ming-che-shihuiowaedu

There are two projects ongoing in my laboratory, which focus on hypoxia signaling mechanisms and on the functional genomics of β-glucosidase and β-galactosidase gene families in Arabidopsis thaliana. Our web site (http://www.biology.uiowa.edu/
arabidopsis/) provides regularly-updated information on the functional genomic project. Below is a brief summary of our research project on the hypoxia signaling mechanisms in Arabidopsis Two major metabolic adjustments are made in Arabidopsis in response to hypoxia stress: (1) the primary carbon metabolism is switched from aerobic respiration to alcoholic fermentation; and (2) the production of ethylene is increased throughout the duration of hypoxia. The increased ethylene triggers a number of cellular responses, including the cell death in leaves. Using a novel genetic approach, we have obtained a class of mutants that are defective in regulating the expression of the ADH gene, which encodes the enzyme alcohol dehydrogenase, during seed germination. We have characterized three recessive mutants, aar1-1, aar2-1, and aar3-1, which belong to three different complementation groups (that is, they define three different genes). Mutations in all three AAR genes affect hypoxia induction of ADH. In addition, mutations in the three AAR genes also affect the induction of ADH by cold stress, but with different organ specificity. Based on these results and other studies, we propose that aar1 and aar2 mutations affect later steps of the hypoxia signaling pathways. We have recently isolated a new class of mutants that are defective in hypoxia responses in mature plants. These mutants are designated hpd (hypoxia defective). We found that four of the twelve Arabidopsis ACS genes, which encode the enzyme ACC synthase that is involved in the biosynthesis of the hormone ethylene, could also be induced during hypoxia. We have examined the patterns of hypoxia induction of ADH and ACS in aar, hpd, and wild-type plants. The results suggest that mutations in aar3 and hpd4 might affect early steps of the hypoxia signaling pathways. Furthermore, our results also indicate that two parallel signaling pathways, one ethylene-dependent and the other ethylene-independent, are triggered during hypoxia. Since these are the first mutations in the hypoxia signal transduction pathway to be isolated, we are in a position to be a leader in the studies of plant response to low oxygen stress. We are currently using map-based cloning strategies to isolate AAR and HPD genes, defined by these mutations. Information on the identity of these genes would allow us, for the first time, to gain insight on the oxygen sensing mechanism and on how the hypoxia signal is transduced in plants.