TAZ couples Hippo/Wnt signalling and insulin sensitivity through Irs1 expression

Jun-Ha Hwang, A Rum Kim, Kyung Min Kim, Jung Park, Ho Taek Oh, Sung A Moon, Mi Ran Byun, Hana Jeong, Hyo Kyung Kim, Michael B. Yaffe, Eun Sook Hwang () and Jeong-Ho Hong ()
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Jun-Ha Hwang: Korea University
A Rum Kim: Korea University
Kyung Min Kim: Korea University
Jung Park: Korea University
Ho Taek Oh: Korea University
Sung A Moon: Korea University
Mi Ran Byun: Korea University
Hana Jeong: Ewha Womans University
Hyo Kyung Kim: Ewha Womans University
Michael B. Yaffe: Massachusetts Institute of Technology
Eun Sook Hwang: Ewha Womans University
Jeong-Ho Hong: Korea University

Nature Communications, 2019, vol. 10, issue 1, 1-11

Abstract: Abstract Insulin regulates blood glucose levels by binding its receptor and stimulating downstream proteins through the insulin receptor substrate (IRS). Impaired insulin signalling leads to metabolic syndrome, but the regulation of this process is not well understood. Here, we describe a novel insulin signalling regulatory pathway involving TAZ. TAZ upregulates IRS1 and stimulates Akt- and Glut4-mediated glucose uptake in muscle cells. Muscle-specific TAZ-knockout mice shows significantly decreased Irs1 expression and insulin sensitivity. Furthermore, TAZ is required for Wnt signalling-induced Irs1 expression, as observed by decreased Irs1 expression and insulin sensitivity in muscle-specific APC- and TAZ-double-knockout mice. TAZ physically interacts with c-Jun and Tead4 to induce Irs1 transcription. Finally, statin administration decreases TAZ, IRS1 level and insulin sensitivity. However, in myoblasts, the statin-mediated decrease in insulin sensitivity is counteracted by the expression of a constitutively active TAZ mutant. These results suggest that TAZ is a novel insulin signalling activator that increases insulin sensitivity and couples Hippo/Wnt signalling and insulin sensitivity.

Date: 2019
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DOI: 10.1038/s41467-019-08287-x

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