One of the biggest welfare issues facing commercial chickens, and in particular layer chickens, is bone health and the risk of fractures, and in particular keel bone fracture. This is due to a blend of issues – bone health is intrinsically linked to egg production, but housing types can also have an effect, and most vitally, genotype can also outweigh all of the above factors. One of the biggest improvements to general bone health has come with the shift from indoor to outdoor environments, however this also leads to an increase in keel bone fractures, to the extent that keel bone fracture is now the largest welfare issue facing layer breeds. Given how density and housing regulations are changing and are shifting towards more outdoor environments where possible, the ability to select for genes that have the greatest effect in specific environments can have the potential for greatly positively impacting bird welfare. To perform, this we require the ability to map genotype x environment interactions in an intercross between a commercial White layer (Bovans Robust/ Deklab White) and a commercial Brown layer (Bovans Brun), and then the ability to actually identify the specific causal genes in the specific cell types, with the specific polymorphisms that underlie them. This will allow actual and tangible enhancements to the keel bone health and welfare to be made through the selection of these specific polymorphisms in commercial-bred flocks.

This will be performed using a selection of intercrosses between the two principal layer breeds (Deklab White and Bovans Brun), complemented by additional studies using free-living feral birds. Commercial White and Brown layers have over 100 years of separation between one another, and each line has specific strengths and weaknesses relating to egg production and longevity/ sociality. Therefore the intercross population will maintain a higher degree of genetic diversity, and allow the identification of genetic loci that yield specific enhancements to keel bone strength in specific environments, in each breed. These results will be complemented by genetic mapping in the feral population, which acts as a counter-point with ideal free-range and density conditions. In addition to post-mortem bone measurements, a variety of behavioural and physiological phenotypes will also be recorded, allowing the identification of specific behaviours and physiological parameters that may predispose to keel bone damage and that can also be selected upon. Finally, these results will be used with in collaboration with our industry partner Hendrix Genetics, to select on the relevant haplotypes and assess the increase in keel bone fracture resistance and production in a commercially relevant setting.

Group members: Gaia Resmini

The predominant view on brain-to-body ratio has for a long time been that there is an allometric relationship between brain and body size, i.e. that you need a certain brain size to maintain a certain body size. However, my group's research has shown that in chickens it is possible to independently select genes for brain size and body size. For example, domestic animals have often been thought of as somewhat less smart, and when one looks at their brain-to-body ratio they have a lower ratio than their wild progenitor.

By looking at the underlying genetic architecture for brain mass and body mass, however, my group has discovered that domestic chickens actually have larger, not smaller, brains than their wild counterparts.  Thus brain size and body size can be decoupled, and it is possible to select for a larger birds without selecting for a larger brain. This can have large repercussions in terms of evolutionary biology, as relative brain size (that is brain size over body size) is often used to compare different species.

If it is possible to select for increased body size without selecting for increased brain size, this method may be flawed. Further to this, by looking at individual substructures of the brain, it is possible to pinpoint the regions that are most associated with domestication selection – in the case of the chicken, the cerebellum seems to be particularly enlarged in the domestic bird.

Group members: Rie Henriksen

Plumage colouration in birds is important for a plethora of reasons, ranging from camouflage, sexual signalling, and species recognition. The genes underlying colour variation have been vital in understanding how genes can affect a phenotype. Multiple genes have been identified that affect plumage variation, but research has principally focused on major-effect genes (such as those causing albinism, barring, and the like), rather than the smaller effect modifier loci that more subtly influence colour. By utilising a domestic x wild advanced intercross with a combination of classical QTL mapping of red colouration as a quantitative trait and a targeted genetical genomics approach, we have identified five separate candidate genes (CREBBP, WDR24, ARL8A, PHLDA3, LAD1) that putatively influence quantitative variation in red-brown colouration in chickens. Such small effect loci are potentially far more prevalent in wild populations, and can therefore potentially be highly relevant to colour evolution. We are now also studying the genetic basis of structural colour, and in particular the genetic regulation of structural iridescence. This structural iridescence refers to the 'metallic' colours that are actually caused by reflecting light waves back in a very focused direction, via the arrangement of layers in the feather and the structural organisation of the (black) melanosomes. To perform this, we are using a population of feral chickens with a wide variation in this type of colour, and also Transmission Electron Microscopy to accurately measure the cellular organisation of these feathers.