Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.

Most organisms are simply diamagnetic, while magnetotactic bacteria and migratory animals are among organisms that exploit magnetism. Biogenic magnetization not only is of fundamental interest, but also has industrial potential. However, the key factor(s) that enable biogenic magnetization in coordi...

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Main Authors: Keiji Nishida, Pamela A Silver
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS Biology
Online Access:http://europepmc.org/articles/PMC3289596?pdf=render
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author Keiji Nishida
Pamela A Silver
author_facet Keiji Nishida
Pamela A Silver
author_sort Keiji Nishida
collection DOAJ
description Most organisms are simply diamagnetic, while magnetotactic bacteria and migratory animals are among organisms that exploit magnetism. Biogenic magnetization not only is of fundamental interest, but also has industrial potential. However, the key factor(s) that enable biogenic magnetization in coordination with other cellular functions and metabolism remain unknown. To address the requirements for induction and the application of synthetic bio-magnetism, we explored the creation of magnetism in a simple model organism. Cell magnetization was first observed by attraction towards a magnet when normally diamagnetic yeast Saccharomyces cerevisiae were grown with ferric citrate. The magnetization was further enhanced by genetic modification of iron homeostasis and introduction of ferritin. The acquired magnetizable properties enabled the cells to be attracted to a magnet, and be trapped by a magnetic column. Superconducting quantum interference device (SQUID) magnetometry confirmed and quantitatively characterized the acquired paramagnetism. Electron microscopy and energy-dispersive X-ray spectroscopy showed electron-dense iron-containing aggregates within the magnetized cells. Magnetization-based screening of gene knockouts identified Tco89p, a component of TORC1 (Target of rapamycin complex 1), as important for magnetization; loss of TCO89 and treatment with rapamycin reduced magnetization in a TCO89-dependent manner. The TCO89 expression level positively correlated with magnetization, enabling inducible magnetization. Several carbon metabolism genes were also shown to affect magnetization. Redox mediators indicated that TCO89 alters the intracellular redox to an oxidized state in a dose-dependent manner. Taken together, we demonstrated that synthetic induction of magnetization is possible and that the key factors are local redox control through carbon metabolism and iron supply.
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spelling doaj.art-87df8cc5de7a49c08097536e777d80fa2022-12-21T22:53:58ZengPublic Library of Science (PLoS)PLoS Biology1544-91731545-78852012-01-01102e100126910.1371/journal.pbio.1001269Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.Keiji NishidaPamela A SilverMost organisms are simply diamagnetic, while magnetotactic bacteria and migratory animals are among organisms that exploit magnetism. Biogenic magnetization not only is of fundamental interest, but also has industrial potential. However, the key factor(s) that enable biogenic magnetization in coordination with other cellular functions and metabolism remain unknown. To address the requirements for induction and the application of synthetic bio-magnetism, we explored the creation of magnetism in a simple model organism. Cell magnetization was first observed by attraction towards a magnet when normally diamagnetic yeast Saccharomyces cerevisiae were grown with ferric citrate. The magnetization was further enhanced by genetic modification of iron homeostasis and introduction of ferritin. The acquired magnetizable properties enabled the cells to be attracted to a magnet, and be trapped by a magnetic column. Superconducting quantum interference device (SQUID) magnetometry confirmed and quantitatively characterized the acquired paramagnetism. Electron microscopy and energy-dispersive X-ray spectroscopy showed electron-dense iron-containing aggregates within the magnetized cells. Magnetization-based screening of gene knockouts identified Tco89p, a component of TORC1 (Target of rapamycin complex 1), as important for magnetization; loss of TCO89 and treatment with rapamycin reduced magnetization in a TCO89-dependent manner. The TCO89 expression level positively correlated with magnetization, enabling inducible magnetization. Several carbon metabolism genes were also shown to affect magnetization. Redox mediators indicated that TCO89 alters the intracellular redox to an oxidized state in a dose-dependent manner. Taken together, we demonstrated that synthetic induction of magnetization is possible and that the key factors are local redox control through carbon metabolism and iron supply.http://europepmc.org/articles/PMC3289596?pdf=render
spellingShingle Keiji Nishida
Pamela A Silver
Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.
PLoS Biology
title Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.
title_full Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.
title_fullStr Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.
title_full_unstemmed Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.
title_short Induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway.
title_sort induction of biogenic magnetization and redox control by a component of the target of rapamycin complex 1 signaling pathway
url http://europepmc.org/articles/PMC3289596?pdf=render
work_keys_str_mv AT keijinishida inductionofbiogenicmagnetizationandredoxcontrolbyacomponentofthetargetofrapamycincomplex1signalingpathway
AT pamelaasilver inductionofbiogenicmagnetizationandredoxcontrolbyacomponentofthetargetofrapamycincomplex1signalingpathway