Poster: Intracellular Signaling

Abs # 830: Hypoxia signal transduction and oxygen sensing mechanism in Arabidopsis

Presenter:	Shih, Ming-Che , mcshih@blue.weeg.uiowa.edu
Authors	Shih, Ming-Che  (A)   Lin, Ter-yun  (A)   Peng, Hsiao-Ping  (A)   Chou, Shu-Jen  (B)   Wu, Shu-Hsing  (B)
Affiliations:	(A): Department of Biological Sciences, University of Iowa, Iowa City, Iowa 52242, USA (B): Botany Institute, Academia Sinica, Nankang, Taipei 11529, Taiwan

We are investigating the hypoxia signaling mechanisms in Arabidopsis thaliana. We have isolated two different classes of mutants, designated aar (allyl alcohol resistant) and hpd (hypoxia defective), that are defective in the hypoxic induction of the ADH gene that encodes alcohol dehydrogenase. We found that two signaling pathways are triggered during hypoxia. One pathway leads to the activation of ADH and the other leads to the induction of several ACS(ACC synthase) genes, which encode a key enzyme in ethylene biosynthesis. Our results show that aar3-1 and hpd4 are defective in early signaling steps before the divergence of the ethylene-dependent and ethylene-independent pathways, whereas aar1 and aar2 are defective in late steps of the ethylene-independent pathway. Map-based cloning of AAR3 is nearing completion. How do plant cells sense oxygen deficiency? The lack of oxygen results in a rapid inhibition of oxidative phosphorylation in mitochondria and therefore a decrease in cellular ATP, an increase in NADH, and changes in a number of cellular metabolites. We propose that plant cells perceive oxygen deficiency by sensing the changes in some of these cellular metabolites in the initial stage of hypoxia. We will present results showing that a decrease in the cellular ATP level and an increase in H₂O₂ level in the early stage of hypoxia may trigger downstream signaling events. To identify additional components in hypoxia signaling pathways, we performed microarray analysis to compare gene expression profiles of wild-type and the hpd4 mutant. The results allowed us to identify several transcription factors that are induced during hypoxia. We are currently examining the effects of T-DNA knockout mutations of these transcription factors on hypoxic responses.