It is known that cells under stress accumulate various dinucleoside polyphosphates, compounds suggested to function as alarmones. In plants, the phenylpropanoid pathways yield metabolites protecting these organisms against various types of stress. Observations reported in this communication link these two phenomena and provide an example of a metabolic “addressee” for an “alarm” signaled by diadenosine triphosphate (Ap3A) or diadenosine tetraphosphate (Ap4A). In response to added Ap3A or Ap4A, seedlings of Arabidopsis thaliana incubated in full nutrition medium increased both the expression of the genes for and the specific activity of phenylalanine ammonia-lyase and 4-coumarate:coenzyme A ligase, enzymes that control the beginning of the phenylpropanoid pathway. Neither adenine mononucleotides (AMP, ADP or ATP) nor adenosine evoked such effects. Reactions catalyzed in vitro by these enzymes were not affected by Ap3A or Ap4A.

Short-term treatment of potato (Solanum tuberosum L.) tuber discs with CdCl 2 solution elevated both the StPCS1 transcript level, phytochelatin synthase (PCS) activity and contents of phytochelatin (PC) and abscisic acid (ABA). Similar effects but less marked were noticed after treatment of tuber tissues with ABA solution. Cd-treatment increased also cysteine (CYS) content but did not change glutathione content. If ABA treatment preceded Cd-treatment, the elevation of CYS and PC contents were limited. The data suggest the participation of ABA in the regulation of PCS.

Treatment of potato (Solanum tuberosum) plants with cadmium or abscisic acid (ABA) enhanced the content of StPCS1 transcript and activity of phytochelatin synthase (PCS) in roots. These treatments enhanced the contents of ABA and expression of genes coding 9-cis-epoxycarotenoid dioxygenase 1 (NCED1) and basic leucine zipper (b-ZIP). Simultaneous treatment of potato plants with Cd and fluridone (Flu), an inhibitor of ABA biosynthesis, completely halted the Cd-induced transcription of StPCS1, NCED1, and StbZIP genes and limited the increases in PCS activity and ABA content. The data suggest that ABA participates in transduction of the Cd signal to the cells of potato roots.

Key words." C a d m i u m , Gh_tthatione, H y d r o g e n peroxide, O x i d a t i v e stress, Phytochclatins, SoZJ, m.m~ mbero,vwn L. AbstractShort-tcm~ treatment of potato tuber (Solcmum tuber(~sum L.} discs wi@ CdC12 (imM) induced all oxidative stress, manifested by higher levels o{I I:-O,, and aclivated the sym'hesi~ of phytochclath~s ((;/--G hL Cys)n-Gly): PC2, 1<'.3 and PCa. l fin the tissues with a bwer GSH level, the oxidative slress was induccd by h-eminent with 3 amhmtriazo] (AT), or with AT arid H:~O2, the Ncv~don or HaO~ and GSI{ levels and lhen some :i

Two barley genotypes, cultivar Aramir and line R567, were subjected to water stress for 24 hours by immersing their roots in polyethylene glycol (PEG 6000) solution of osmotic potential -1.0 MPa. The relative water content (RWC) in the leaves of both genotypes lowered under the stress conditions. Reduction of RWC led to membrane disorganization, which is evidenced by the injury index data. The injury index was lower in the leaves of cv. Aramir as compared with line R567. The level of lipid peroxidation decreased under stress conditions in the leaves of both genotypes. Hydrogen peroxide content also decreased in the leaves of stressed plants relative to the control ones. The decrease was higher in line R567 and was accompanied by a decrease in ascorbic acid level in the leaves of that genotype. In the leaves of cv. Aramir water stress did not affect the ascorbic acid content. The examined genotypes showed little or no changes in the activity of ascorbic acid peroxidase in the response to water stress. No evidence of an increase in the level of oxidative stress during water depletion in studied genotypes was seen. Water stress-induced decrease in the level of hydrogen peroxide without an increase in the activity of ascorbic acid peroxidase indicate that other mechanisms may be involved in the detoxification of hydrogen peroxide