Hyperosmotic stress induces the myo‐inositol pathway by several orders of magnitude in tilapia (Oreochromis mossambicus) gill epithelium

Abstract

Myo‐inositol (MI) biosynthesis from glucose is one mechanism by which organisms can accumulate compatible organic osmolytes to counteract hyperosmotic stress. Here we show that the entire MI pathway is strongly induced by hyperosmotic stress in tilapia gill epithelium. We found that the second enzyme of this two‐step pathway, inositol monophosphatase (IMPA), is strongly up‐regulated by hyperosmotic stress at the protein level as shown by online LCMS. Using quantitative real‐time PCR we have investigated the level of induction of the MI biosynthesis pathway in gill epithelium after acclimating tilapia acutely and gradually from fresh water to either 34, 70 or 90 ppt salinity. Two distinct myo‐inositol‐phosphate synthase (MIPS) transcripts of the same gene showed similarly high levels of mRNA up‐regulation during all types of hyperosmotic stress. While only a single MIPS gene was found we detected at least two distinct IMPA genes in the tilapia genome. The IMPA1 gene that was highly up‐regulated after hyperosmotic stress at the protein level was also found highly up‐regulated at the mRNA level during all types of hyperosmotic stress. In contrast, IMPA2 was not up‐regulated suggesting that it lacks osmoresponsive enhancers. We conclude that the MI biosynthesis pathway represents a major hyperosmotic stress coping mechanism for euryhaline fish such as tilapia. Supported by NSF grant IOS‐1049780.