Ej klar.
The noble crayfish, Astacus astacus is both an important food commodity and a key component of freshwater ecosystems in many European countries. This species was once widely distributed in Sweden, but is now at risk of extinction because of crayfish plague disease outbreaks. The crayfish plague is caused by a parasitic fungus, Aphanomyces astaci, which is carried by the North American signal crayfish as a subclinical infection but it is acutely pathogenic to the noble crayfish. The noble crayfish has significant economic value for Sweden and other North European countries. However, crayfish plague remains a major hindering factor in the successful production of noble crayfish in an aquaculture setting.
For designing efficient anti-infective strategies against plague in noble crayfish, it is vital to understand the mechanisms by which animals acquire resistance against this pathogen. The resistance mechanisms of the signal crayfish against plague are the result of a long co-evolutionary history between host and pathogen. However, noble crayfish has not yet acquired resistance against the plague in nature, except a few individuals under laboratory conditions. In signal crayfish, a known reason behind plague resistance is the animals ability to restrict the colonization of the pathogen to the cuticle and joints by the process of melanization - an innate immune response. However, melanization in noble crayfish occurs at a much slower rate compared to signal crayfish and, therefore, animals are highly prone to the fungal infection.
A previous study conducted on the crustacean Artemia model, showed that in response to environmental cues, modifications of the epigenetic marks led to a significant change in the expression of immune-related genes, and to the development of resistant phenotypes, both within and across generations. Our hypothesis is that epigenetic programming of the immune-related genes might be an important mechanism behind increased plague resistance.
This study aims at identifying the genetic and epigenetic factors underlying resistance against A. astaci fungal infection. This will allow development of molecular markers behind the two resistant and susceptible phenotypes in signal crayfish and noble crayfish, respectively. Furthermore, it will form the basis for studies focusing on elucidating the molecular mechanisms for innate immune activation in crayfish in particular and crustaceans in general.
Task 1: Whole-genome sequencing of signal and noble crayfish to identify genetic variants that can be used to genotype resistant signal crayfish and susceptibile noble crayfish species towards A. astaci (0-12 months).
Task 2: Whole-genome bisulfite sequencing analysis for assessing the differences in the resistance level between signal and noble crayfish towards A. astaci (6-12 months)
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