β-adrenergic receptor regulates embryonic epithelial extensibility through actomyosin inhibition

Yohei Mizoguchi; Kaoru Nakashima; Ayato Sato; Asako Shindo

doi:10.1016/j.isci.2023.108469

β-adrenergic receptor regulates embryonic epithelial extensibility through actomyosin inhibition

iScience. 2023 Nov 15;26(12):108469. doi: 10.1016/j.isci.2023.108469. eCollection 2023 Dec 15.

Authors

Yohei Mizoguchi¹, Kaoru Nakashima², Ayato Sato³, Asako Shindo²

Affiliations

¹ Division of Biological Sciences, Department of Molecular Biology, Nagoya University Graduate School of Science, Nagoya 464-8602, Japan.
² Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto 860-0811, Japan.
³ Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Nagoya 464-8601, Japan.

Abstract

During morphogenesis, epithelial tissues reshape and expand to cover the body and organs. The molecular mechanisms of this deformability remain elusive. Here, we investigate the role of the β-adrenergic receptor (ADRB) in orchestrating actomyosin contractility, pivotal for epithelial extensibility. Chemical screens on Xenopus laevis embryos pinpointed ADRB2 as a principal regulator. ADRB2 promotes actomyosin relaxation, facilitating apical cell area expansion during body elongation. In contrast, ADRB2 knockdown results in heightened cell contraction, marked by synchronous oscillation of F-actin and myosin, impeding body elongation. ADRB2 mutants with reduced affinity for ligand binding lack the function to induce cellular relaxation, highlighting the ligand's essential roles even in the developing epidermis. Our findings unveil ADRB2's critical contribution to extensibility of the epidermis and subsequent body elongation during development. This study also offers insights into the physiology of mature epithelial organs deformed by the smooth muscle response to the adrenergic autonomic nervous system.

Keywords: Bioengineering; Tissue engineering.