Dr Thomas Price

I am trying to understand the population dynamics of the selfish X chromosome SRS in the European fruit fly Drosophila subobscura. In Tunisian populations about 20% of flies carry a driving X chromosome called SRS. Normal X chromosomes are passed on to half a male’s offspring, while the other half inherits his Y chromosome. But when males carry the SRS chromosome all their Y bearing sperm die and all their offspring inherit the SRS X chromosome. This allows the SRS chromosome to spread as it is passed on to more offspring that the normal X, but it also causes male carriers to only have daughters, and to produce less sperm than normal males. This can cause populations to mostly consist of females, and potentially could wipe entire populations out due to a total lack of males. Work in related species has shown that if females mate with multiple males the small amounts of sperm produced by carrier males is usually swamped by the large amounts of sperm transferred by normal males, and the driving X cannot spread. But in D. subobscura, SRS is only found in the Southern populations where females remate, and is never found in the Northern populations where females mate once. It’s a bit of a mystery.

I am trying to understand the molecular and genetic basis of the drive mechanism in this species, and releted ones. Ultimately, if we can understand sex chromosome drive, we might be able to use it to control pest species, or to modify the sex ratio of important agricultural animals. But our understanding of how these mechanisms work, how they evolve, and how they persist, is still at a very early stage.

Some female animals mate once in their life while others mate with many males each day. This results in big differences between species in everything from their physiology and behaviour, to how their social systems are arranged. A male fathers fewer offspring if a female he mates with goes on to mate with another male. This has caused the evolution of male traits that reduce female remating rates. The establishment of harems in red deer and gorillas are well known examples. Male honeybees genitalia burst inside the female in an effort to block her reproductive tract and prevent her mating with other males. Females in turn have often evolved traits that allow them to avoid control by males, and remate with males of their choosing.Finding the genes underlying female remating would be a big step forward in understanding all this variation, and I am searching for these genes using the fruit flies Drosophila pseudoosbcura and D. subobscura.

I am also interested in how environmental and genetic differences, including meiotic drive (see above), can impact on fertility, particularly male fertility. We know that sperm is hard to produce at high temperatures, which is why many mammals have external testes that keep their sperm cool, and birds also have sperm cooling mechanisms. But how will ectotherms cope if they are exposed to increasing temperatures as climate change progresses? I am trying to find out, using a variety of fruit fly species.

I also work on how fertility, particularly male fertility, can be damaged by high temperatures. Many organisms, including important crop plants, pollinating insects, farm animals and even humans, lose fertility at temperatures far lower than their lethal limits. However, we really know very little about why this occurs, and have only recently begun exploring the consequences. Given the warming of the planet, infertility caused by heat stress may have major consequences for conservation, agriculture, and the spread of disease. It amazes me that there are species that can remain fertile in the hottest deserts, while closely related species lose fertility at temperatures seen in summer in England. Why are some species so vulnerable?

I am trying to understand this at every level, from the genes and proteins that protect fertility at high temperatures, to the impacts on population dynamics, to the evolutionary theory that might explain why fertility is so vulnerable. Are males particularly affected? Are aquatic species more or less vulnerable than land species? How quickly can species evolve increased resistance to high temperatures? I believe we urgently need to answer these questions if we are going to maintain agriculture and conserve species in a warming world.

I co-founded the European Thermal Fertility Network to unite researchers interested in these questions. If you are interested in this, please check us out at https://thermal-fertility-network-eseb.com/

If you are interested in joining, please email me!