Photo: Collected
A multi-faceted approach combining genetics, nutrition, rearing practices, and housing design is required to improve skeletal health and enhance the welfare and sustainable performance of laying hens.
That was the message from Professor Ian Dunn of The Roslin Institute and Royal (Dick) School of Veterinary Studies at the University of Edinburgh when he recently delivered the UK branch of the World Poultry Society’s Gordon Memorial lecture.
In the lecture, which has now been published in the British Poultry Science journal, Dunn reviewed the issue of bone quality in laying hens from a genetic perspective, noting the irony that the transition from cages to non-cage environments had increased keel bone damage, despite improving overall skeletal health.
It is a welfare paradox that improving the hen’s environment through legislation – as seen in the US and EU – has often been accompanied by greater skeletal damage.
To tackle the paradox, Dunn said it is possible to take a number of approaches with scientists saying the constructed environment can be adapted to reduce the damage of transitions; the bird itself could be bred to have a stronger skeleton and there are behavioural traits that could be potentially selected. Nutrition must also be considered.
Importance of laying hen bone health
In his presentation, Dunn said laying hen bone health has been an issue going back to Darwin in 1868, but the recent problem of keel bone health has reached the European Parliament, resulting in questioning of breeding practices for laying hens.
Hens in multi-tier housing have more damage to their keel bones than those in single-tier housing. The issue is also seen in free-range organic production.
Keel bone damage – too many eggs?
It is not the number of eggs that hens lay that is an issue, but simply the fact that they lay eggs, said Dunn. Looking at historical data, there were no genetic correlations between a range of bone quality traits and the number of eggs hens laid.
Puberty
Genetic studies have demonstrated that it is not the number of eggs laid, but rather the timing of puberty, measurable as the onset of egg laying, that is clearly important in determining skeletal health. However, in other research, looking at hens that laid brown eggs, no effect of puberty was apparent, so it can’t be recognized as a factor in all cases.
Genetics and nutrition
Decades of work have been devoted to understanding the genetic contribution to bone quality in laying hens. As the pace of genetic tool delivery has quickened, association studies have been possible using single nucleotide polymorphisms (SNP) that fine-map the loci in the pure line and allow tracking through successive generations.
One genetic region has been pinpointed with a relatively small number of genetic markers that defined 2 different haplotypes. It has been possible to use bone samples from haplotypes that had a large difference in bone quality to compare the expression of genes, so-called transcriptomics.
Having access to large populations has enabled the control of variables that are known to alter bone quality. This includes the time of day, which influences egg formation and, therefore, the status of the bone, to get hens that were similar physiologically but their genotype at the genome location differed. Only a small number of genes were different between the 2 genotypes.
Enzymes
One of them stood out in terms of its significance and that was an enzyme cystathionine beta synthase. This gene was located within the region of the chromosome that had already been identified as the location of the effect. This was strong evidence that this gene was likely to be causative for the observed difference in bone quality between the genotypes and its substrate, homocysteine, was found to differ between the haplotypes.
Homocysteine is known in hindsight to potentially affect bones, but cystathionine-β-synthase was not a gene that would necessarily have ever been identified as being a cause of differences in bone quality.
Cystathionine-β-synthase is an important component of the one-carbon pathway, as it is central to cell metabolism. Its substrate, homocysteine, is an amino acid but is not used directly in protein synthesis. It does, however, inhibit the actions of cross-linking between cysteine bonds by inhibiting lysyl oxidase expression and enzyme activity through the formation of homocysteine thiolactone. Cross-linking is important for the quality of collagen. The collagen matrix is the structure in which mineralization occurs and gives plastic or ductile properties to bone.
Next steps
What can be done with this information? Most studies go no further than listing what genes may differ between different states, he said. Few studies have identified a causative gene for a trait. In this case, it has been possible to both demonstrate a functional effect and provide a potential nutritional solution.
Cystathionine-β-synthase is involved in the conversion of homocysteine into cystathionine as part of the one-carbon pathway and, given a large amount of biochemistry in this pathway, it is possible to manipulate it to reduce its concentration.
The re-methylation of homocysteine into methionine, which is a limiting amino acid, should reduce homocysteine concentrations. Betaine, or trimethylamine, is a proven feed additive that facilitates the re-methylation of homocysteine to methionine which reduces the concentrations of homocysteine. The hypothesis that reducing homocysteine by feeding betaine would improve bone quality has been tested. The concentration of homocysteine was reduced and bone-breaking strength and density were higher when hens were fed betaine. Going from basic genetics, it has been possible to work through an inexpensive method to improve bone quality.
Conclusions
In the review, Dunn presented a genetic perspective on improving bone quality, and direct genetic selection can work. A practical phenotype is key to progress, and there is finally one method based on tibiatarsus density on live hens.
This may need further development or simplification. Efforts are being made to automate aspects of the process, and it is hoped that poultry breeders will embrace the opportunity to reduce bone damage with this or better methods. This will be a key step in improving the future sustainability of the industry.
Research to improve bone quality should target traits that have good evidence for being important and measurable. Bone quality can be measured directly, although correlated traits, such as age at puberty or body weight, which is, in part, a consequence of age at puberty, are all measurable and have known effects on bone quality. There is little proven support for the hypothesis that an increase in the number of eggs produced by modern hens is the cause of poor bone quality.
Using genetics to find the genes controlling bone quality is not a waste of time if it brings knowledge of function which might lead to innovative solutions. Cystathionine-β-synthase has led to new nutritional interventions and there are many other genome locations awaiting exploration for controlling bone quality.
Nobel Prize-winning biologist Sidney Brenner said “There is a gene for every scientist”, and there is certainly a genetic loci for every scientist. Understanding the consequences of these loci will potentially bring resolutions to important issues. The genetic markers associated with cystathionine-β-synthase alone could improve flock bone strength by 6-18% (and there is plenty of evidence that genomic selection would be possible for bone quality, which can help make the task easier as this technology is now widely used.
Genetics has provided solutions, but it is not the only solution, as rearing, nutrition, and housing design are all important. A comprehensive approach will be needed to optimize the welfare of the future long-life layer under conditions that consumers and retailers are increasingly demanding.
Source: Email/GFMM
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