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Bmi1 regulates mitochondrial function and the DNA damage response pathway.

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Title: Bmi1 regulates mitochondrial function and the DNA damage response pathway.
Authors: Liu, Jie, Cao, Liu, Chen, Jichun, Song, Shiwei, Lee, In Hye, Quijano, Celia, Liu, Hongjun, Keyvanfar, Keyvan, Chen, Haoqian, Cao, Long-Yue, Ahn, Bong-Hyun, Kumar, Neil G., Rovira, Ilsa I., Xu, Xiao-Ling, van Lohuizen, Maarten, Motoyama, Noboru, Deng, Chu-Xia, Finkel, Toren
Source: Nature. 5/21/2009, Vol. 459 Issue 7245, p387-392. 6p. 1 Color Photograph, 3 Graphs.
Subjects: Mitochondria, DNA damage, Genetic repressors, Stem cell research, Phenotypes, Active oxygen in the body, Laboratory mice, Metabolic regulation
Abstract: Mice deficient in the Polycomb repressor Bmi1 develop numerous abnormalities including a severe defect in stem cell self-renewal, alterations in thymocyte maturation and a shortened lifespan. Previous work has implicated de-repression of the Ink4a/Arf (also known as Cdkn2a) locus as mediating many of the aspects of the Bmi1-/- phenotype. Here we demonstrate that cells derived from Bmi1-/- mice also have impaired mitochondrial function, a marked increase in the intracellular levels of reactive oxygen species and subsequent engagement of the DNA damage response pathway. Furthermore, many of the deficiencies normally observed in Bmi1-/- mice improve after either pharmacological treatment with the antioxidant N-acetylcysteine or genetic disruption of the DNA damage response pathway by Chk2 (also known as Chek2) deletion. These results demonstrate that Bmi1 has an unexpected role in maintaining mitochondrial function and redox homeostasis and indicate that the Polycomb family of proteins can coordinately regulate cellular metabolism with stem and progenitor cell function. [ABSTRACT FROM AUTHOR]
Copyright of Nature is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: <searchLink fieldCode="AR" term="%22Liu%2C+Jie%22">Liu, Jie</searchLink><br /><searchLink fieldCode="AR" term="%22Cao%2C+Liu%22">Cao, Liu</searchLink><br /><searchLink fieldCode="AR" term="%22Chen%2C+Jichun%22">Chen, Jichun</searchLink><br /><searchLink fieldCode="AR" term="%22Song%2C+Shiwei%22">Song, Shiwei</searchLink><br /><searchLink fieldCode="AR" term="%22Lee%2C+In+Hye%22">Lee, In Hye</searchLink><br /><searchLink fieldCode="AR" term="%22Quijano%2C+Celia%22">Quijano, Celia</searchLink><br /><searchLink fieldCode="AR" term="%22Liu%2C+Hongjun%22">Liu, Hongjun</searchLink><br /><searchLink fieldCode="AR" term="%22Keyvanfar%2C+Keyvan%22">Keyvanfar, Keyvan</searchLink><br /><searchLink fieldCode="AR" term="%22Chen%2C+Haoqian%22">Chen, Haoqian</searchLink><br /><searchLink fieldCode="AR" term="%22Cao%2C+Long-Yue%22">Cao, Long-Yue</searchLink><br /><searchLink fieldCode="AR" term="%22Ahn%2C+Bong-Hyun%22">Ahn, Bong-Hyun</searchLink><br /><searchLink fieldCode="AR" term="%22Kumar%2C+Neil+G%2E%22">Kumar, Neil G.</searchLink><br /><searchLink fieldCode="AR" term="%22Rovira%2C+Ilsa+I%2E%22">Rovira, Ilsa I.</searchLink><br /><searchLink fieldCode="AR" term="%22Xu%2C+Xiao-Ling%22">Xu, Xiao-Ling</searchLink><br /><searchLink fieldCode="AR" term="%22van+Lohuizen%2C+Maarten%22">van Lohuizen, Maarten</searchLink><br /><searchLink fieldCode="AR" term="%22Motoyama%2C+Noboru%22">Motoyama, Noboru</searchLink><br /><searchLink fieldCode="AR" term="%22Deng%2C+Chu-Xia%22">Deng, Chu-Xia</searchLink><br /><searchLink fieldCode="AR" term="%22Finkel%2C+Toren%22">Finkel, Toren</searchLink>
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  Data: Mice deficient in the Polycomb repressor Bmi1 develop numerous abnormalities including a severe defect in stem cell self-renewal, alterations in thymocyte maturation and a shortened lifespan. Previous work has implicated de-repression of the Ink4a/Arf (also known as Cdkn2a) locus as mediating many of the aspects of the Bmi1-/- phenotype. Here we demonstrate that cells derived from Bmi1-/- mice also have impaired mitochondrial function, a marked increase in the intracellular levels of reactive oxygen species and subsequent engagement of the DNA damage response pathway. Furthermore, many of the deficiencies normally observed in Bmi1-/- mice improve after either pharmacological treatment with the antioxidant N-acetylcysteine or genetic disruption of the DNA damage response pathway by Chk2 (also known as Chek2) deletion. These results demonstrate that Bmi1 has an unexpected role in maintaining mitochondrial function and redox homeostasis and indicate that the Polycomb family of proteins can coordinately regulate cellular metabolism with stem and progenitor cell function. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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