funding and make sure there will be a public discussion on the issue? Getting renowned scientists in the UK to get involved was an obvious choice, and we spent a couple of weeks contacting them. At one point, I remember making the wild suggestion of cold emailing Prof Stephen Hawking, which other committee members thought was a good idea – I can’t tell you how surprised and delighted I when I got an email back, fully supporting the campaign!

So the campaign was launched with a letter in the Daily Telegraph signed by more than 50 prominent scientists in the UK, including Stephen Hawking, Martin Rees, Brian Cox, Paul Nurse and ICaMB’s own Jeff Errington.

We are asking the Government to show a clear long-term commitment to science in UK and set a target to increase public investment in R&D to 0.8% GDP – the G8 average – so we will regain our leading position and compete more effectively with the leading economies of the world.

Public spending in R&D as a percentage of GDP (via scienceogram.org)

Science funding in UK needs your help

Now, it’s your turn to help and support us.

We want to prepare a report, detailing the effects of the current cash-freeze is already having in the research community and alerting the Government for the dangers in pursuing the current policy of managed declined. For that, we need data. So please take our survey and tell us what you think.

We have prepared a public petition and ask you all to sign it. Importantly, we need to spread the word. As in 2010, we have used social media networks to tell people about the campaign. So please, sign it and tell everyone you know.

Also, you can write to your MP to get them involved in the discussion.

Science in UK needs you now. We only have a few weeks to get this important message across: Science is Vital for the UK.


A scientific note:


60 years ago today,  a ground breaking discovery was printed in Nature:

James Watson and Francis Crick published their proposed DNA structure, based on X-ray data collected by Rosalind Franklin, then working with Maurice Wilkins. There is hardly a need to explain the immense impact this paper had in science, medicine and our views of the world.

The fact that this was carried out in UK labs, with public funding, is one of the many examples of excellence in UK science.


We can not let this leading position be eroded, so what better way to celebrate it than join a campaign to help reverse science funding?


Science is Vital http://scienceisvital.org.uk/
R&D 0.8% campaign http://scienceisvital.org.uk/latest/
CaSE http://sciencecampaign.org.uk/

ICaMB Postgraduate Research Symposium – students’ views


Once a year the final year PhD students in ICaMB have a one day symposium to present their data.  Here we ask some of these students to tell us how they found the occasion and discuss the projects they found particularly interesting.

 By Thomas Kinsman, Alexander Egan, Emma Button and Nichola Conlon

The ICaMB PGR Symposium was held on 25 March 2013. This annual symposium provides not only an excellent opportunity for final year PhD students to present their work to a mixed scientific audience of fellow students, research technicians, post docs and more senior researchers, but is also an excellent demonstration of the diversity of top quality research that is going on in ICaMB labs. The symposium and lunch were generously sponsored by GT Vision.

Session 1 – Reported by Thomas Kinsman (Lewis Lab)

The first session was centred on the study of DNA, yet talks ranged from the molecular biology of DNA polymerase processivity to the role of extracellular DNA in dental plaque biofilms. In addition to enabling me to gain a greater appreciation of the work that goes on in other labs within ICaMB, it was interesting that one of the speakers made a point of saying that preparing their talk had been very useful because it had made them realise they had enough results to write-up their PhD – I had not fully appreciated that this was another value of these talks!

Session 2 – Reported by Alex Egan (Vollmer Lab)

The second session of the symposium featured the work of students who look at various aspects of bacterial cell biology including; cell wall synthesis and cell division, bacterial cell motility, copper transport and storage and DNA replication. What immediately stands out from that list is the vast range of biological problems we work on here in ICaMB, and that’s just a small representation of the bacterial labs here. A positive impact of this vast range is that it creates an excellent centre for diverse knowledge, not just in gross terms, but in the myriad of different cellular and molecular techniques. With use of relatively simple yet elegant microscopy to study biological problems on cellular levels to the use of biochemical approaches to characterise the molecular basis of bacterial processes, it highlights that there’ll always be someone with experience who can provide advice and insight into almost any approach to biology. Having been on both the giving and receiving end of this, I believe it’s one of the great strengths of the symposium.

Session 3 – Reported by Emma Button (Veal Lab)

Session three was an exciting session in which talks ranged from the important interactions between the host and gut microbiota to mathematical equations used to refine a statistical modelling process that identifies subtle interactions involved telomere maintenance. Highlights of the session included a talk on the diverse roles of a peroxiredoxin (PRDX-6) in stress resistance and ageing, and a description of the importance of a DNA licensing protein (Cdt-1) and how it controlled DNA replication during embryo development in the African clawed frog, Xenopus laevis.

Session 4 – Reported by Nichola Conlon (Thwaites Lab)

The final session had talks that were all related to the gut, yet ranged from studies at a molecular level to in vivo human clinical trials. The first talk demonstrated how understanding the structure of mammalian amino acid transporter proteins in the plasma membrane is vital in understanding the pathology of gastrointestinal diseases and in improving drug specificity and targeting. An interesting insight followed into the mystery surrounding the mechanisms by which enteropathogenic E.coli (EPEC) disrupts the intestinal epithelium to cause diarrhoeal disease. The talk described the ways in which EPEC targets host cell proteins and pathways and highlighted the complexity in understanding such a common disease. Focus then shifted to the gut in its entirety with an intriguing description of an in vitro ‘model gut’, which is used to study the effects of various compounds on digestion. This model has proved effective in identifying alginate as a novel lipase inhibitor that can inhibit fat digestion similar to a current commercially available drug that is plagued by unwanted side effects. In vitro then moved to in vivo with the final talk which described a human clinical study in which ileostomy patients were used to assess the ability of alginate-enriched bread to inhibit fat digestion in vivo. Preliminary results revealed that, as observed in the model gut, alginate can also inhibit fat digestion in vivo when added as a supplement to food. The idea is that alginate could be incorporated into everyday foods, such as a loaf of bread, to try and combat obesity in a ‘health by stealth’ manner.

Personally, I found the symposium a complete success: everybody in attendance, students and staff alike, seemed to benefit in different ways from the experience. As a first year student in my lab said to me, they are looking forward to their turn in two years time.

You don’t always want what your mother gives you! – can we prevent mitochondrial disease?


By Professor Robert Lightowlers

In 1988, scientists in the UK and US recognised that certain diseases were caused by mutations in mtDNA . Over the following 20 years, mtDNA defects have been shown to cause a range of debilitating diseases many affecting different parts of the body. However, the main disorders relate to your muscle tissue and the brain.

Human muscle fibres stained for mitochondrial function. As can be seen in B, some of the fibres show no activity. This is because these fibres have high levels of mutated mitochondrial DNA.

It is estimated that at least 1:10,000 people suffer from disorders associated with defects in Mitochondrial DNA (mtDNA) – that’s more than 6,000 people in the UK. Even so, it is only recently that the importance of mitochondrial diseases have hit the general media.

Many of you will have seen the debate on correcting mitochondrial diseases in the newspapers (for example, see the Guardian, Telegraph) and on television recently, but not be aware of the central role that Newcastle researchers have played in making this exciting, or to some, controversial, new therapy closer to becoming a reality.  Here, Bob Lightowlers ICAMB Director and senior member of the Wellcome Trust Centre for Mitochondrial Research (WTCMR) reflects on the role mitochondrial research in Newcastle has played in this process over the last 20 years and tells us some of the story behind the headlines.

What are Mitochondria?

Electron micrograph of a cell (coloured blue) revealing part of the mitochondrial structure (orange) within. The entire length of the mitochondrion is about 5 micrometres.


These crucial structures found in all the trillions of cells in our body have many essential functions. One very important role they play is to take our common foodstuffs such as fats and sugars and turn them into energy for our body’s to function.

A single human cell showing the nucleus (green), the mitochondrial network (red) and the mitochondrial DNA within the network (yellow)




One surprising element of these structures is that they contain their own genetic element, mitochondrial (mt) DNA. Much smaller than our chromosomes, mtDNA is essential for energy production.




OK, so this is important, but why have mitochondria and mtDNA begun to work their way into the common conversation of the nation?

Answer: Our mothers!

What has this got to do with our mothers ? Mitochondrial DNA is only transmitted to babies by their mothers. This is different to all our other DNA where copies are made and transmitted from both parents. Unfortunately, as you inherit your mothers mitochondria, diseases caused by mtDNA mutations are inadvertently transmitted from the mother.

How does this relate to Newcastle based Mitochondrial Research?

My colleague Doug Turnbull, a neurologist here in Newcastle (and Director of the WTCMR) and I have been intrigued by these mtDNA mutations since it first became clear that they could cause disease. Back in the early ‘90’s, we discussed whether some day it would be possible to try and prevent the transmission of the faulty mtDNA from the mothers to their children. Of course, at that stage, it was just wishful thinking. As the Mitochondrial Research Group (MRG) began to grow and mature in Newcastle, we often returned to one question:

What if the nucleus from the diseased egg could be transferred to a healthy egg whose nucleus had been removed, in essence leaving all the affected mtDNA behind ?

If it was indeed possible, this reconstituted egg could be fertilised and implanted back into the mother by standard techniques used routinely in fertility clinics throughout the world. We also would consider when would such a technique be most efficient: before or after fertilisation of the egg? On paper both options looked possible, but there are many complications.

Technical Concept: achieving the switch of nuclei without some of the faulty mtDNA being inadvertently taken along for the ride.

Towards the end of the 90’s, scientists working in Canada were able to show that the level of mtDNA inadvertently transferred when the nucleus was switched into a recipient cell lacking a nucleus, was low. This was a promising result, but it led to two central questions:

•   Could this be repeated with human cells?

•   Was this technique morally and ethically acceptable to everyone?

The ethical debate: Debate raged as to whether this technique would constitute genetic manipulation of humans, which of course would be illegal. Further, it was not possible to perform these types of reconstruction experiments in man, as using viable human fertilised cells for research was also, understandably, illegal.

Professor Mary Herbert working at the nearby Human Fertility Centre came up with an intriguing proposal. She explained that unfortunately, during the standard process of in vitro fertilisation, many eggs became incorrectly fertilised. These eggs are unable to grow correctly and have to be discarded. One way of determining whether it would be possible to swap mtDNA in humans, she suggested, was to use these incorrectly fertilised eggs. As this procedure would still require the manipulation of fertilised human eggs, a licence would need to be applied for from the Human Fertilisation and Embryological Authority (HFEA). Following lengthy and extensive debate, including members of the research team being called to the House of Commons, a licence was eventually awarded in 2005.  Five years later, with the essential help of colleagues in the Fertility Centre, Mary, Doug and a group of us from the MRG were able to show that such a swap could be performed without any or very low levels of the defective mtDNA being transferred. Importantly, there was also no defect detectable in the reconstituted cells . In 2011, this very promising result, along with many other important contributions made by the Newcastle MRG to understanding mitochondrial biology in health and disease was recognised by the Wellcome Trust who funded the establishment of a new Research Centre in Newcastle, the Wellcome Trust Centre for Mitochondrial Research.

Getting acceptance of the technique

It was important to know whether the people of the UK agreed that such reconstitution technology was ethically acceptable. In August 2012, the government asked the Human Fertility and Embryological Authority (HFEA) to find out what the general public thought of the procedure .  The results were collated last month and the Human Fertility and Embryological Authority made a recommendation to Government. There was an overall support for the new technology with only 10% being fairly or strongly against the concept of mitochondrial gene replacement ) This is an endorsement of the method but there is still a long way to go before the technique can be performed in the clinic.

Its amazing to think how far this concept has come in 20 years. Perhaps in another 20 years we may be able to look back and celebrate how this dream has helped to provide a realistic method to help prevent the transmission of a debilitating disease for many couples.


Wellcome Trust Centre for Mitochondrial Research http://www.newcastle-mitochondria.com/
Human Fertility and Embryological Authority (HFEA) http://www.hfea.gov.uk/index.html
HFEA mitochondria puclib consultation 2012 http://www.hfea.gov.uk/6896.html