I completed my PhD in Biosciences at The University of Birmingham in 2003, studying the role of Rho small GTPases in keratinocyte function. Following this I undertook a postdoc at the MRC Laboratory for Molecular Cell Biology investigating the function of Rho family small GTPases during neurotransmitter release in Caenorhabditis elegans.
In 2010 I became a Wellcome Trust Career Development Fellow at Imperial College using C. elegans to study the relationships between the nervous and immune systems the mediate responses to infection.
I joined the School of Life, Health and Chemical Sciences in 2015 as a lecturer.
1999 BSc Biochemistry and Molecular Cell Biology The University of Birmingham
2003 PhD Biosciences The University of Birmingham
Avoidance behaviours are the first line of defence against pathogens and have been selected for throughout evolution; simply put animals that avoid situations where the risk of infectious disease is high are more likely to survive and procreate. The human emotion of disgust is an adaptive disease avoidance system that could be harnessed to prevent infectious disease spread. Since human disgust must share common ancestry with pathogen avoidance behaviours in other animals we can begin to understand disgust through experimental studies of pathogen avoidance in animals.
The nematode worm Caenorhabditis elegans is routinely used as a genetic model to dissect complex behaviours. We and others have established C. elegans as a cost-effective invertebrate model of pathogen avoidance. This model will provide a platform for further investigations into the evolutionary role of pathogen avoidance behaviours in host defence and the effect of life-traits such as ageing on pathogen avoidance behaviour.
A full understanding of the evolution of pathogen avoidance behaviours could be used to inform the design of public health interventions that will be important in disease control. Interventions based on emotional drivers of behavior, including disgust, have been used to improve hygiene and handwashing rates in rural India (the SuperAmma trial).
In collaboration with Dr Gini Harrison (Psychology)
Previous research has reported a link between exposure to organophosphate (OP) pesticides, mood disorders and suicidal behaviour. The mechanism through which OP exposure may result in mood disorders is unclear. Some researchers have suggested that they may also cause changes to serotonergic and dopaminergic pathways, which are systems involved in mood and stress regulation. Using behavioural assays in C. elegans we are studying how the long-term, low level OP exposure that has been associated with mood disorders affects neuronal development and function.
Anderson A. and McMullan R. From head to tail it's a two way street for neuro-immune communication Worm 3(3) e959425
Anderson A, Laurenson-Schafer H, Partridge F, Hodgkin J, McMullan R. 2013, Serotonergic Chemosensory Neurons Modify the C. elegans Immune Response by Regulating G-protein Signalling in Epithelial Cells, PLOS Pathogens Vol:9(12), e1003787
Anderson A, Kang S, McMullan R, 2013, A simple method for quantifying M. nematophilum clearance from the rectal opening of C. elegans, Worm Breeders Gazette, Vol:19 (4), Pages: 15-16
Anderson A, McMullan E, 2013, A modified leaving assay to study pathogen avoidance, Worm Breeders Gazette, Vol:19 (4), Pages: 13-14
Anderson A, McMullan R, G-proteins: Fighting infection on two fronts, Worm, Vol:1, ISSN:2162-4046, Pages:196-201
McMullan R, Anderson A, Nurrish S, 2012, Behavioral and Immune Responses to Infection Require G alpha q- RhoA Signaling in C. elegans, PLOS Pathogens, Vol:8, ISSN:1553-7366, Pages:e1002530-e1002530
Currently teaching on the following modules;
SK320 Infectious disease and public health
S350 Evaluating contemporary science
SDK228 The science of the mind-investigating mental health
SXHL288 Practical Science: biology and health
I am currently a STEM ambassador and Nuffield placement provider
I have been a competitor in "I'm a scientist get me out of here" and presented "The Disgust Instinct" with Valerie Curtis (London School of Hygiene and Tropical Medicine) at the 2016 Cheltenham Science Festival.
I have recently organising the Royal Society Evolution of Pathogen and Parasite Avoidance meeting that took place at Chichley Hall, UK in June 2017. You can listen to the presentations here
Find out more about my recent talk at RSC Science and the Assembly 2017 here
Member Genie (Group of elegans new investigators in europe)
|Role||Start date||End date||Funding source|
|Lead||18/May/2015||31/Jan/2016||WELLCOME Wellcome Trust|
Rho signaling has been extensively studied using biochemistry and cell-based assays that have demonstrated roles for Rho in many basic cell functions. These studies have told us a lot about the functions of Rho, however little about their importance in a whole animal. Rho signaling is essential during development making it difficult to study Rho’s role in adult animals. Analysis of adult Rho signaling pathways is important because aberrant signaling by these pathways has been implicated in human disease. In this study I aim to define the Rho pathways that act in adult animals. In particular I will identify those pathways that trigger changes in cell morphology as part of the C. elegans innate immune response. By identifying effectors important for this phenotype we will better understand Rho’s role in controlling cell morphology in adult animals. The innate immune system is evolutionarily conserved, for example, both Rho and MAPKinase function in the mammalian immune system and this is also true in C. elegans. In addition cross talk between Rho and MAPKinase pathways has been suggested to contribute to the action of oncogenic Ras. The molecular interactions that mediate this cross talk and Rho’s activation during the immune response remain poorly described and this phenotype provides a genetic model to dissect them. Defining these pathways and the relationships between them in C. elegans is likely to tell us more about how they are involved in innate immunity and misregulated in diseases such as cancer.