SUMO and cellular adaptive mechanisms

Stress response: how cells wrestle with SUMO disruption Cellular stress caused by disrupting attachment of the ubiquitous small ubiquitin-like modifier (SUMO) proteins, which are present in most organisms and regulate numerous DNA processes and stress responses by attaching to key proteins, results...

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Main Authors: Hong-Yeoul Ryu, Seong Hoon Ahn, Mark Hochstrasser
Format: Article
Language:English
Published: Nature Publishing Group 2020-06-01
Series:Experimental and Molecular Medicine
Online Access:https://doi.org/10.1038/s12276-020-0457-2
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spelling doaj-e284bab50fa64d9ab5b52117e9c0a65e2021-06-27T11:44:52ZengNature Publishing GroupExperimental and Molecular Medicine1226-36132092-64132020-06-0152693193910.1038/s12276-020-0457-2SUMO and cellular adaptive mechanismsHong-Yeoul Ryu0Seong Hoon Ahn1Mark Hochstrasser2School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, College of National Sciences, Kyungpook National UniversityDepartment of Molecular and Life Science, College of Science and Convergence Technology, Hanyang UniversityDepartment of Molecular Biophysics and Biochemistry, Yale UniversityStress response: how cells wrestle with SUMO disruption Cellular stress caused by disrupting attachment of the ubiquitous small ubiquitin-like modifier (SUMO) proteins, which are present in most organisms and regulate numerous DNA processes and stress responses by attaching to key proteins, results in some remarkable adaptations. Mark Hochstrasser at Yale University, New Haven, USA, and co-workers review how this “sumoylation” is reversed by protease enzymes, and how imbalances between sumoylation and desumoylation may be linked to diseases including cancer. When certain SUMO proteases are deliberately disrupted, the cells quickly become aneuploid, i.e., carry an abnormal number of chromosomes. These cells show severe growth defects, but over many generations they regain the normal number of chromosomes. They also undergo genetic changes that promote alternative mechanisms that compensate for losing the SUMO protease and facilitate the same efficient stress responses as the original cells.https://doi.org/10.1038/s12276-020-0457-2
collection DOAJ
language English
format Article
sources DOAJ
author Hong-Yeoul Ryu
Seong Hoon Ahn
Mark Hochstrasser
spellingShingle Hong-Yeoul Ryu
Seong Hoon Ahn
Mark Hochstrasser
SUMO and cellular adaptive mechanisms
Experimental and Molecular Medicine
author_facet Hong-Yeoul Ryu
Seong Hoon Ahn
Mark Hochstrasser
author_sort Hong-Yeoul Ryu
title SUMO and cellular adaptive mechanisms
title_short SUMO and cellular adaptive mechanisms
title_full SUMO and cellular adaptive mechanisms
title_fullStr SUMO and cellular adaptive mechanisms
title_full_unstemmed SUMO and cellular adaptive mechanisms
title_sort sumo and cellular adaptive mechanisms
publisher Nature Publishing Group
series Experimental and Molecular Medicine
issn 1226-3613
2092-6413
publishDate 2020-06-01
description Stress response: how cells wrestle with SUMO disruption Cellular stress caused by disrupting attachment of the ubiquitous small ubiquitin-like modifier (SUMO) proteins, which are present in most organisms and regulate numerous DNA processes and stress responses by attaching to key proteins, results in some remarkable adaptations. Mark Hochstrasser at Yale University, New Haven, USA, and co-workers review how this “sumoylation” is reversed by protease enzymes, and how imbalances between sumoylation and desumoylation may be linked to diseases including cancer. When certain SUMO proteases are deliberately disrupted, the cells quickly become aneuploid, i.e., carry an abnormal number of chromosomes. These cells show severe growth defects, but over many generations they regain the normal number of chromosomes. They also undergo genetic changes that promote alternative mechanisms that compensate for losing the SUMO protease and facilitate the same efficient stress responses as the original cells.
url https://doi.org/10.1038/s12276-020-0457-2
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