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Mol. Cells 2012; 34(2): 127-132

Published online July 24, 2012

https://doi.org/10.1007/s10059-012-2242-0

© The Korean Society for Molecular and Cellular Biology

Expression Profiling Reveals an Unexpected Growth-Stimulating Effect of Surplus Iron on the Yeast Saccharomyces cerevisiae

Yang Du, Wang Cheng, and Wei-Fang Li*

School of Life Sciences, University of Science and Technology of China, People’s Republic of China

Correspondence to : *Correspondence: liwf@ustc.edu.cn

Received: October 31, 2011; Revised: May 20, 2012; Accepted: May 25, 2012

Abstract

Iron homeostasis plays a crucial role in growth and divi-sion of cells in all kingdoms of life. Although yeast iron metabolism has been extensively studied, little is known about the molecular mechanism of response to surplus iron. In this study, expression profiling of Saccharomyces cerevisiae in the presence of surplus iron revealed a dual effect at 1 and 4 h. A cluster of stress-responsive genes was upregulated via activation of the stress-resistance transcription factor Msn4, which indicated the stress effect of surplus iron on yeast metabolism. Genes involved in aerobic metabolism and several anabolic pathways are also upregulated in iron-surplus conditions, which could significantly accelerate yeast growth. This dual effect suggested that surplus iron might participate in a more complex metabolic network, in addition to serving as a stress inducer. These findings contribute to our understanding of the global response of yeast to the fluctuating availability of iron in the environment.

Keywords aerobic metabolism, expression profiling, Msn4, Saccharomyces cerevisiae, stress response

Article

Research Article

Mol. Cells 2012; 34(2): 127-132

Published online August 31, 2012 https://doi.org/10.1007/s10059-012-2242-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Expression Profiling Reveals an Unexpected Growth-Stimulating Effect of Surplus Iron on the Yeast Saccharomyces cerevisiae

Yang Du, Wang Cheng, and Wei-Fang Li*

School of Life Sciences, University of Science and Technology of China, People’s Republic of China

Correspondence to:*Correspondence: liwf@ustc.edu.cn

Received: October 31, 2011; Revised: May 20, 2012; Accepted: May 25, 2012

Abstract

Iron homeostasis plays a crucial role in growth and divi-sion of cells in all kingdoms of life. Although yeast iron metabolism has been extensively studied, little is known about the molecular mechanism of response to surplus iron. In this study, expression profiling of Saccharomyces cerevisiae in the presence of surplus iron revealed a dual effect at 1 and 4 h. A cluster of stress-responsive genes was upregulated via activation of the stress-resistance transcription factor Msn4, which indicated the stress effect of surplus iron on yeast metabolism. Genes involved in aerobic metabolism and several anabolic pathways are also upregulated in iron-surplus conditions, which could significantly accelerate yeast growth. This dual effect suggested that surplus iron might participate in a more complex metabolic network, in addition to serving as a stress inducer. These findings contribute to our understanding of the global response of yeast to the fluctuating availability of iron in the environment.

Keywords: aerobic metabolism, expression profiling, Msn4, Saccharomyces cerevisiae, stress response

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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