Oxidative burst in Chenopodium rubrum suspension cells:

Abstract

Lowering of the osmotic value of the medium has been tive compound tested, giving maximum rates of indicator reported previously to induce an oxidative burst in plant oxidation corresponding to the formation of 4 ×10 − 15 mol cells. This has been explained by a sequence of events, in-H 2 O 2 cell − 1 min − 1 . Auxin analogous (10 mM) exhibited cluding solute influx, cellular swelling and the activation of the following order of effectiveness: 4-chloride indoleacetic stretch-regulated channels, triggering the production of reac-acid (100%), indoleacetic acid (80%), 2,4-dichlorophenoxyacetic acid (75%), 2-naphthylacetic acid (52%) and 1-naph-tive oxygen species. Moreover, it is known that the plant growth hormone auxin induces protoplast swelling. Together, thylacetic acid (47%). Benzoic acid (23%) was used as a these findings prompted the hypothesis that plant cells can control. Fusicoccin (35%) showed only slight stimulation in conjunction with complex kinetics. The detection of oxida-respond to auxin-treatment with an oxidative burst. We tested this hypothesis using suspension cultured cells from tive burst responses to 10 nM indoleacetic acid revealed a high sensitivity of the assay for auxin. Cell-free medium Chenopodium rubrum L. and 2,7-dichlorodihydrofluorescein from aged batch cultures and light were also found to stimu-as the indicator for reactive oxygen species. An auxin-inlate the production of reactive oxygen species. These data duced oxidative burst was found similar to an osmotically induced burst. Osmotic treatment consisted of a shift from indicate that reactive oxygen species can transduce and integrate developmental and environmental signals and thus play 110 mOsm to 40 mOsm. The naturally occurring haloa general role in plant growth regulation. genated auxin 4-chloroindole-3-acetic acid was the most acfast elongation growth. In fact, it has been reported that auxin increases swelling of oat coleoptile protoplasts by 40% (Keller and Van Volkenburgh 1996). However, it is known that the isolation of protoplasts changes some physiological properties of the cells like membrane potential (Assmann et al. 1985, Barbier-Brygoo et al. 1991 and membrane lipid content (Webb and Williams 1984). Thus, a parameter to follow auxin action in intact plant cells could give further insight. In this context the finding of an osmotically induced oxidative burst in intact soybean cells (Yahraus et al. 1995) is of interest. It can lead to the working hypothesis that auxin-induced swelling mentioned before (Keller and Van Volkenburgh 1996) may be associated with an osmotically induced oxidative burst in plant cells.

Clustering of Microarray Data Reveals Transcript Patterns Associated with Somatic Embryogenesis in Soybean,

“…Although all the intermediates of the response to auxin are not known, it is established that 2,4-D and light can induce an oxidative burst in the target tissue by generating reactive oxygen species (ROS; Pfeiffer and Hoftberger, 2001). Consistent with these findings, we observed many genes, characteristic of a response to oxidative burst, up-regulated in the cotyledons during the first 14 d on 2,4-D (Fig.…”

“…It suggests that an oxidative burst, most probably caused by 2,4-D (Pfeiffer and Hoftberger, 2001), occurs during the development of somatic embryos and might lead to PCD of certain cells (Fig. 6).…”

Components of apoplastic ascorbate use in Betula pendula leaves exposed to CO2 and O3 enrichment

“…Similarly, from (Schraudner et al, 1998, their Fig. 2 (Pfeiffer & Höftberger, 2001). Spotty H 2 O 2 accumulation in cell walls and on plasma membrane has also been observed in Betula pendula leaves under acute exposure to 150 ppb O 3 (Pellinen et al, 1999).…”

Induction of somatic embryogenesis as an example of stress-related plant reactions

“…Although not all of the intermediates of the auxin response are known, it is established that 2,4-D and light are able to induce an oxidative burst in the target tissue by generating ROS (Pfeiffer and Höftberger, 2001). The drastic changes in the cellular environment of the in vitro culture, induced by a 'stressor' in the culture medium or in the physical environment of the culture, are responsible for reprogramming of gene expression.…”