High impact information on APX2

• The mutant regulator of APX2 1-1 (rax1-1) was identified in Arabidopsis thaliana that constitutively expressed normally photooxidative stress-inducible ASCORBATE PEROXIDASE2 (APX2) and had >/=50% lowered foliar glutathione levels [1].
• This signal, which preceded the photooxidative burst of hydrogen peroxide (H2O2) associated with photoinhibition of photosynthesis, resulted in a rapid increase (within 15 min) in mRNA levels of two cytosolic ascorbate peroxidase genes (APX1 and APX2) [2].
• In the HsfA2-overexpressing Arabidopsis (Pro(35S):HsfA2) plants, 46 genes, including a large number of heat-shock proteins, ascorbate peroxidase 2 and galactinol synthase 1 and 2, were highly expressed compared with those in the wild-type plants [3].
• Thus, the weak induction of APX2 expression in wounded leaves may require H(2)O(2) and PET only [4].
• Signalling pathways dependent upon jasmonic acid (JA), chitosan and ABA were not involved in the wound-induced expression of APX2, but were shown to require PET and were preceded by a depressed rate of CO(2) fixation [4].

Biological context of APX2

• This regulation of APX2 may reflect a functional organisation of the leaf to resolve two conflicting physiological requirements of protecting the sites of primary photosynthesis from ROS and, at the same time, stimulating ROS accumulation to signal responses to changes in the light environment [5].
• Imaging of chlorophyll fluorescence and the production of reactive oxygen species (ROS) indicated that APX2 expression followed a localised increase in hydrogen peroxide (H2O2) resulting from photosynthetic electron transport in the bundle sheath cells [5].
• By deletion analysis the promoter region of the strongest affected target gene APX2 was functionally mapped in detail to verify potential HsfA2 binding sites [6].
• Singlet oxygen and superoxide production were found to be primarily located in mesophyll tissues whereas hydrogen peroxide accumulation and APX2 gene expression were primarily localized in the vascular tissues [7].
• We have applied a genetic approach to understanding the mechanisms of photoprotection, using APX2 as an indicator of oxidative stress [8].

Anatomical context of APX2

• Our data suggest that Apx2 is a novel heat shock gene and that the enzymatic activity of APX2/APX(S) is required to compensate heat stress-dependent decline of APX1 activity in the cytosol [9].

Associations of APX2 with chemical compounds

• ABA appears to augment the role of H2O2 in initiating APX2 expression [5].
• Abscisic acid stimulated APX2 expression [5].

Other interactions of APX2

• In Arabidopsis leaves, high light stress induces rapid expression of a gene encoding a cytosolic ascorbate peroxidase (APX2), whose expression is restricted to bundle sheath cells of the vascular tissue [5].
• Exposure of ABA-insensitive mutants (abi1-1, abi2-1) to excess light resulted in reduced levels of APX2 expression and confirmed a role for ABA in the signalling pathway [5].
• On the other hand, the native ELIP2 gene as well as the APX2 gene was activated by the hydrogen peroxide [10].

References