| Description: | In higher eukaryotes, the regulation of programmed cell death (pcd) and cell growth is often coupled. Using a dominant gain-of-function mutation in the Arabidopsis ACD6 gene, we recently showed that plants, like animals, have coupled regulation of cell death and cell growth responses (Rate et al., Plant Cell 11, 1695-1708, 1999). acd6-1 plants show constitutive activation of cell death, cell growth and pathogen defenses and require at least two signals that act together to achieve these phenotypes. One of these signal molecules is salicylic acid (SA). Our goal is to determine the identity of the second signal and determine how it acts with SA to regulate cell fate. SA is absolutely required for the regulation of defenses in plants and it is sometimes required for the regulation of cell death. Until now, SA was not known to play a clear role in cell growth responses. Removal of SA from acd6 plants using a nahG transgene, whose product metabolizes SA, completely suppresses all the acd6 phenotypes. The acd6-conferred phenotypes are restored and hyperactivated by treatment of the acd6nahG plants with low levels a synthetic analogue of SA. Activation of the SA pathway does not induce cell death or cell growth in wild type plants. This led us to propose that SA acts with a second signal to regulate these cell fate changes. Because reactivation of the SA pathway hyperactivates the acd6 phenotypes, SA likely negatively regulates the second signal.s level or activity. Using the microarray technology could point us to candidate genes and pathways that are regulated by the second signal. In acd6nahG plants, the second signal should be building up so that when we reactivate the SA pathway, we get a hyperactivated response. By comparing the gene expression patterns from nahG and nahGacd6 plants, we will identify SA-independent genes regulated by the second pathway. If the regulatory signal is already known for these genes, then we will be in a position to directly test the interaction between it and SA in inducing cell growth and cell death. We believe that to interpret this experiment, it needs to be accompanied by a comparison between nahG and wild type, to establish what pathways that are acd6-independent might be affected by the SA pathway. This is basic information that would be useful for the community of researchers interested in SA-dependent responses. Our experiments require RNA prepared from the following leaf samples: acd6nahG, nahG, wild type (Columbia) |
NASCArrays Information at The BAR
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