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过氧化物酶体的维持依赖于从头形成过氧化物酶体,这在酵母分裂和遗传缺陷的过氧化物酶体突变体中是缺陷的。

Peroxisome Maintenance Depends on De Novo Peroxisome Formation in Yeast Mutants Defective in Peroxisome Fission and Inheritance.

机构信息

Molecular Cell Biology, Groningen Biomolecular Sciences and Biotechnology Institute (BBA), University of Groningen, PO Box 11103, 9300 CC Groningen, The Netherlands.

出版信息

Int J Mol Sci. 2019 Aug 17;20(16):4023. doi: 10.3390/ijms20164023.

Abstract

There is an ongoing debate on how peroxisomes form: by growth and fission of pre-existing peroxisomes or de novo from another membrane. It has been proposed that, in wild type yeast cells, peroxisome fission and careful segregation of the organelles over mother cells and buds is essential for organelle maintenance. Using live cell imaging we observed that cells of the yeast , lacking the peroxisome fission protein Pex11, still show peroxisome fission and inheritance. Also, in cells of mutants without the peroxisome inheritance protein Inp2 peroxisome segregation can still occur. In contrast, peroxisome fission and inheritance were not observed in cells of a double deletion strain. In buds of cells of this double mutant, new organelles likely appear de novo. Growth of cells on methanol, a growth substrate that requires functional peroxisomes, is retarded relative to the wild type control. Based on these observations we conclude that in de novo peroxisome formation is a rescue mechanism, which is less efficient than organelle fission and inheritance to maintain functional peroxisomes.

摘要

关于过氧化物酶体如何形成,一直存在争议:是通过先前存在的过氧化物酶体的生长和分裂,还是从头在另一种膜上形成。有人提出,在野生型酵母细胞中,过氧化物酶体的分裂和细胞器在母细胞和芽之间的精细分离对于细胞器的维持是必不可少的。通过活细胞成像,我们观察到缺乏过氧化物酶体分裂蛋白 Pex11 的酵母细胞仍然显示出过氧化物酶体的分裂和遗传。此外,在没有过氧化物酶体遗传蛋白 Inp2 的突变体细胞中仍然可以发生过氧化物酶体的分离。相比之下,在双缺失菌株的细胞中没有观察到过氧化物酶体的分裂和遗传。在这个双突变体的芽细胞中,新的细胞器可能是从头出现的。与野生型对照相比,在甲醇上生长的细胞(甲醇是一种需要功能性过氧化物酶体的生长基质)的生长速度较慢。基于这些观察结果,我们得出结论,在 中,从头形成过氧化物酶体是一种挽救机制,其效率低于细胞器的分裂和遗传,以维持功能性过氧化物酶体。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8003/6719073/c0b28a6d6442/ijms-20-04023-g001.jpg

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