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235 Ethylene Signaling Components Are Involved in Polycyclic Aromatic Hydrocarbon Stress<br />

Responses in Arabidopsis thaliana<br />

Adan Colon-Carmona, Merianne Alkio, David Weisman<br />

University of Massachusetts-Boston<br />

With the growing awareness of hazardous polycyclic aromatic hydrocarbons (PAHs) to humans, the interest in<br />

plant responses to these environmental pollutants is increasing. We studied ethylene signaling in plant PAH stress by 1)<br />

analyzing stress responses of Arabidopsis mutants, defective in different components of the ethylene-signaling pathway,<br />

to the model PAH, phenanthrene; 2) studying ethylene-inducible gene expression in PAH-exposed GUS-reporter plants<br />

and 3) comparing global gene expression changes of PAH- and ethylene-exposed plants. Results: 1) PAH-exposed wild<br />

type plants (wt) had shorter hypocotyls and roots than wt grown on control medium. However, growth of some ethylene<br />

insensitive mutants (etr1-1, ers2-1, ein2, ein6) was even more inhibited by PAH than that of wt, whereas constitutive<br />

ethylene signaling mutants (eto3, ctr1-1, and the triple mutants etr1-6xetr2-3xein4-4 and etr2-3xers2-3xein4-4) generally<br />

appeared resistant to the inhibition of organ elongation, and often even had longer roots on PAH than on control medium.<br />

The mutants did not differ from wt in respect to PAH-induced oxidative stress. However, compared to wt, the rosettes<br />

ctr1-1 and etr1-7 were more reduced in size and more chlorotic, indicating greater PAH sensitivity. 2) After PAHexposure,<br />

GUS expression was slightly induced in chitinase-GUS plants but strongly induced in GSTF2-GUS plants. 3)<br />

DNA microarray analyses (our own, and published data) support the view that parts of the ethylene signaling pathway<br />

are involved in the PAH response, although ethylene signaling pathway as a whole is not switched on. We conclude that<br />

while PAH stress signaling in plants overlaps <strong>with</strong> other signaling pathways, it involves a unique subset of the known<br />

molecular players as well as unidentified cellular components.<br />

Funded by NSF-IBN 0343856<br />

236 The Magnitude of Phosphate-Starvation Responses is Determined by the Rate of Plant<br />

Growth and Cell Division<br />

Fan Lai, Peter Doerner<br />

Edinburgh University<br />

Plants require adequate and balanced quantities of mineral nutrients for optimal growth, but such conditions are rarely<br />

found in nature. For example phosphate (Pi) is required for RNA and DNA synthesis, phospho-lipids, in intermediate<br />

energy metabolism and to regulate protein function. We examined the relationship between Pi starvation responses and<br />

plant growth. To assess Pi starvation responses, we quantified gene expression responses of a set of Pi-responsive genes.<br />

When plant growth was globally enhanced, e.g. by supply of sugars, Pi starvation responses were enhanced. We examined<br />

whether this was a nutrient-specific effect or caused by altered growth magnitude. When plant growth was selectively<br />

inhibited (e.g by osmotic stress) starvation responses were significantly reduced. Selective growth inhibition (for example<br />

of root growth by elevated nitrogen supply) led to reduced Pi starvation responses in roots. These data show that the<br />

magnitude of Pi starvation responses is determined by the demand for phosphate. We found that the magnitude of cell<br />

proliferation, not cell expansion was responsible for setting phosphate demand. Moreover, starvation responses appear<br />

to be controlled organ autonomously. This is in contrast to previous suggestions that plant phosphate status is sensed<br />

in the shoot (Burleigh and Harrison 1999). We propose a model in which growth control networks regulating meristem<br />

activity and therefore shoot-root mass ratios, which then sets the level of demand for phosphate in plant organs. Altered<br />

allocation of growth potential, e.g. by altering carbon-nitrogen ratios, is independent of phosphate nutritional status and<br />

dominates over phosphate starvation-induced growth responses.<br />

Burleigh, S. H. and M. J. Harrison (1999). Plant Physiology 119: 241-248.

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