Life in extreme environments: adaptation and evolution of a soda lake cichlid; Alcolapia alcalica

Alcolapia are the only vertebrates to survive the harsh conditions of Lake Natron, this requires multiple adaptations. Due to their evolution under extreme conditions they present themselves as naturally occurring biological experiments and potential model organisms in the study of adaptation to change and evolution under stressful conditions.
Alcolapia are reportedly the only 100% ureotelic teleost, unable to excrete ammonia due to their high pH environment. Lab acclimated A. alcalica are not 100% ureotelic as previously reported, although most waste is still excreted as urea. To accommodate this the ornithine urea enzyme, carbamoyl-phosphate synthetase (CPS), has evolved in function and expression. Usually isolated to liver tissue, in Alcolapia it is found in muscle and convergently evolved in function to bind ammonia, as done by terrestrial vertebrates, rather than fish CPS which binds glutamate. A proportion of A. alcalica nitrogenous waste was excreted as ammonia, with the ammonia transporters rhesus glycoproteins acting to move ammonia in two orthologous systems. These proteins have potentially evolved to move ammonia against a concentration gradient.
Protocols were adapted and good husbandry established for Alcolapia, and although no gene editing technology was effective, A. alcalica are clearly an interesting study animal. Differences in gene structure and gene expression were notable when comparing A. alcalica to model species. The presence of a poly-serine region within the MyoD1 protein of A. alcalica and other non-model species shows more information could be gained with more access to non-model species. This region was only present in the MyoD1 of species which retain a MyoD2 gene. Preliminary analysis suggests this region increases protein stability. Pax-6, Pax-6-like and Pax-10 show spatiotemporal subfunctionalisation of expression across the developing eye and nervous system of A. alcalica. MyoD1 and MyoD2 also show subfunctionalisation within muscle tissue showing a likely conserved function of these genes.