Tom Houslay

PhD Research Student

MSc Bioinformatics, University of Manchester (2004)
BSc (Hons) Computer Science, University of Lancaster (2002)

Supervisor: Dr. Luc Bussière

Start Date: 1st March 2010

Research Project

Sexual selection and life history allocation in Gryllodes sigillatus

I am interested in sexual selection, especially regarding the evolution and maintenance of preference in systems where there are no apparent direct benefits to the ‘choosy’ gender (typically females). Variation in male fitness depends on differences in multiple traits, including - but not limited to - sexually-selected characters, such as exaggerated ornaments and weapons. A comprehensive explanation for sexual trait diversity depends on integrating life history theory and sexual selection to compare costs and benefits of sexual traits. A universal cost for all such traits involves the resources required to create and maintain them, which are consequently unavailable to other life history characters. This resource trade-off typically causes covariance between an organism’s resource budget and its level of sexual trait expression, which is known as condition-dependence. Condition-dependence has several implications. It may be particularly important for ornaments signalling genetic quality, by helping to maintain the genetic variation that favours mate choice. It may also reduce extinction risk in sexually selected populations. I use the decorated cricket (Gryllodes sigillatus) to study the interdependence of resource budgets and allocation strategies in a species where males express a sexually-selected trait repeatedly across their lifetime.

 

Other Information

Personal background

I gained my undergraduate degree in Computer Science from Lancaster University (2002), and a Master’s degree (with distinction) in Bioinformatics from the University of Manchester ( 2004). Part of my postgraduate degree was spent at Novartis AG in Basel, Switzerland, after which I returned to the UK to work as a research assistant at the University of Glasgow’s Bioinformatics Research Centre, providing support to various laboratories in addition to pursuing some short research projects. In 2006 I moved to AstraZeneca’s Advanced Science and Technology Lab, where I worked as a computational biologist with a focus on designing algorithms for high-throughput image analysis (mostly with the Definiens suite of resources). My return to university was prompted by a desire to pursue my own research in an area that I feel passionate about.

Publications

University of Stirling

Houslay TM, Bussiere LF. 2012. Sexual Selection and Life History Allocation. In: eLS 2012, John Wiley & Sons, Ltd: Chichester. [LINK]

AstraZeneca

Caie PD, Walls RE, Ingleston-Orme A, Daya S, Houslay TM, Eagle R, Roberts ME, Carragher NO. 2010. High-content phenotypic profiling of drug response signatures across distinct cancer cells. Molecular Cancer Therapeutics 9(6):1913-1926.

University of Glasgow

Xu T-R, Baillie GS, Bhari N, Houslay TM, Pitt AM, Adams DR, Kolch W, Houslay MD, Milligan G. 2008. Mutations of beta-arrestin 2 that limit self-association also interfere with interactions with the beta(2)-adrenoceptor and the ERK1/2 MAPKs: implications for beta(2)-adrenoceptor signalling via the ERK1/2 MAPKs. Biochemical Journal 413:51-60.

Smith KJ, Baillie GS, Hyde EI, Li X, Houslay TM, McCahill A, Dunlop AJ, Bolger GB, Klussmann E, Adams DR, Houslay MD. 2007. H-1 NMR structural and functional characterisation of a cAMP-specific phosphodiesterase-4D5 (PDE4D5) N-terminal region peptide that disrupts PDE4D5 interaction with the signalling scaffold proteins, arrestin and RACK1. Cellular Signalling 19(12):2612-2624.

Baillie GS, Adams DR, Bhari N, Houslay TM, Vadrevu S, Meng D, Li X, Dunlop A, Milligan G, Bolger GB, Klussmann E, Houslay MD. 2007. Mapping binding sites for the PDE4D5 cAMP-specific phosphodiesterase to the N- and C-domains of beta-arrestin using spot-immobilized peptide arrays. Biochemical Journal 404:71-80.

Huston E, Gall I, Houslay TM, Houslay MD. 2006. Helix-1 of the cAMP-specific phosphodiesterase PDE4A1 regulates its phospholipase-D-dependent redistribution in response to release of Ca2+. Journal of Cell Science 119(18):3799-3810.

Huston E, Houslay TM, Baillie GS, Houslay MD. 2006. cAMP phosphodiesterase-4A1 (PDE4A1) has provided the paradigm for the intracellular targeting of phosphodiesterases, a process that underpins compartmentalized cAMP signalling. Biochemical Society Transactions 34:504-509.

Wallace DA, Johnston LA, Huston E, MacMaster D, Houslay TM, Cheung YF, Campbell L, Millen JE, Smith RA, Gall I, Knowles RG, Sullivan M, Houslay MD. 2005. Identification and characterization of PDE4A11, a novel, widely expressed long isoform encoded by the human PDE4A cAMP phosphodiesterase gene. Molecular Pharmacology 67(6):1920-1934.

Links

Personal website

Photography

Twitter

Academia.edu page

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