Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 1 May 2007
Vol. 2007, Issue 384, p. tw153
[DOI: 10.1126/stke.3842007tw153]

EDITORS' CHOICE

Molecular Biology The Heart of Stress Responses

Beverly Purnell

Science, AAAS, Washington, DC 20005, USA

Two myosin heavy chain (MHC) genes are expressed in opposing manners in the mouse heart; betaMHC is expressed embryonically, whereas {alpha}MHC is up-regulated postnatally. Cardiac stress shifts this ratio toward betaMHC with negative effects on cardiac function, and previous work has identified microRNAs (miRNAs) as possible regulators of cardiac growth and function. Van Rooij et al. now show that miR-208, which is encoded by an intron of the {alpha}MHC gene, is a cardiac-specific regulator of betaMHC expression in response to stress and hypothyroidism in the heart. Deletion of the coding region of miR-208 resulted in inhibition of betaMHC expression and a reduced stress response in the heart. Thus, miR-208 may act through thyroid signaling to regulate betaMHC expression, possibly by repressing expression of the thyroid receptor coregulator THRAP1.

E. van Rooij, L. B. Sutherland, X. Qi, J. A. Richardson, J. Hill, E. N. Olson, Control of stress-dependent cardiac growth and gene expression by a microRNA. Science 316, 575-579 (2007). [Abstract] [Full Text]

Citation: B. Purnell, The Heart of Stress Responses. Sci. STKE 2007, tw153 (2007).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882