Department of Biology, University of Missouri, St. Louis, Missouri 63121, USA.
Plant Physiol. 2010 Dec;154(4):1602-15. doi: 10.1104/pp.110.162479. Epub 2010 Oct 25.
PEX5 and PEX7 are receptors required for the import of peroxisome-bound proteins containing one of two peroxisomal targeting signals (PTS1 or PTS2). To better understand the role of PEX5 in plant peroxisomal import, we characterized the Arabidopsis (Arabidopsis thaliana) pex5-10 mutant, which has a T-DNA insertion in exon 5 of the PEX5 gene. Sequencing results revealed that exon 5, along with the T-DNA, is removed in this mutant, resulting in a truncated pex5 protein. The pex5-10 mutant has germination defects and is completely dependent on exogenous Suc for early seedling establishment, based on poor utilization of seed-storage fatty acids. This mutant also has delayed development and reduced fertility, although adult pex5-10 plants appear normal. Peroxisomal metabolism of indole-3-butyric acid, propionate, and isobutyrate also is disrupted. The pex5-10 mutant has reduced import of both PTS1 and PTS2 proteins, and enzymatic processes that occur in peroxisomes are disrupted. To specifically study the import and importance of PTS1 proteins, we made a truncated PEX5 construct lacking the PTS1-binding region (PEX5(454)). Transformation of this construct into pex5-10 resulted in the rescue of PTS2 import, thereby creating a line with PTS1-specific import defects. The pex5-10 (PEX5(454)) plants still had developmental defects, although restoring PTS2 import resulted in a less severe mutant phenotype. Comparison of pex5-10 and pex5-10 (PEX5(454)) phenotypes can separate the import mechanisms for enzymes acting in different peroxisomal processes, including indole-3-butyric acid/2,4-dichlorophenoxybutyric acid oxidation, isobutyrate and propionate metabolism, and photorespiration.
PEX5 和 PEX7 是将含有两种过氧化物酶体靶向信号(PTS1 或 PTS2)之一的过氧化物酶体结合蛋白导入过氧化物酶体所需的受体。为了更好地了解 PEX5 在植物过氧化物酶体导入中的作用,我们对拟南芥(Arabidopsis thaliana)pex5-10 突变体进行了特征描述,该突变体在 PEX5 基因的外显子 5 中插入了 T-DNA。测序结果表明,该突变体中外显子 5 和 T-DNA 均被切除,导致截短的 pex5 蛋白。pex5-10 突变体的萌发缺陷以及完全依赖外源蔗糖来建立早期幼苗,这是基于种子储存脂肪酸的利用不良。尽管成年 pex5-10 植物看起来正常,但该突变体的发育也延迟且育性降低。吲哚-3-丁酸、丙酸盐和异丁酸盐的过氧化物酶体代谢也被打乱。pex5-10 突变体的 PTS1 和 PTS2 蛋白导入减少,并且过氧化物酶体中发生的酶过程被打乱。为了专门研究 PTS1 蛋白的导入和重要性,我们构建了一个缺失 PTS1 结合区域的截短 PEX5 构建体(PEX5(454))。将该构建体转化到 pex5-10 中导致 PTS2 导入的恢复,从而产生具有 PTS1 特异性导入缺陷的品系。pex5-10(PEX5(454))植物仍存在发育缺陷,尽管恢复 PTS2 导入导致突变表型不那么严重。pex5-10 和 pex5-10(PEX5(454))表型的比较可以分离作用于不同过氧化物酶体过程的酶的导入机制,包括吲哚-3-丁酸/2,4-二氯苯氧丁酸氧化、异丁酸和丙酸盐代谢以及光呼吸。