Wu Fei, de Boer Rinse, Krikken Arjen M, Akşit Arman, Bordin Nicola, Devos Damien P, van der Klei Ida J
Molecular Cell Biology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, 9300CC Groningen, The Netherlands.
Centro Andaluz de Biología del Desarrollo, CSIC, Universidad Pablo de Olavide, Carretera de Utrera, Km.1, Seville 41013, Spain.
J Cell Sci. 2020 Aug 17;133(16):jcs246983. doi: 10.1242/jcs.246983.
The yeast contains four members of the Pex23 family of peroxins, which characteristically contain a DysF domain. Here we show that all four Pex23 family proteins localize to the endoplasmic reticulum (ER). Pex24 and Pex32, but not Pex23 and Pex29, predominantly accumulate at peroxisome-ER contacts. Upon deletion of or - and to a much lesser extent, of or - peroxisome-ER contacts are lost, concomitant with defects in peroxisomal matrix protein import, membrane growth, and organelle proliferation, positioning and segregation. These defects are suppressed by the introduction of an artificial peroxisome-ER tether, indicating that Pex24 and Pex32 contribute to tethering of peroxisomes to the ER. Accumulation of Pex32 at these contact sites is lost in cells lacking the peroxisomal membrane protein Pex11, in conjunction with disruption of the contacts. This indicates that Pex11 contributes to Pex32-dependent peroxisome-ER contact formation. The absence of Pex32 has no major effect on pre-peroxisomal vesicles that occur in deletion cells.
该酵母含有过氧化物酶体生物发生因子23（Pex23）家族的四个成员，其特征是含有一个DysF结构域。在此我们表明，所有四个Pex23家族蛋白都定位于内质网（ER）。Pex24和Pex32主要在内质网与过氧化物酶体的接触点积累，而Pex23和Pex29则不然。缺失Pex24或Pex32以及在较小程度上缺失Pex23或Pex29后，内质网与过氧化物酶体的接触会丧失，同时伴有过氧化物酶体基质蛋白输入、膜生长以及细胞器增殖、定位和分离方面的缺陷。通过引入人工内质网与过氧化物酶体连接体，这些缺陷得以抑制，这表明Pex24和Pex32有助于内质网与过氧化物酶体的连接。在缺乏过氧化物酶体膜蛋白Pex11的细胞中，Pex32在这些接触位点的积累会丧失，同时接触也会被破坏。这表明Pex11有助于依赖Pex32的内质网与过氧化物酶体接触的形成。Pex32的缺失对Pex24缺失细胞中出现的前过氧化物酶体小泡没有重大影响。
