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野生型和玫瑰色突变型黑腹果蝇中的过氧化物酶体。

Peroxisomes in wild-type and rosy mutant Drosophila melanogaster.

作者信息

Beard M E, Holtzman E

机构信息

Department of Biological Sciences, Columbia University, New York, NY 10027.

出版信息

Proc Natl Acad Sci U S A. 1987 Nov;84(21):7433-7. doi: 10.1073/pnas.84.21.7433.

DOI:10.1073/pnas.84.21.7433
PMID:3118368
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC299310/
Abstract

This study shows that peroxisomes are abundant in the Malpighian tubule and gut of wild-type Oregon R Drosophila melanogaster and that the peroxisomal population of the rosy-506 eye-color mutant differs from that of the wild type. Catalase activity in wild-type flies is demonstrable in bodies of appearance and centrifugal behavior comparable to the peroxisomes of vertebrate tissues. Xanthine oxidase (xanthine:oxygen oxidoreductase, EC 1.1.3.22) activity of the Malpighian tubule of wild-type flies is demonstrable cytochemically in bodies like those containing catalase. The rosy-506 mutant flies, with a deletion in the structural gene for xanthine dehydrogenase (xanthine:NAD+ oxidoreductase, EC 1.1.1.204), lack cytochemically demonstrable peroxisomal xanthine oxidase activity. In addition, peroxisomes in the rosy-506 mutants show less intense cytochemical staining for catalase than those in wild-type flies, and biochemical assays indicate that catalase in the rosy mutant is much more accessible to substrate in the absence of detergent than in the wild type. Thus, the rosy-506 mutation appears to affect peroxisomes and may mimic aspects of the defects of peroxisomes in some human metabolic disorders.

摘要

本研究表明,过氧化物酶体在野生型俄勒冈R黑腹果蝇的马氏管和肠道中大量存在,并且玫瑰红-506眼色突变体的过氧化物酶体群体与野生型不同。野生型果蝇中的过氧化氢酶活性在外观和离心行为与脊椎动物组织的过氧化物酶体相当的物体中是可证实的。野生型果蝇马氏管的黄嘌呤氧化酶(黄嘌呤:氧氧化还原酶,EC 1.1.3.22)活性在含有过氧化氢酶的物体中通过细胞化学方法可证实。玫瑰红-506突变果蝇在黄嘌呤脱氢酶(黄嘌呤:NAD +氧化还原酶,EC 1.1.1.204)的结构基因中有缺失,缺乏细胞化学可证实的过氧化物酶体黄嘌呤氧化酶活性。此外,玫瑰红-506突变体中的过氧化物酶体对过氧化氢酶的细胞化学染色强度低于野生型果蝇,并且生化分析表明,在没有去污剂的情况下,玫瑰红突变体中的过氧化氢酶比野生型更容易接近底物。因此,玫瑰红-506突变似乎影响过氧化物酶体,并且可能模拟某些人类代谢紊乱中过氧化物酶体缺陷的某些方面。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/393e94c857e5/pnas00336-0085-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/1a03e4301bfc/pnas00336-0084-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/0568b1b557f4/pnas00336-0084-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/0065c2b646e5/pnas00336-0084-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/8a5e0acd45c9/pnas00336-0085-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/393e94c857e5/pnas00336-0085-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/1a03e4301bfc/pnas00336-0084-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/0568b1b557f4/pnas00336-0084-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/0065c2b646e5/pnas00336-0084-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/8a5e0acd45c9/pnas00336-0085-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc12/299310/393e94c857e5/pnas00336-0085-b.jpg

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Dysfunctional peroxisomes compromise gut structure and host defense by increased cell death and Tor-dependent autophagy.功能失调的过氧化物酶体通过增加细胞死亡和 Tor 依赖性自噬来损害肠道结构和宿主防御。
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