ULTRAVIOLET-B-INDUCED RESPONSES IN ARABIDOPSIS-THALIANA - ROLE OF SALICYLIC-ACID AND REACTIVE OXYGEN SPECIES IN THE REGULATION OF TRANSCRIPTS ENCODING PHOTOSYNTHETIC AND ACIDIC PATHOGENESIS-RELATED PROTEINS
Sl. Surplus et al., ULTRAVIOLET-B-INDUCED RESPONSES IN ARABIDOPSIS-THALIANA - ROLE OF SALICYLIC-ACID AND REACTIVE OXYGEN SPECIES IN THE REGULATION OF TRANSCRIPTS ENCODING PHOTOSYNTHETIC AND ACIDIC PATHOGENESIS-RELATED PROTEINS, Plant, cell and environment, 21(7), 1998, pp. 685-694
Supplementary UV-B was shown to lead to a decrease in transcripts enco
ding the photosynthetic genes Lhcb and psbA and a concomitant increase
in transcripts encoding three acid-type pathogenesis-related proteins
, PR-1, PR-2 and PR-5, in Arabidopsis thaliana, UV-B radiation has bee
n reported to lead to the generation of reactive oxygen species (ROS),
Here we report that ROS are required for UV-B-induced down-regulation
of the photosynthetic genes and up-regulation of PR genes, as the add
ition of antioxidants before W-B treatment resulted in a marked reduct
ion in the effect of UVB on both sets of gents. Rises in ROS are frequ
ently accompanied by increases in salicylic acid (SA) accumulation. UV
-B treatment of transgenic NahG Arabidopsis plants, which are unable t
o accumulate SA, showed that the increase in PR transcripts, but not t
he decrease in photosynthetic transcripts, was dependent on the increa
se in SA, In addition, a 3 d exposure to UV-B radiation resulted in a
7-fold increase in SA levels. Oxidant treatment of NahG plants indicat
ed that ROS could not up-regulate PR genes in the absence of SA accumu
lation; however, the down-regulation of photosynthetic transcripts was
unchanged from that in wild-type plants. The results indicate that th
e effects of UV-B on the two sets of genes are mediated through two di
stinct signal tranduction pathways. One pathway is ROS-dependent but S
A-independent and mediates the down-regulation of photosynthetic genes
. The other is SA- and ROS-dependent and mediates the up-regulation of
the acidic-type PR genes.