Twist3 is required for dedifferentiation during extraocular muscle regeneration in adult zebrafish

被引：5

作者：

Zhao, Yi ^{[1
]}

Louie, Ke'ale W. ^{[2
]}

Tingle, Christina F. ^{[1
]}

Sha, Cuilee ^{[1
]}

Heisel, Curtis J. ^{[1
]}

Unsworth, Shelby P. ^{[1
]}

Kish, Phillip E. ^{[1
]}

Kahana, Alon ^{[1
]}

机构：

[1] Univ Michigan, Kellogg Eye Ctr, Dept Ophthalmol & Visual Sci, Ann Arbor, MI 48109 USA

[2] Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA

来源：

PLOS ONE | 2020年 / 15卷 / 04期

关键词：

RETINOIC ACID; GENE-TRANSFER; EXPRESSION; CELLS; ELECTROPORATION; ROLES; FGF; PROTEIN; TISSUE; MODEL;

D O I：

10.1371/journal.pone.0231963

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Severely damaged adult zebrafish extraocular muscles (EOMs) regenerate through dedifferentiation of residual myocytes involving a muscle-to-mesenchyme transition. Members of the Twist family of basic helix-loop-helix transcription factors (TFs) are key regulators of the epithelial-mesenchymal transition (EMT) and are also involved in craniofacial development in humans and animal models. During zebrafish embryogenesis, twist family members (twist1a, twist1b, twist2, and twist3) function to regulate craniofacial skeletal development. Because of their roles as master regulators of stem cell biology, we hypothesized that twist TFs regulate adult EOM repair and regeneration. In this study, utilizing an adult zebrafish EOM regeneration model, we demonstrate that inhibiting twist3 function using translationblocking morpholino oligonucleotides (MOs) impairs muscle regeneration by reducing myocyte dedifferentiation and proliferation in the regenerating muscle. This supports our hypothesis that twist TFs are involved in the early steps of dedifferentiation and highlights the importance of twist3 during EOM regeneration.

引用

页数：15

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