Speciation by genetic conflict


Aim: to determine whether selfish chromosomes that kill sperm create reproductive isolation

How new species form is a major question in biology. Key to this is reproductive isolation- the factors that prevent two populations interbreeding. Traditionally, ecological differences between populations have been thought to create reproductive isolation. But recently, a new theory has arisen that conflict within the genome drives speciation.

Many species harbour selfish genetic elements that spread by manipulating reproduction. For example, some X chromosomes kill Y chromosome sperm, so all offspring inherit the driving X, and all offspring are female. These selfish elements create intense conflict over reproduction, as the driver evolves to drive more effectively, and the rest of the genome evolves mechanisms to stop it. This intragenomic conflict rapidly alters genes involved in making gametes in population that carry the selfish genetic elements.

One key prediction of conflictual speciation theory is that selfish genetic elements will be adapted to their local population, and will perform poorly in hybrids. When a driver enters a naïve population with no defences against drive, the drive is expected to attack too strongly, sterilising hybrids. So drive will not be able to spread between species. However, it is possible that this is wrong, and instead drivers will spread rapidly through naïve populations and species, potentially homogenising them.

In this project you will investigate how selfish meiotic drivers interact with hybridisation. We will use a suite of meiotic drive systems in various Drosophila species. We will first cross each species to closely related species to establish which can hybridise. We will then repeat the crosses with individuals bearing meiotic drive chromosomes. Can drivers spread rapidly through naïve species, having a homogenising effect? Or will the cost of drivers kill or sterilise drive-bearing hybrids?


Notes and details of how to apply are available here: https://accedtp.ac.uk/acce-dtp-phd-opportunities-at-university-of-liverpool/

All applicants to ACCE must complete the ACCE personal statement proforma. This is instead of a normal personal/supporting statement/cover letter. The proforma is designed to standardise this part of the application to minimise the difference between those who are given support and those who are not.

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Open to students worldwide

Funding information

Funded studentship

NERC ACCE DTP in Ecology and Evolution, programme starts October 2023.
UKRI provide the following funding for 3.5 years:
• Stipend (2022/23 UKRI rate £17,668)
• Tuition Fees at UK fee rate (2022/23 rate £4,596)
• Research support and training grant (RTSG)
Note - UKRI funding only covers UK (Home) fees (£4,596 at 2022/23 rate). A limited number of international fee bursaries will be awarded on a competitive basis. However, if selected International and EU fee rate candidates may need to cover the remaining amount of tuition fees by securing additional funding. International fees for 2022/23 entry were £25,950 (full time) per annum.



Price, Verspoor, and Wedell N. 2019 Ancient gene drives: an evolutionary paradox. Proc. R. Soc. B 286: 20192267
Verspoor, Smith, Mannion, Hurst, and Price. 2018 Strong hybrid male incompatibilities impede the spread of a selfish chromosome between populations of a fly." Evolution Letters 2: 169-179
Tom AR Price, Nikolai Windbichler, Robert L Unckless, Andreas Sutter, Jan‐Niklas Runge, Perran A Ross, Andrew Pomiankowski, Nicole L Nuckolls, Catherine Montchamp‐Moreau, Nicole Mideo, Oliver Y Martin, Andri Manser, Mathieu Legros, Amanda M Larracuente, Luke Holman, John Godwin, Neil Gemmell, Cécile Courret, Anna Buchman, Luke G Barrett, Anna K Lindholm. 2016 The ecology and evolutionary dynamics of meiotic drive. Trends in Ecology & Evolution 31: 315-326
M.N. Brien, J. Enciso Romero, A.J. Parnell, P.A. Salazar, C. Morochz, D. Chala, H.E. Bainbridge, T. Zinn, E.V. Curran, N.J. Nadeau 2018 Phenotypic variation in Heliconius erato crosses shows iridescent structural colour is sex-linked and controlled by multiple genes. Interface Focus 9: 20180047.