| First Author | Hayashi M | Year | 2000 |
| Journal | EMBO J | Volume | 19 |
| Issue | 21 | Pages | 5701-10 |
| PubMed ID | 11060021 | Mgi Jnum | J:65672 |
| Mgi Id | MGI:1927034 | Doi | 10.1093/emboj/19.21.5701 |
| Citation | Hayashi M, et al. (2000) AtPex14p maintains peroxisomal functions by determining protein targeting to three kinds of plant peroxisomes. EMBO J 19(21):5701-10 |
| abstractText | We previously isolated an ARABIDOPSIS: peroxisome-deficient ped2 mutant by its resistance to 2,4-dichlorophenoxybutyric acid. Here, we describe the isolation of a gene responsible for this deficiency, called the PED2 gene, by positional cloning and confirmed its identity by complementation analysis. The amino acid sequence of the predicted protein product is similar to that of human Pex14p, which is a key component of the peroxisomal protein import machinery. Therefore, we decided to call it AT:Pex14p. Analyses of the ped2 mutant revealed that AT:Pex14p controls intracellular transport of both peroxisome targeting signal (PTS)1- and PTS2-containing proteins into three different types of peroxisomes, namely glyoxysomes, leaf peroxisomes and unspecialized peroxisomes. Mutation in the PED2 gene results in reduction of enzymes in all of these functionally differentiated peroxisomes. The reduction in these enzymes induces pleiotropic defects, such as fatty acid degradation, photorespiration and the morphology of peroxisomes. These data suggest that the AT:Pex14p has a common role in maintaining physiological functions of each of these three kinds of plant peroxisomes by determining peroxisomal protein targeting. |
