The Snail Family Gene Snai3 Is Not Essential for Embryogenesis in Mice

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.

The Snail Family in Normal and Malignant Haematopoiesis

“…Additionally, a profound reduction in the numbers of immature and mature B cells in the bone marrow was observed. This was in striking contrast to the normal B-cell development previously found in the individual Snai2-and Snai3-KO mouse models [Inoue et al, 2002;Perez-Losada et al, 2002;Bradley et al, 2013;Pioli et al, 2013]. The DKO mice also had an increased proportion of neutrophils in the blood, and a concomitant enrichment of macrophages and granulocytes in the spleen.…”

“…Two individual Snai3-KO models have been generated, with no overt haematopoietic abnormalities apparent. It is important to note, however, that stress haematopoiesis was not studied in either of these models [Bradley et al, 2013;Pioli et al, 2013]. In contrast, retroviral-mediated overexpression of Snai3 in bone marrow HSPCs did have a profound effect on both lymphoid and myeloid development [Dahlem et al, 2012].…”

“…Snai2 is expressed in all subsets of haematopoietic stem and progenitor cells (HSPCs), but not in more differentiated blood cells [Inoue et al, 2002;Pioli et al, 2013]. Snai1 has been detected at a low level in mature T, B, and myeloid lineage cells, while Snai3 has been detected primarily in T and B cells [Bradley et al, 2013;Pioli et al, 2013].…”

“…In contrast to Snai1-and Snai2-KO mice, loss of Snai3 had no effect on normal embryonic and adult mouse development [Bradley et al, 2013;Pioli et al, 2013]. Given their strong homology and conservation throughout evolution, it is likely that the different Snail family members can compensate for each other's loss of function.…”

Sub-circuits of a gene regulatory network control a developmental epithelial-mesenchymal transition

“…These transcription factors were then discovered in vertebrates (Sargent and Bennett, 1990;Hopwood et al, 1989) where expanded genomes included families of genes: SNAI1 (Snail, Snail1, Sna), SNAI2 (Snail2, Slug), SNAI3 (Snail3, Smuc), TWIST1 (Twist), TWIST2, ZEB1 (BZP) and ZEB2 (SIP-1). The case of SNAI3 is still slightly ambiguous (Kataoka et al, 2000;Bradley et al, 2013), but these TFs are all considered to be E-cadherin repressors and have been proposed to be the 'master regulators' that are capable of inducing the full EMT program (Zheng and Kang, 2013).…”