The effects of ABA on channel-mediated K(+) transport across higher plant roots.

The transport and accumulation of K(+) in higher plant roots is regulated by ABA. Molecular and electrophysiological techniques have identified a number of discrete transporters which are involved in the translocation of K(+) from the soil solution to the shoots of higher plants. Furthermore, recent reports have shown that ABA regulates K(+) channel activity in maize and Arabidopsis roots which suggests that ABA regulation of K(+) transport in roots is, at least in part, ion channel-mediated. The signalling processes which underlie the ABA regulation of K(+) channels have been investigated. The effects of ABA on the membrane potential of intact maize root cells were also studied. It was found that ABA regulated the membrane potential of root cells and that this regulation is consistent with the hypothesis that ABA-induced K(+) accumulation in roots is mediated by K(+) channels.

Alterations in the actin cytoskeleton of pollen tubes are induced by the self-incompatibility reaction in Papaver rhoeas.

Self-incompatibility (SI) is a genetically controlled process used to prevent self-pollination. In Papaver rhoeas, the induction of SI is triggered by a Ca(2)+-dependent signaling pathway that results in the rapid and S allele-specific inhibition of pollen tube tip growth. Tip growth of cells is dependent on a functioning actin cytoskeleton. We have investigated the effect of self-incompatibility (S) proteins on the actin cytoskeleton in poppy pollen tubes. Here, we report that the actin cytoskeleton of incompatible pollen tubes is rapidly and dramatically rearranged during the SI response, not only in our in vitro SI system but also in vivo. We demonstrate that nonspecific inhibition of growth does not result in similar actin rearrangements. Because the SI-induced alterations are not observed if growth stops, this clearly demonstrates that these alterations are triggered by the SI signaling cascade rather than merely resulting from the consequent inhibition of growth. We establish a detailed time course of events and discuss the mechanisms that might be involved. Our data strongly implicate a role for the actin cytoskeleton as a target for signaling pathways involved in the SI response of P. rhoeas.