Despite the fast growing knowledge about the components of the signalling pathways involved in the activation of drought-, cold-, osmotic stress- and salt-responsive genes, relatively little is known about the sensor types responsible for the induction of the pathways. It is thought that different signals have their own cognate receptors which independently, or in cooperation, initiate a downstream signalling cascade (Xiong and Zhu 2002). On the other hand, the stress level-dependent activation of different receptors has been proposed in plants responding to osmotic stress (Munnik and Meijer 2001). The question arises as to whether the activation of different signalling systems will depend on the nature of the sensors or on the stress-induced primary event, which may differ in cells subjected to moderate or severe stress. In this article, a discussion is given of the available literature data concerning this controversial question. It is proposed that, in plants responding to mild stress, a disturbance of water balance is the primary stress-induced event affecting the cell wall–plasma membrane interactions, resulting in the activation of receptor-like kinases, including wall-associated kinases, cytoskeleton-related mechanosensors, stretch-dependent ion (calcium) channels and redox-mediated systems. The mild stress-sensing systems, assisted by an increased supply of abscisic acid, seem to be involved in the activation of the pathways that enable the adjustment of plant growth and metabolism to the stressful conditions, i.e. allowing acclimation. Severe or suddenly acting stressors are sensed by membrane destabilization (membrane depolarization, alterations in ion transport systems), which results in the triggering of phospholipid signalling. This may lead to the increased production of reactive oxygen species, the accumulation of H2O2, lipid peroxidation and increased synthesis of hormones such as jasmonates and ethylene. These are characteristic features of the alarm situation, which may result in irreversible injury and cell death, or in cell recovery, depending on stress impact.