Reversibility of peroxisomal differentiation in higher plants.

已知高等植物细胞中的过氧化物酶体根据细胞类型在功能上有分化。通过对拟南芥全基因组过氧化物酶体基因的全面调查，我们发现286个过氧化物酶体候选基因。它们包括了迄今为止报道的所有过氧化物酶酶基因，其中大多数编码过氧化物酶体中功能未知的蛋白质。基因表达谱分析表明，过氧化物酶体分化是由特定器官中诱导的特定基因的表达引起的，而不是由组成性表达基因引起的。聚类分析表明，过氧化物酶体的基本功能是β-氧化、H_2O_2降解、支链氨基酸分解代谢和一些未知的功能，幼苗、子叶、叶片和根中的过氧化物酶体是通过器官特异性表达基因分化的。在其中一种突变体apm1中，过氧化物酶体变长，数量减少，这显然是分裂受到抑制的结果。我们发现APM1编码DRP3A（动力蛋白相关蛋白3A），并且APM1/DRP3A的突变也会导致线粒体形态的异常。瞬时表达分析表明，DRP3A与过氧化物酶体的细胞质侧相关。这些发现表明，在高等植物中，相同的动力蛋白分子参与过氧化物酶体和线粒体的分裂。通过对apm2和apm4突变体的分析，我们确定了apm2和apm4基因分别编码过氧化物酶13 （PEX13）和PEX12，并揭示了它们与过氧化物酶体膜上的pts2以及pts1依赖蛋白有关。

Peroxisomes in higher plantcells are known to differentiate in function depending on the cell type. By a comprehensive survey of peroxisomal genes in the entire Arabidopsis genome, we found 286 candidates of peroxisomal genes. They included all genes for peroxisomal enzymes reported up to date, and most of them encoded functionally unknown proteins in peroxisomes. Analyses of gene expression profiles revealed that peroxisomal differentiation is caused by the expression of specific genes that are induced in specific organs in addition to constitutively expressed genes. The clustering analyses suggested that basic functions of peroxisomewereβ-oxidation, H_2O_2 degradation, branched chain amino acid catabolism and some unknown functions, and that peroxisomesinseedlings, cotyledons, leavesand roots were differentiated by organ-specific expressed genes.In one of these mutants, apm1, the peroxisomes are long and reduced in number, apparently as a result of inhibition of division. We showed that APM1 encodes DRP3A (dynamin-related protein 3A), and that mutations in APM1/DRP3A also caused aberrant morphology of mitochondria. The transient expression analysis showed that DRP3A is associated with the cytosolicsideofperoxisomes. Thesesfindingsindicate that the same dynamin molecule is involved in peroxisomal and mitochondrialdivision in higherplants.From analyses of apm2 and apm4 mutants which are difectiveinproteintransportbyPTS1-dependent pathway, we determined that APM2 and APM4 genes encode PEROXIN13 (PEX13) and PEX12, respectively, and revealed that they are responsible for PTS2-as well as PTS1-dependent protein on the peroxisomal membrane.