The yeast Hansenula polymorpha contains four members of the Pex23 family of peroxins, which characteristically contain a DysF domain. Here we show that all four H. polymorpha 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 PEX24 or PEX32 – and to a much lesser extent, of PEX23 or PEX29 – 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 pex3 atg1 deletion cells.

多形汉逊酵母含有过氧化物酶 Pex23 家族的四个成员，其特征是含有 DysF 结构域。在这里，我们展示了所有四种多形菌Pex23 家族蛋白都定位于内质网 (ER)。Pex24 和 Pex32，但不是 Pex23 和 Pex29，主要在过氧化物酶体-ER 接触处积累。删除PEX24或PEX32（以及较小程度的PEX23或PEX29）后，过氧化物酶体 - ER 接触就会丢失，并伴随着过氧化物酶体基质蛋白输入、膜生长以及细胞器增殖、定位和分离的缺陷。这些缺陷通过引入人工过氧化物酶体-ER 系链得到抑制，表明 Pex24 和 Pex32 有助于过氧化物酶体与 ER 的系链。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丢失，同时接触也会受到破坏。这表明 Pex11 有助于 Pex32 依赖性过氧化物酶体-ER 接触的形成。Pex32 的缺失对pex3 atg1缺失细胞中出现的前过氧化物酶体囊泡没有重大影响。