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Plant Physiology Preview Published on August 17, 2007; 10.1104/pp.107.103432
OPEN ACCESS ARTICLE
Received June 8, 2007 AtHIPM, an Ortholog of the Apple HrpN-interacting Protein, Is a Negative Regulator of Plant Growth and Mediates the Growth-enhancing Effect of HrpN in Arabidopsis
Department of Plant Pathology, Cornell University, Ithaca, NY 14853, USA * Corresponding author; email: svb1{at}cornell.edu.
HrpN (harpin) protein is critical to the virulence of the fire blight pathogen, Erwinia amylovora, in host plants like apple. Moreover, exogenous treatment of Arabidopsis, a non-host plant, with partially purified HrpN enhances growth. To address the bases of the effects of HrpN in disease, we sought a HrpN-interacting protein(s) in apple, using a yeast two-hybrid assay. A single positive clone, designated HIPM (HrpN-interacting protein from Malus) was found. HIPM, a 6.5-kDa protein, interacted with HrpN in yeast and in vitro. Deletion analysis showed that the N-terminal 198 of 403 amino acids of HrpN are required for interaction with HIPM. HIPM orthologs were found in Arabidopsis thaliana (AtHIPM) and Oryzae sativa, rice (OsHIPM). HrpN also interacted with AtHIPM in yeast and in vitro. In silico analyses revealed that the three plant proteins contain putative signal peptides and putative transmembrane domains. We showed that both HIPM and AtHIPM have functional signal peptides and GFP-tagged HIPM and AtHIPM associated, in clusters, with plasma membranes. Both HIPM and AtHIPM are expressed constitutively; however, they are expressed more strongly in apple and Arabidopsis flowers than in leaves and stems. The size of AtHIPM knock-out mutants of Arabidopsis was slightly larger than the wild-type plants. Interestingly, the knock-out mutant did not exhibit enhanced plant growth in response to treatment with HrpN. Over-expression of AtHIPM conversely resulted in smaller plants. These results indicate that AtHIPM functions as a negative regulator of plant growth and mediates enhanced growth that results from treatment with HrpN.
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