Determining the effects of genetic variation and early life stress on the regulation of the galanin gene in fat and alcohol selection.
Lead Research Organisation:
University of Aberdeen
Department Name: Sch of Medicine, Medical Sci & Nutrition
Abstract
Overindulgence in high calorie nutrients, which include fat and alcohol, has had a major effect on the health of the UK population where 67% of males and 57% of females are classed as overweight. Because obesity is linked to type 2 diabetes and cardiovascular disease we need to find the causes of this calorie overconsumption and a major source of the calories consumed by the UK population come in the form of fat and alcohol. In addition to cardiovascular disease and cancer, excessive alcohol consumption is also linked to liver cirrhosis and pancreatitis. Many of us are susceptible to over consume fat and alcohol as a result of differences in our DNA but there is also evidence that environmental factors such as early life stress also play a role. However, we still know very little about the mechanisms that influence our intake of fat and alcohol and how these mechanisms are affected by genetic variation and environment. Important clues have emerged. For example, a small neuropeptide, called galanin is expressed in a region of the brain called the hypothalamus that controls fat and alcohol intake. Removal of the gene which encodes galanin reduces fat and alcohol intake and decreases weight gain. A critical aspect of the function of galanin is that it should be expressed in the correct cells, in the correct amount and in response to the correct stimuli. However, nothing was known about the mechanisms controlling the production of galanin in the hypothalamus or how differences in the regions of DNA that control this expression might affect fat and alcohol intake. We first discovered a DNA switch sequence that was an excellent candidate for the undiscovered switch sequence that controls galanin in the hypothalamus. We then found that sequence changes within this switch that exist within the human population, and were linked to alcohol abuse, increased the strength of this switch in the hypothalamus. We also found epigenetic changes within the switch, called DNA methylation, that were altered by stress and seemed to also change the strength of the switch. We hypothesise that these sequence changes and methylation changes within the GAL gene switch work together to alter the production of galanin in the hypothalamus and to influence fat and alcohol intake. To address this hypothesis we used a remarkable new method called CRISPr genome editing to quickly and efficiently delete the switch from the genome. We will initially determine the effects of removing the switch on galanin production in the hypothalamus and determine its effects on fat and alcohol selection. We will use CRISPr technology again to reproduce known human sequence changes within the switch (a process known as humanisation) to model their effects on galanin production and fat and alcohol intake. We will then use these "humanised" models to determine the effects of early life stress on the methylation of the switch sequence and how this methylation affects its function. Using this revolutionary CRISPr technology we will determine how changes that occur naturally in the human population, as a result of genetics or environment, affect our fat and alcohol intake. Considering the huge problem of obesity and excessive alcohol intake in our society these studies will open avenues for not only understanding the role of genetics and environment in excess fat and alcohol intake but will also provide novel opportunities for reducing susceptibility to obesity by controlling excess calorie intake in the human population.
Technical Summary
We will determine the effects of genetics and epigenetics on the mechanisms that control galanin gene (GAL) expression in the paraventricular nucleus (PVN) where galanin controls fat and alcohol intake. Excess fat and alcohol contribute to obesity that is a risk factor in diabetes and cardiovascular disease. Alcohol abuse is also linked to cirrhosis and pancreatitis. We need to know;
1. What happens to the expression of galanin and fat and alcohol intake when you remove the regulatory elements that control GAL expression in PVN.
2. What are the effects of genetic variation on these regulatory elements and in fat and alcohol intake.
3. How are these regulatory elements affected by epigenetic modification as a result of early life stress.
We identified a regulatory element (GAL5.1) that is active in GAL expressing cells of the PVN. Polymorphisms within GAL5.1, associated with alcohol abuse, have a significant effect on its activity. Early life stress was shown to increase GAL mRNA in the PVN and led to changes in GAL5.1 methylation. We hypothesise that GAL5.1 is important in the regulation of GAL in the PVN and that polymorphisms and epigenetic modification influence the expression of GAL that, in turn, influence fat and alcohol intake. We have used CRISPr technologies to knock out GAL5.1 from the mouse genome and will use GAL mRNA expression analysis and fat/alcohol intake tests to determine the effects of GAL5.1 deletion. Humanisation of GAL5.1 in mice using CRISPr technologies to reproduce both human polymorphisms will permit a comparison of alleles on GAL expression and alcohol/fat intake. Humanisation will also permit an analysis of the effects of early life stress on the methylation of the human GAL5.1 in-vivo whose CpG content and distribution differs from mouse. The unique studies described in this proposal will revolutionise our understanding of the roles of gene regulation in nutrition and will have important ramifications for obesity research.
1. What happens to the expression of galanin and fat and alcohol intake when you remove the regulatory elements that control GAL expression in PVN.
2. What are the effects of genetic variation on these regulatory elements and in fat and alcohol intake.
3. How are these regulatory elements affected by epigenetic modification as a result of early life stress.
We identified a regulatory element (GAL5.1) that is active in GAL expressing cells of the PVN. Polymorphisms within GAL5.1, associated with alcohol abuse, have a significant effect on its activity. Early life stress was shown to increase GAL mRNA in the PVN and led to changes in GAL5.1 methylation. We hypothesise that GAL5.1 is important in the regulation of GAL in the PVN and that polymorphisms and epigenetic modification influence the expression of GAL that, in turn, influence fat and alcohol intake. We have used CRISPr technologies to knock out GAL5.1 from the mouse genome and will use GAL mRNA expression analysis and fat/alcohol intake tests to determine the effects of GAL5.1 deletion. Humanisation of GAL5.1 in mice using CRISPr technologies to reproduce both human polymorphisms will permit a comparison of alleles on GAL expression and alcohol/fat intake. Humanisation will also permit an analysis of the effects of early life stress on the methylation of the human GAL5.1 in-vivo whose CpG content and distribution differs from mouse. The unique studies described in this proposal will revolutionise our understanding of the roles of gene regulation in nutrition and will have important ramifications for obesity research.
Planned Impact
Our research will contribute fundamental new knowledge relating to the mechanisms regulating fat and alcohol intake with a range of potential beneficiaries in the academic, commercial and public sectors. To maximise engagement with these stakeholders and deliver the widest possible impact from our findings, we will pursue the following specific objectives:
1: Impact through training. The current proposal will permit the further training of a highly skilled and motivated post-doctoral scientist; Scott Davidson, in the role of genetics and epigenetics in the control of fat/alcohol intake. Dr. Davidson will receive training in new and powerful technologies such as CAS9/CRISPr genome editing, that Dr. MacKenzie has adopted and mastered in Aberdeen, epigenetic analysis of early life stress, genomics, mRNA expression analysis and in-vivo physiological and metabolic studies. This training will allow Dr. Davidson to eventually progress as an independent researcher within the UK.
2: Expansion of current public engagement activities.
An immediate impact of this project is its opportunity to raise public awareness and understanding of the role of gene regulation in the control of appetite and nutrient selection. Additionally, engaging with school children is vital, not only for educating in the benefits of a healthy diet and the role of genetics and environment in its control but also for inspiring the next generation of researchers in nutrition. Throughout the project, we will engage with the public in the following ways:
(a)To maximise the availability of our research, we will publish the results from this project in high-impact journals with Open Access Compliant policies. We will also promote the findings of our studies on our respective University web pages and in the national and international press.
(b)We will continue to make use of the University of Aberdeen Press Office, as well as the BBSRC media services, to disseminate our findings as widely as possible to the general public.
(c)At least once a year we will continue our outreach activities with school children .
(d)Once a year we will engage the public through public seminars and science festivals.
(e)We will continue to use the University of Aberdeen Public Engagement with Science Unit (PERU) to keep us updated on additional public engagement opportunities to expand our current activities.
3: Establish formal links with clinical science .
Our published work the identification of functional variation within the GAL5.1 enhancer has inspired at least two major patient based association analysis that established a significant association between GAL5.1 haplotypes and increased alcohol consumption in certain populations. We will continue to engage the clinical community by;
(i) Publishing our results in a timely manner and continuing to chair and deliver presentations at national and international conferences attended by both scientists and clinicians.
(ii) Seek formal collaborations with clinicians to explore potential clinical applications of the planned research.
4: Commercial exploitation of research outcomes.
We have had success in collaborating with industrial partners as reflected by our current partnership with GW Pharmaceuticals. We will continue to seek further industrial collaborations and have organised meetings with representatives from Eli Lilly, Alder pharmaceuticals and Pharmnovo who I have invited to speak at Neuropeptides-2015 (a conference organised by AM in Sept 2015) and who have an interest in discussing the implications of genetic and epigenetic variation on appetite and patient drug responses. We will also seek assistance of University bodies such as the Kosterlitz Centre to seek further links with academic and industrial partners. We will also work with the Research and Innovation Department at The University of Aberdeen who will review opportunities for commercialisation throughout the project.
1: Impact through training. The current proposal will permit the further training of a highly skilled and motivated post-doctoral scientist; Scott Davidson, in the role of genetics and epigenetics in the control of fat/alcohol intake. Dr. Davidson will receive training in new and powerful technologies such as CAS9/CRISPr genome editing, that Dr. MacKenzie has adopted and mastered in Aberdeen, epigenetic analysis of early life stress, genomics, mRNA expression analysis and in-vivo physiological and metabolic studies. This training will allow Dr. Davidson to eventually progress as an independent researcher within the UK.
2: Expansion of current public engagement activities.
An immediate impact of this project is its opportunity to raise public awareness and understanding of the role of gene regulation in the control of appetite and nutrient selection. Additionally, engaging with school children is vital, not only for educating in the benefits of a healthy diet and the role of genetics and environment in its control but also for inspiring the next generation of researchers in nutrition. Throughout the project, we will engage with the public in the following ways:
(a)To maximise the availability of our research, we will publish the results from this project in high-impact journals with Open Access Compliant policies. We will also promote the findings of our studies on our respective University web pages and in the national and international press.
(b)We will continue to make use of the University of Aberdeen Press Office, as well as the BBSRC media services, to disseminate our findings as widely as possible to the general public.
(c)At least once a year we will continue our outreach activities with school children .
(d)Once a year we will engage the public through public seminars and science festivals.
(e)We will continue to use the University of Aberdeen Public Engagement with Science Unit (PERU) to keep us updated on additional public engagement opportunities to expand our current activities.
3: Establish formal links with clinical science .
Our published work the identification of functional variation within the GAL5.1 enhancer has inspired at least two major patient based association analysis that established a significant association between GAL5.1 haplotypes and increased alcohol consumption in certain populations. We will continue to engage the clinical community by;
(i) Publishing our results in a timely manner and continuing to chair and deliver presentations at national and international conferences attended by both scientists and clinicians.
(ii) Seek formal collaborations with clinicians to explore potential clinical applications of the planned research.
4: Commercial exploitation of research outcomes.
We have had success in collaborating with industrial partners as reflected by our current partnership with GW Pharmaceuticals. We will continue to seek further industrial collaborations and have organised meetings with representatives from Eli Lilly, Alder pharmaceuticals and Pharmnovo who I have invited to speak at Neuropeptides-2015 (a conference organised by AM in Sept 2015) and who have an interest in discussing the implications of genetic and epigenetic variation on appetite and patient drug responses. We will also seek assistance of University bodies such as the Kosterlitz Centre to seek further links with academic and industrial partners. We will also work with the Research and Innovation Department at The University of Aberdeen who will review opportunities for commercialisation throughout the project.
Publications
Hay EA
(2017)
Using the CRISPR/Cas9 system to understand neuropeptide biology and regulation.
in Neuropeptides
Leeson-Payne, A.
(2024)
Loss of GPR75 protects against non-alcoholic fatty liver disease and body fat accumulation
in Cell Metabolism
MacKenzie A
(2017)
Neuropeptides-2015, Aberdeen University, Scotland.
in Neuropeptides
MacKenzie A
(2022)
Context-dependant enhancers as a reservoir of functional polymorphisms and epigenetic markers linked to alcohol use disorders and comorbidities.
in Addiction neuroscience
McEwan A
(2021)
The anxiety and ethanol intake controlling GAL5.1 enhancer is epigenetically modulated by, and controls preference for, high-fat diet.
in Cellular and molecular life sciences : CMLS
Description | Excessive alcohol intake is associated with 5.9% of global deaths. However, this figure is especially acute in men such that 7.6% of deaths can be attributed to alcohol intake. Previous studies identified a significant interaction between genotypes of the galanin (GAL) gene with anxiety and alcohol abuse in different male populations but were unable to define a mechanism. To address these issues the current study analysed the human UK Biobank cohort and identified a significant interaction (n=115,865; p=0.0007) between allelic variation (GG or CA genotypes) in the highly conserved human GAL5.1 enhancer, alcohol intake (AUDIT questionnaire scores) and anxiety in men. Critically, disruption of GAL5.1 in mice using CRISPR genome editing significantly reduced GAL expression in the amygdala and hypothalamus whilst producing a corresponding reduction in ethanol intake in KO mice. Intriguingly, we also found evidence of reduced anxiety-like behaviour in male GAL5.1KO animals mirroring that seen in humans that was consistent with our previous UK Biobank studies. Using bioinformatic analysis and co-transfection studies we further identified the EGR1 transcription factor, that is co expressed with GAL in amygdala and hypothalamus, as being important in the protein kinase C (PKC) supported activity of the GG genotype of GAL5.1 but less so in the CA genotype. Further analysis of the GAL5.1KO line demonstrated a reduction in intake of highfat diet (HFD) compared to wild type littermates which was published in Cell. Mol. Life Sci. This study also showed that exposure of pregnant females to HFD altered DNA-methylation within GAL5.1 in male offspring. Our unique study uses a novel combination of human association analysis, CRISPR genome editing in mice, animal behavioural analysis and cell culture studies to identify a highly conserved regulatory mechanism linking anxiety and alcohol intake that might contribute to increased susceptibility to anxiety and alcohol abuse in men. This study has been accepted for publication by the journal Molecular Psychiatry which is one of the top journals in the field. |
Exploitation Route | Our data suggests that comparative genomics, CRISPR genome editing and mouse behavioural analysis are highly effective methods of determining the role of the non-coding genome in health and disease. In addition, by collaborating with Andrew McIntosh and Toni Clarke at the University of Edinburgh we have found a significant association between increased alcohol intake in human males the GG allele of our enhancer and anxiety. These studies have been published on line (MS ID#: BIORXIV/2019/572065 MS TITLE: CRISPR disruption and UK Biobank analysis of a highly conserved polymorphic enhancer suggests its role in anxiety and male alcohol intake.). We have also been able to complete another manuscript (MS ID#: BIORXIV/2019/544585 MS TITLE: Genetic, epigenetic and pharmacological influences modulating tissue specific regulation of the cannabinoid receptor -1 (CB1) gene; implications for cannabinoid pharmacogenetics.) whose work was also partially funded by the BBSRC grant. I have also just completed an article in collaboration with The Conversation. |
Sectors | Agriculture Food and Drink Creative Economy Education Healthcare Pharmaceuticals and Medical Biotechnology Other |
URL | https://www.biorxiv.org/content/10.1101/572065v2 |
Description | My Findings have been published in a number of articles in publications such as "The conversation" which have collectively been read by over 100k people. In addition I was recently interviewed by the "Evening express" who were interested on the role of anxiety and fear surrounding Halloween. I have also took part in a 4 week series on Gaelic Radio devoted to advances in Genetics. |
First Year Of Impact | 2018 |
Sector | Agriculture, Food and Drink,Education,Pharmaceuticals and Medical Biotechnology,Other |
Impact Types | Cultural Societal |
Description | A novel in-vivo CRISPR enhancer screen to identify polymorphic regulatory regions controlling the hypothalamic expression of appetite regulating neuropeptides. |
Amount | £25,000 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 09/2017 |
End | 04/2018 |
Description | Characterisation of a novel selectable cell-surface regulator of cardiovascular progenitors for stem cell-mediated regeneration. |
Amount | £196,608 (GBP) |
Organisation | British Heart Foundation (BHF) |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 09/2019 |
End | 11/2022 |
Description | Determining how the anxiety and alcohol intake modulating GAL5.1 enhancer works |
Amount | £12,000 (GBP) |
Organisation | Tenovus Cancer Care |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 11/2019 |
End | 12/2020 |
Description | Determining the biological basis for, and de-stigmatising, problematic alcohol use and anxiety |
Amount | £130,000 (GBP) |
Funding ID | PHD-50366-2021 |
Organisation | Medical Research Scotland |
Sector | Charity/Non Profit |
Country | United Kingdom |
Start | 09/2022 |
End | 09/2026 |
Description | Determining the effects of genetic variation and early life stress on the regulation of the galanin gene in fat and alcohol selection. |
Amount | £418,914 (GBP) |
Funding ID | BB/N017544/1 |
Organisation | Biotechnology and Biological Sciences Research Council (BBSRC) |
Sector | Public |
Country | United Kingdom |
Start | 09/2016 |
End | 09/2019 |
Description | How do genetics and epigenetics interact to influence the activity of a context specific enhancer? |
Amount | £720,962 (GBP) |
Organisation | Manchester Metropolitan University |
Sector | Academic/University |
Country | United Kingdom |
Start | 03/2023 |
End | 02/2026 |
Description | How do genetics and epigenetics interact to influence the activity of a context specific enhancer? |
Amount | £720,962 (GBP) |
Funding ID | BB/W017598/1 |
Organisation | Biotechnology and Biological Sciences Research Council (BBSRC) |
Sector | Public |
Country | United Kingdom |
Start | 03/2023 |
End | 02/2026 |
Title | Production of ECR1 enhancer knockout mice using CRISPR genome editing |
Description | We have used CRISPR genome editing to produce a knockout mouse lacking the polymorphic ECR1 enhancer that resides in intron 2 of the cannabinoid-1 receptor gene (CNR1). Analysis of this line demonstrates a reduction of CNR1 expression in the hippocampus and hypothalamus with concurrent changes in ethanol intake and hypothermia response following agonism of the CB1 receptor. |
Type Of Material | Model of mechanisms or symptoms - mammalian in vivo |
Year Produced | 2017 |
Provided To Others? | Yes |
Impact | We are in the process of completing a manuscript describing our findings to two journals; Neuropsychopharmacology and Neuroinflammation. |
Title | Production of GAL5.1 enhancer knockout mice using CRISPR genome editing |
Description | We used CRISPR genome editing to delete an enhancer that controls the expression of the galanin gene in the PVN of the mouse. Analysis of this knock out line shows a decrease in GAL expression in the PVN and a significant reduction in fat and alcohol intake. A manuscript describing these findings is being revised with a view to publication in Cell Reports. |
Type Of Material | Model of mechanisms or symptoms - mammalian in vivo |
Year Produced | 2017 |
Provided To Others? | Yes |
Impact | A manuscript describing these findings is being revised with a view to publication in Cell Reports. |
Title | Transgenic animal models |
Description | Transgenic animal lines containing reporter constructs driven by enhancers of the TAC1, GAL and CNR1 genes |
Type Of Material | Model of mechanisms or symptoms - mammalian in vivo |
Year Produced | 2009 |
Provided To Others? | Yes |
Impact | Expression data produced using these transgenic models have contributed to a great many research papers (see outputs). |
Description | Determining the biological basis for, and de-stigmatising, problematic alcohol use and anxiety. |
Organisation | NHS Grampian |
Department | Aberdeenshire Community Health Partnership |
Country | United Kingdom |
Sector | Public |
PI Contribution | We wrote and provided preliminary data for the award. |
Collaborator Contribution | Our partners at NHS provided advise and support and helped writethe application |
Impact | None yet |
Start Year | 2022 |
Description | Organisation of conference entitled "Functional Regulatory Genomics and Disease". |
Organisation | University of Edinburgh |
Department | Institute of Genetics & Molecular Medicine |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | I have personally been involved in organising this event |
Collaborator Contribution | My partners have made a major contribution in organising this event. |
Impact | Still to be determined |
Start Year | 2019 |
Description | Contributed an article in "The Conversation" about human evolution |
Form Of Engagement Activity | Engagement focused website, blog or social media channel |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | The title of the piece was " Its time we stopped human evolution" and it received 80k reads and 120 contacts. |
Year(s) Of Engagement Activity | 2019 |
URL | https://theconversation.com/its-time-we-stopped-human-evolution-geneticist-116544#comment_1945368 |
Description | Contributed an article in "The Conversation" about the genome. |
Form Of Engagement Activity | Engagement focused website, blog or social media channel |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | I was asked to produce an article for "The Conversation" by the Scotland editor Steve Vass. |
Year(s) Of Engagement Activity | 2019 |
URL | https://theconversation.com/human-genome-project-new-alcohol-abuse-study-could-help-us-finally-unloc... |
Description | Interview on Gaelic Radio about bacteria and human health |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | National |
Primary Audience | Public/other audiences |
Results and Impact | I was interviewed about the role of bacteria in health and disease. The programme has yet to be scheduled. |
Year(s) Of Engagement Activity | 2019 |
Description | Interview on Gaelic Radio about enhancers and human health |
Form Of Engagement Activity | A broadcast e.g. TV/radio/film/podcast (other than news/press) |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | Interview on press release related to 2024 McEwan paper. |
Year(s) Of Engagement Activity | 2024 |
Description | Interview on SHMU radio |
Form Of Engagement Activity | A broadcast e.g. TV/radio/film/podcast (other than news/press) |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | An interview on SHMU FM about my career as a scientist and the subject of my current studies |
Year(s) Of Engagement Activity | 2017 |
Description | Multimedia press release on publication of Mol Psych article. |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | A press release publicising our paper "An ancient polymorphic regulatory region within the BDNF gene associated with obesity modulates anxiety-like behaviour in mice and humans" garnered a great deal of media interest and was released through the following outlets;The Independent, The Mail Online, BBC Alba, BBC Radio Scotland, STV, The Times, The Mirror, The Evening Standard, Northsound, Radio News Hub, The Belfast Times, the Shropshire Star etc.... |
Year(s) Of Engagement Activity | 2024 |
URL | https://www.abdn.ac.uk/news/22898/?dm_i=5EH4,ZV6I,2MQGHE,42CML,1 |
Description | Opinion piece published in the "Conversation" entitled 'The human genome at 20: how biology's most-hyped breakthrough led to anticlimax and arrests" |
Form Of Engagement Activity | Engagement focused website, blog or social media channel |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | The article received nearly 40k reads in its first week. |
Year(s) Of Engagement Activity | 2021 |
URL | https://theconversation.com/the-human-genome-at-20-how-biologys-most-hyped-breakthrough-led-to-antic... |
Description | Oral presentation at the World Congress of Psychiatric Genetics entitled "CRISPR and UK Biobank Analysis of an Enhancer That Modulates Fat and Alcohol Intake and Mood Suggests a Role in Male Alcohol Abuse and Anxiety" |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Professional Practitioners |
Results and Impact | Delivery of Conference paper. |
Year(s) Of Engagement Activity | 2020 |
URL | https://ispg.net/wcpg-2020/ |
Description | Talk at Cafe Scientifique entitled "Health and the disposable cave man; understanding disease using evolution." |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | A talk on my research for a general audience. Attended by nearly 100 members of the public who took a great interest. My work on CRISPR genome editing forged a collaboration with a Prof of Rice genomics who was in the audience (Prof Alan Price) and we wrote a grant together to the BBSRC. The outcome is pending. |
Year(s) Of Engagement Activity | 2017 |
Description | Talk at the the Aberdeen Science centre as part of British science week entitled "Tales form the dark side". |
Form Of Engagement Activity | A talk or presentation |
Part Of Official Scheme? | No |
Geographic Reach | Regional |
Primary Audience | Public/other audiences |
Results and Impact | 60 members of the general public attended a talk to introduce the subject and justification for my research. I was told afterwards that the talk was pitched at the right level and a great deal of discussion followed from interested members of the general public. |
Year(s) Of Engagement Activity | 2019 |
URL | https://www.facebook.com/events/248617896013636/ |