Toraason Katrina, Johnson Nathan, Guernsey Jenna, Laughon Allen
Undergraduate Program in Genetics, University of Wisconsin-Madison, Madison, Wisconsin, United States.
Department of Genetics, Department of Medical Genetics, University of Wisconsin-Madison, Madison, Wisconsin, United States.
MicroPubl Biol. 2024 Jan 26;2024. doi: 10.17912/micropub.biology.001066. eCollection 2024.
The Smad-interacting co-factor, Schnurri (Shn) confers transcriptional repression in response to Decapentaplegic (Dpp) signaling. Shn zinc fingers 6-8 mediate this Smad interaction but are lacking in vertebrate Shn homologs. In contrast, the vertebrate-conserved zinc finger 1,2 and 4,5 pairs have been reported to engage in Smad-mediated transcriptional activation in fly and vertebrate systems, and to contribute to Dpp-dependent tissue repair in the fly retina. We report that mutation of zinc coordination residues within vertebrate-conserved Shn zinc finger pairs 1,2 and 4,5 results in ectopic venation that is sensitive to Dpp signaling.
与Smad相互作用的辅助因子施努里(Shn)在响应Decapentaplegic(Dpp)信号时赋予转录抑制作用。Shn锌指6 - 8介导这种Smad相互作用,但在脊椎动物Shn同源物中不存在。相比之下,脊椎动物保守的锌指1、2和4、5对已被报道在果蝇和脊椎动物系统中参与Smad介导的转录激活,并有助于果蝇视网膜中Dpp依赖的组织修复。我们报告称,脊椎动物保守的Shn锌指对1、2和4、5内锌配位残基的突变导致对Dpp信号敏感的异位脉管形成。