Poster: Transcription Regulation
Abs #
1048: Molecular characterization of the phosphoenolpyruvate-carboxylase kinase (PpcK) multigene family in soybean (Glycine max)
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Presenter: |
Chollet, Raymond , rchollet1@unl.edu |
Authors | Chollet, Raymond (A) Xu, Wenxin (A) | | Affiliations: |
(A): Biochemistry Department, University of Nebraska-Lincoln
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Various isoforms of plant phosphoenolpyruvate carboxylase (PEPC [Ppc]) are controlled posttranslationally by an intricate interaction between allosteric regulation and reversible protein phosphorylation. In leaves and legume root-nodules, these changes in PEPC phosphorylation-state are governed primarily by PEPC-kinase (PpcK), a novel, "minimal but functional" Ser/Thr kinase. As an important extension of our earlier biochemical studies on this kinase and PEPC phosphorylation in soybean nodules, we analyzed in molecular and biochemical terms the first legume PpcK (accession AY143660; Plant J. (2003) 34, in press), which encodes a functional, 31.0-kDa nodule-enhanced PpcK (NE-PpcK). Besides displaying organ, developmental and spatial expression properties that are strikingly up-regulated in mature nodules, this transcript's expression pattern is distinct from that of a second soybean PpcK isogene (GmPpcK, accessions AY143661/AF203479). The up-/down-regulation of NE-PpcK transcript level by photosynthate supply from the shoots occurs in concert with corresponding changes in nodule PpcK activity, the phosphorylation-state of PEPC, and the abundance of a previously identified, nodule-enhanced transcript (GmPEPC7) that encodes the target enzyme (NE-Ppc). These and recent findings with Arabidopsis implicate the existence of multiple PpcK-Ppc "expression-partners" in plants. Following the appearance of a third soybean PpcK ORF (GmPpcK3, accession AY144184) in the NCBI database, we analyzed its transcript pattern, which was quite similar but not identical to that of NE-PpcK. To further elucidate the regulation and expression of these G. max PpcK isogenes, the expression of reporter genes such as GUS and/or GFP driven by the various PpcK promoters will be investigated.