Lingard Matthew J, Trelease Richard N
School of Life Sciences, Arizona State University, PO Box 874501, Tempe, AZ 85287-4501, USA.
J Cell Sci. 2006 May 1;119(Pt 9):1961-72. doi: 10.1242/jcs.02904.
Pex11 homologs and dynamin-related proteins uniquely regulate peroxisome division (cell-cycle-dependent duplication) and proliferation (cell-cycle-independent multiplication). Arabidopsis plants possess five Pex11 homologs designated in this study as AtPex11a, -b, -c, -d and -e. Transcripts for four isoforms were found in Arabidopsis plant parts and in cells in suspension culture; by contrast, AtPex11a transcripts were found only in developing siliques. Within 2.5 hours after biolistic bombardments, myc-tagged or GFP-tagged AtPex11 a, -b, -c, -d and -e individually sorted from the cytosol directly to peroxisomes; none trafficked indirectly through the endoplasmic reticulum. Both termini of myc-tagged AtPex11 b, -c, -d and -e faced the cytosol, whereas the N- and C-termini of myc-AtPex11a faced the cytosol and matrix, respectively. In AtPex11a- or AtPex11e-transformed cells, peroxisomes doubled in number. Those peroxisomes bearing myc-AtPex11a, but not myc-AtPex11e, elongated prior to duplication. In cells transformed with AtPex11c or AtPex11d, peroxisomes elongated without subsequent fission. In AtPex11b-transformed cells, peroxisomes were aggregated and rounded. A C-terminal dilysine motif, present in AtPex11c, -d and -e, was not necessary for AtPex11d-induced peroxisome elongation. However, deletion of the motif from myc-AtPex11e led to peroxisome elongation and fission, indicating that the motif in this isoform promotes fission without elongation. In summary, all five overexpressed AtPex11 isoforms sort directly to peroxisomal membranes where they individually promote duplication (AtPex11a, -e), aggregation (AtPex11b), or elongation without fission (AtPex11c, -d).
Pex11 同源物和发动蛋白相关蛋白独特地调节过氧化物酶体分裂（细胞周期依赖性复制）和增殖（细胞周期非依赖性倍增）。拟南芥植物拥有五个在本研究中命名为 AtPex11a、-b、-c、-d 和 -e 的 Pex11 同源物。在拟南芥植物各部分和悬浮培养细胞中发现了四种异构体的转录本；相比之下，仅在发育中的角果中发现了 AtPex11a 转录本。在生物弹道轰击后 2.5 小时内，带有 myc 标签或 GFP 标签的 AtPex11a、-b、-c、-d 和 -e 分别从细胞质直接分选到过氧化物酶体；没有一个通过内质网间接运输。带有 myc 标签的 AtPex11b、-c、-d 和 -e 的两个末端都面向细胞质，而 myc-AtPex11a 的 N 端和 C 端分别面向细胞质和基质。在 AtPex11a 或 AtPex11e 转化的细胞中，过氧化物酶体数量翻倍。那些带有 myc-AtPex11a 而不是 myc-AtPex11e 的过氧化物酶体在复制前伸长。在用 AtPex11c 或 AtPex11d 转化的细胞中，过氧化物酶体伸长但随后没有分裂。在 AtPex11b 转化的细胞中，过氧化物酶体聚集并呈圆形。存在于 AtPex11c、-d 和 -e 中的 C 端双赖氨酸基序对于 AtPexIId 诱导的过氧化物酶体伸长不是必需的。然而，从 myc-AtPex11e 中删除该基序会导致过氧化物酶体伸长和分裂，表明该异构体中的基序促进分裂而不伸长。总之，所有五个过表达的 AtPex11 异构体都直接分选到过氧化物酶体膜上，在那里它们分别促进复制（AtPex11a、-e）、聚集（AtPex11b）或伸长而不分裂（AtPex11c、-d）。
