期刊
DEVELOPMENTAL DYNAMICS
卷 236, 期 8, 页码 2159-2171出版社
WILEY
DOI: 10.1002/dvdy.21233
关键词
xenopus; influenza; M2(H37A); rimantadine; amantadine; conditional; toxic; cell-ablation; death; heart; development; macrophage; myeloid; embryo; transgenesis
资金
- Medical Research Council [MC_U117562103] Funding Source: Medline
- MRC [MC_U117562103] Funding Source: UKRI
- Medical Research Council [MC_U117562103] Funding Source: researchfish
Harnessing toxic proteins to destroy selective cells in an embryo is an attractive method for exploring details of cell fate and cell-cell interdependency. However, no existing suicide gene system has proved suitable for aquatic vertebrates. We use the M2(H37A) toxic ion channel of the influenza-A virus to induce cell-ablations in Xenopus laevis. M2(H37A) RNA injected into blastomeres of early stage embryos causes death of their progeny by late-blastula stages. Moreover, M2(H37A) toxicity can be controlled using the M2 inhibitor rimantadine. We have tested the ablation system using transgenesis to target M2(H37A) expression to selected cells in the embryo. Using the myocardial MLC2 promoter, M2(H37A)-mediated cell death causes dramatic loss of cardiac structure and function by stage 39. With the LURP1. promoter, we induce cell-ablations of macrophages. These experiments demonstrate the effectiveness of M2(H37A)ablation in Xenopus and its utility in monitoring the progression of developmental abnormalities during targeted cell death experiments.
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