Abstract
The Snail gene family encodes zinc finger-containing transcriptional repressor proteins. Three members of the Snail gene family have been described in mammals, encoded by the Snai1, Snai2, and Snai3 genes. The function of the Snai1 and Snai2 genes have been studied extensively during both vertebrate embryogenesis and tumor progression and metastasis, and play critically important roles during these processes. However, little is known about the function of the Snai3 gene and protein. We describe here generation and analysis of Snai3 conditional and null mutant mice. We also generated an EYFP-tagged Snai3 null allele that accurately reflects endogenous Snai3 gene expression, with the highest levels of expression detected in thymus and skeletal muscle. Snai3 null mutant homozygous mice are viable and fertile, and exhibit no obvious phenotypic defects. These results demonstrate that Snai3 gene function is not essential for embryogenesis in mice.
Highlights
The Snail gene family encodes zinc finger proteins that function primarily as transcriptional repressors [1,2]
Generation of Snai3flox, Snai3null, and Snai3-EYFP Mice In order to assess whether the Snai3 gene plays an essential in vivo role in mice, we created three Snai3 targeted mutant alleles: a Snai3flox allele for conditional Snai3 gene inactivation (Fig. 1A), a Snai3null allele, and a Snai3-EYFP knock-in allele that is a Snai3 null allele (Fig. 1B)
The Snai3null allele was generated by Cre recombinase-mediated deletion of the Snai3flox allele, which results in deletion of Snai3 promoter sequences and the first exon of the Snai3 gene
Summary
The Snail gene family encodes zinc finger proteins that function primarily as transcriptional repressors [1,2]. The SNAI1 and SNAI2 proteins are key regulators of the epithelialmesenchymal transition, directly repressing transcription of genes encoding components of cell-cell adhesive complexes in epithelia. A recent study utilized ChIP-Seq and gene expression analyses to demonstrate that a Snai1-HDAC1/2 repressive complex bound and excluded the myogenic transcription factor MyoD from its targets [5]. These authors further showed that a regulatory network involving myogenic regulatory factors, Snai1/2, and the microRNAs miR30a and miR-206 acted as a molecular switch controlling entry into myogenic differentiation
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