ABIOTIC STRESS SIGNALLING IN THE FUCUS EMBRYO

Abstract

Fucoid algae live in the intertidal region where they experience daily fluctuations in light and external osmotic environment. High light, especially in combination with ultraviolet (UV) radiation and hyper-osmotic stress affected the cellular physiology of Fucus embryos. Two photoinhibition responses were recognised. Firstly, a rapid decline of the photosystem II (PSII) efficiency, linked with the operation of the xanthophyl cycle, followed by a slower decline correlated with reactive oxygen species (ROS) production. As a result of enhanced ROS production, a slower repair of the PSII efficiency was observed, particularly with increased UV-B doses. Development of the embryos was transiently affected by UV-B. The cellular signal transduction pathway during hyper-osmotic stress was investigated. ROS production in response to hyperosmotic stress comprised two distinct components. The first ROS component coincided closely with the origin of a Ca2+ wave in the peripheral cytosol at the growing cell apex, had an extracellular origin, and was necessary for the Ca2+ wave. Patch clamp experiments showed that a non-selective cation channel was stimulated by H2O2, and may underlie the initial cytosolic Ca2+ elevation. The spatio-temporal pattern of the Ca2+ wave was thus determined by peripheral ROS production. The second, later ROS component localised to the mitochondria and was a direct consequence of the Ca2+ wave. The first, but not the second component was required for short-term adaptation to osmotic stress, probably through the activity of cell wall bromoperoxidases. Mitogen-activated protein kinases may be involved in the hyper-osmotic stress response downstream or independently of the mitochondrial ROS production.