Dealing with salt stress in animal cells: The role and regulation of glycine betaine concentrations

Abstract

AbstractGlycine betaine is the end product of a two step oxidation of choline. Although glycine betaine is a common osmolyte in the cells of many species, the mechanism(s) regulating its synthesis in response to hyperosmotic stress has not been thoroughly studied in animals. We localized glycine betaine production in the mitochondrial matrix of cardiac cells from the horseshoe crab (Limulus polyphemus). Isolated Limulus mitochondria take up choline and convert it to glycine betaine. The uptake rate is stimulated by exposure to hyperosmotic medium and mediated in part by a Na+‐dependent, high affinity transporter. The increased choline concentrations in hyperosmotically stressed mitochondria result in increased glycine betaine concentrations. Thus, choline transport by Limulus mitochondria is the rate‐limiting step in glycine betaine synthesis. Oysters (Crassostrea virginica) appear to have a different regulatory strategy. Oysters from the Atlantic Ocean accumulate more glycine betaine than oysters from the Chesapeake Bay when hyperosmotically stressed. Gill mitochondria isolated from both oyster populations take up choline at similar rates. However, the Atlantic Coast oyster mitochondria synthesize 3–4 times as much glycine betaine as their Bay counterparts. Thus, in oysters, the regulatory step may be at the level of the synthetic enzymes. © 1994 Wiley‐Liss, Inc.